Operative Techniques in Laryngology

Clark A. Rosen, C. Blake Simpson Operative Techniques in Laryngology

Clark A. Rosen C. Blake Simpson

Operative Techniques in Laryngology Forewords by Hans von Leden and Robert H. Ossoff

With 390 Figures and 11 Tables

123

Clark A. Rosen, M.D.

C. Blake Simpson, M.D.

University of Pittsburgh Voice Center UPMC Mercy Hospital 1400 Locust Street, 2100 Bldg D Pittsburgh, PA 15219, USA E-mail: [email protected]

The University of Texas Health Science Center Department of Otolaryngology 7703 Floyd Curl Drive MC-7777 San Antonio, TX 78229-390, USA E-mail: [email protected]

ISBN  978-3-540-25806-3     e-ISBN  978-3-540-68107-6 Library of Congress Control Number: 2008926220 © 2008 Springer-Verlag Berlin Heidelberg This work is subject to copyright. All rights are reserved, whether the whole or part of the material is concerned, specifically the rights of translation, reprinting, reuse of illustrations, recitation, broadcasting, reproduction on microfilm or in any other way, and storage in data banks. Duplication of this publication or parts thereof is permitted only under the provisions of the German Copyright Law of September 9, 1965, in its current version, and permission for use must always be obtained from Springer Verlag. Violations are liable to prosecution under the German Copyright Law. The use of general descriptive names, registered names, trademarks, etc. in this publication does not imply, even in the absence of a specific statement, that such names are exempt from the relevant protective laws and regulations and therefore free for general use. Product liability: The publishers cannot guarantee the accuracy of any information about dosage and application contained in this book. In every individual case the user must check such information by consulting the relevant literature. Cover design: eStudio Calamar, Spain Production: le-tex publishing services oHG, Leipzig Printed on acid-free paper 987654321 springer.com

 



Dedication

I have had the incredible good fortune to be blessed with supportive family, teachers, and friends. It is imperative that I recognize the huge impact of some of these individuals on my personal and professional development and growth. I would like to dedicate this book to my parents, Paul Jack Rosen, M.D., and Shirley Maureen Orr Rosen, who worked tirelessly to provide the optimal growth environment for me and instill in me the best possible work ethic. Over my many years of education, I have had many wonderful teachers. However, one has had the greatest impact, not only on my knowledge base, but also on my approach to learning, teaching, and academic life. I would like to thank Jamie Cohen, M.D., Ph.D., for being an outstanding role model, mentor, and friend. Eugene N. Myers, M.D. has been vital to me from a professional and career development perspective, for providing me the opportunity to achieve my dreams and goals. Without his support, this book would not have been possible. I would like to acknowledge the primal role of Blake Simpson, M.D., in the development of this book from con-

cept to completion. I have grown as a laryngologist due to our “mind meld” of laryngologic experience and philosophy while writing this book together. I am indebted to the wonderful group of teachers and colleagues with whom I have had the pleasure and privilege to work: Gayle Woodson, M.D.; Thomas Murry, Ph.D.; Robert Buckmire, M.D.; Lori Lombard, Ph.D.; and Jackie GartnerSchmidt, Ph.D. I would like to acknowledge the importance of my Fellows and OR staff, without whom many of the concepts in this book would not exist: AT, TK, PK, MJB, AF, TC, SR, SO, NS, CP, MB, Icarus, and MLL. Lastly and most importantly, I dedicate this book to Monica Anne Linde, without whose support, energy and love, none of my professional success would have been possible. Sincerely and with deepest gratitude, Clark A. Rosen M.D. Pittsburgh, Pennsylvania March 2008

 



Dedication

This work is dedicated to my wife, Cristina, and my twin daughters, Juliana and Audrey. I am eternally grateful for all the love and support you have given me. C. Blake Simpson, M.D. San Antonio, Texas March 2008

 



Foreword

In this age of communication, the care of the human voice and the vocal organ has assumed greater and greater importance. The maintenance of good vocal health and the treatment of the diseased larynx are essential for all members of society—from heads of state to the receptionist with the golden voice on the telephone. The necessity for the restoration of pathologic changes in the larynx has resulted in the application of numerous operative techniques, which may bewilder the clinician. There is a real need for a comprehensive educational resource like Operative Techniques in Laryngology. The two authors of this textbook, Clark A. Rosen and C. Blake Simpson, both leading scholars and experienced surgeons at major medical centers, have created a superb treatise, which expertly details the surgical care of different laryngeal pathologies. The introductory chapters call attention to the current methods of clinical evaluation for laryngeal disorders, including videostroboscopy and flexible laryngoscopy, as well as the medical treatment of patients with vocal problems. The indicated preoperative measures are discussed in detail, and the importance of anesthesia and airway management during surgical procedures within the larynx are stressed. Subsequent chapters advance the reader from the fundamental principals of laryngeal surgery to such major surgical techniques as phonomicrosurgery, laser surgery, vocal fold augmentation, and surgery of the laryngeal framework. In successive chapters, each pathologic entity is presented in detail, including the etiology, history, vocal quality, physical examination, surgical intervention, postoperative care, and potential complications. Specific microsurgical procedures are

recommended for all common benign lesions and for localized neoplasms of the vocal folds. The use of lasers is described for stenosis of the vocal folds and circumscribed malignant lesions. The chapters on vocal fold augmentation include precise information on injection techniques via microlaryngoscopy, as well as peroral and percutaneous approaches. Specific chapters are devoted to the principles of operative care for laryngeal framework surgery. These procedures range medialization laryngoplasty or arytenoid adduction to problems more complex such as cricothyroid subluxation, laryngeal fractures, sulcus vocalis, and stenosis of the larynx and trachea. The reader will be impressed with the clarity of the presentations, which is enhanced by the use of systematic headings, and by the precision and the rich color of the illustrations within each chapter. An abundance of carefully selected references enables the prospective surgeon to pursue further detailed information from various experts as desired. It is apparent that the authors and the publisher have combined their expertise to present an outstanding educational and inspirational textbook for both the clinical otorhinolaryngologist as well as the experienced laryngeal surgeon. I shall cherish my own copy of this exciting edition. Hans von Leden, M.D., Sc.D. Professor Emeritus University of Southern California Los Angeles, California February 2008

 



Foreword

The subspecialty of laryngology has gone through a tremendous period of growth and maturation during the past 20 years. Fellowships dedicated to advanced training in laryngology, neurolaryngology, and voice care are now available at several academic health centers and private practices. Furthermore, it is now very common to find at least one fellowship-trained laryngologist on the full-time faculty of many of our resident education programs in otolaryngology–head and neck surgery in the United States and Canada. The quality of resident education, patient care, and laryngology-related research has improved because of the advances in this subspecialty promoted by this growing critical mass of individuals who have completed fellowships in laryngology and voice care after their formal residency training in otolaryngology. Now, the cycle has come full circle, with several of the earlier fellowship-trained laryngologists directing laryngology fellowship training programs of their own. Drs. Blake Simpson and Clark Rosen are excellent examples of this training model. Blake spent a year at Vanderbilt in fellowship with me and my colleagues, and Clark spent a year of fellowship training at the University of Tennessee with Dr. Gayle Woodson. Now, both Blake and Clark direct fellowship training programs at their respective institutions. Operative Techniques in Laryngology fills a real void in the field of laryngology and voice care. Drs. Simpson and Rosen present us with a surgical atlas dedicated to and highlighting modern techniques for microlaryngeal surgery and laryngeal framework surgery. They have selected an outstanding group of experts in the field to whose contributions include not only

the step-by-step surgical approach to the many problems covered in the atlas, but also addressing the important medical information associated with the various conditions requiring the surgical procedures highlighted in this book. The quality of the illustrations are excellent, and the reader will feel very confident using this atlas as a primary reference for managing appropriate cases in the operating theatre. This atlas represents a major contribution to our laryngology literature, and it should find its way to the office of all laryngologists, laryngology fellows, resident education program libraries, and many community-based otolaryngologist–head and neck surgeons who perform a moderated volume of laryngeal surgery in their practices. I am very proud of Blake and Clark for realizing the vision of the growing need for an atlas of surgical techniques in laryngology. I am honored to have had the opportunity to serve as Blake’s fellowship mentor and to have had Clark spend a visiting fellow week at Vanderbilt during his fellowship year with Dr. Woodson. I am further honored to be asked by Blake and Clark to write this foreword to their excellent and very important book. Robert H. Ossoff, D.M.D., M.D. Guy M. Maness Professor and Chairman Department of Otolaryngology Vanderbilt University Medical Center Nashville, Tennessee March 2008

 



Preface

The field of laryngeal surgery for voice and airway pathologic conditions has dramatically changed over the last 20 years, and the impetus for this book was to reflect these major paradigm shifts, and bring together in one place essential information on the rapidly growing and changing field of laryngeal surgery. The book was written to provide the laryngeal surgeon with: (1) essential background information in voice disorders, (2) step-by-step surgical information for laryngeal surgery, and (3) key pearls and pitfalls about indications, surgical steps, and postoperative management of laryngeal surgeries. The book provides essential “background” information of which any laryngeal surgeon must have mastery. We feel strongly that a true surgeon is a physician first, and must always approach each patient in a holistic manner, and thus understand the essential anatomy and pathology of voice disorders, as well as the nonsurgical treatment modalities. This supports the concept of vocal medicine, not just vocal surgery. Once surgery has been chosen as a treatment modality, the surgeon must carefully consider timing, planning, anesthesia, and airway considerations. These important issues are reviewed in Chaps. 8 and 9. The book encompasses a wide range of laryngeal procedures, and it has been organized around the broad categories of phonomicrosurgery and laryngeal framework surgery. Within phonomicrosurgery, detailed information is provided regarding surgery for benign and malignant vocal fold lesions, vocal fold augmentation, and laser laryngeal surgery. The laryngeal framework surgery sections include essential chapters on “open” treatment for unilateral vocal fold paralysis, bilateral vocal fold paralysis, laryngeal trauma, airway stenosis (glottic, subglottic and tracheal), and vocal fold scar/sulcus vocalis.

All the chapters have been designed to allow the reader to understand indications, contraindications, equipment required, step-by-step aspects of the procedure, perioperative care, and management of complications. In almost every chapter, one will find important insights or pearls that, until now, have only been taught verbally by mentor to student. We feel that this book will become essential reading for all students of laryngology, and general otolaryngologists performing laryngeal surgery. We have written each chapter of this book; however, for selected chapters, we have been honored to have leaders in our field with whom we collaborated. We would like to thank all of these truly gifted surgeons for sharing their knowledge and expertise. This surgical atlas is richly illustrated with detailed, colorful artwork as well as essential photographic documentation. This book would not have been possible without the hard work and phenomenal talent of the medical illustration team at the University of Texas Health Science Center, San Antonio. We would like to personally thank these gifted and insightful individuals: David Baker, David Aten, and Chris McKee. In closing, we feel that this book brings together a wide variety of new and exciting surgical procedures involving the larynx and upper airway. We would like to thank our supporting staff of Diane Keane and Veronica Aleman, as well as Springer for valuable support from their staff, including Marion M. Philipp and Irmela Bohn. Clark A. Rosen, M.D. C. Blake Simpson, M.D.

 



Acknowledgements

The authors wish to thank the following individuals for their important contributions to the book: Kristin J. Otto, M.D., Chap. 1 Phillip Song, M.D., Chap. 2 Scott M. Green, Chap. 13 Paolo Pontez, M.D., Chap. 23 Robert Eller, M.D., Chap. 25 J. Michael King, M.D., Chap. 34 S. Carter Wright, Jr., M.D., Chap. 39 Each one of these individuals contributed a portion of the chapter’s contents or supplied the initial draft prior to editing. The authors would like to thank the superb team of medical illustrators at the University of Texas Health Science Center, San Antonio: David Baker David Aten Chris McKee

These individuals worked closely with the authors over a fouryear period during the writing of this book. The illustrators went the extra mile, studying cadaveric specimens, attending surgical procedures, and reviewing surgical photos from multiple perspectives. Their mastery of laryngeal anatomy and the surgical perspectives of laryngeal surgery are without peer. Their efforts ultimately resulted in, we believe, the highest quality laryngeal surgical illustrations to date. The authors wish to express thanks to the following companies for their financial support in the making of this book: Olympus Surgical Medtronic ENT Kay Pentax Karl Storz Endoscopy America Salary support for the medical illustrators was significantly funded though generous donations from these corporations. Without their support, this book would not have been possible.

 



Contents

Part A Clinical Evaluation of Laryngeal Disorders 1 1.1 1.1.1 1.1.1.1 1.1.1.2 1.1.1.3 1.1.1.4 1.1.1.5 1.1.2 1.1.2.1 1.1.2.2 1.1.3 1.1.3.1 1.1.3.2 1.1.4 1.1.4.1 1.1.4.2 1.1.5 1.1.6 1.1.7 1.2 1.2.1 1.2.1.1

2 2.1 2.2 2.3 2.4 2.5 2.6 2.7 2.8 2.9 2.10 2.11 2.12

Anatomy and Physiology of the Larynx  . . . . . . . Anatomy  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Laryngeal Cartilages  . . . . . . . . . . . . . . . . . . . . . . . . Thyroid  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Cricoid  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Arytenoid   . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Accessory Cartilages: Cuneiform and Corniculate  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Epiglottis  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Laryngeal Joints  . . . . . . . . . . . . . . . . . . . . . . . . . . . . Cricothyroid Joint  . . . . . . . . . . . . . . . . . . . . . . . . . . Cricoarytenoid Joint  . . . . . . . . . . . . . . . . . . . . . . . . Laryngeal Musculature  . . . . . . . . . . . . . . . . . . . . . . Intrinsic Laryngeal Muscles  . . . . . . . . . . . . . . . . . . Extrinsic Laryngeal Muscles  . . . . . . . . . . . . . . . . . Fibroelastic Tissue of the Larynx  . . . . . . . . . . . . . Quadrangular Membrane  . . . . . . . . . . . . . . . . . . . Conus Elasticus  . . . . . . . . . . . . . . . . . . . . . . . . . . . . Microanatomy of the Vocal Fold  . . . . . . . . . . . . . . Vasculature  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Innervation  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Physiology  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Major Laryngeal Functions: Lower Airway Protection, Respiration, and Phonation  . . . . . . . . Phonation  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Key Points  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Selected Bibliography  . . . . . . . . . . . . . . . . . . . . . . .

3  3  3  3  3  3  3  3  4  4  4  4  4  4  5  5  5  5  6  6  6  7  7  7  8  8

Principles of Clinical Evaluation for Voice Disorders  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   9 Fundamental and Related Chapters  . . . . . . . . . . .   9 Introduction  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   9 Gathering a Patient History  . . . . . . . . . . . . . . . . . .   9 History of Present Illness  . . . . . . . . . . . . . . . . . . . .   9 Past Medical History  . . . . . . . . . . . . . . . . . . . . . . . .   10 Past Surgical History  . . . . . . . . . . . . . . . . . . . . . . . .   11 Social History  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   11 Occupational History  . . . . . . . . . . . . . . . . . . . . . . .   11 Listening to the Voice  . . . . . . . . . . . . . . . . . . . . . . .   11 Perceptual Analysis  . . . . . . . . . . . . . . . . . . . . . . . . .   12 Quality-of-Life Questionnaires  . . . . . . . . . . . . . . .   12 Professional Speaking/Singing Voice  . . . . . . . . . .   12 Key Points  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   14 Selected Bibliography  . . . . . . . . . . . . . . . . . . . . . . .   14

3.1 3.2 3.3 3.4 3.4.1 3.4.2 3.4.3 3.4.4 3.5

4 4.1 4.2 4.3 4.3.1 4.3.2 4.3.3 4.3.4 4.4 4.4.1 4.4.2 4.4.3 4.4.4 4.4.5 4.4.6 4.4.7 4.4.8 4.4.9 4.5 4.5.1 4.5.2 4.5.3 4.5.4 4.5.5

Videostroboscopy and Dynamic Voice Evaluation with Flexible Laryngoscopy  . . . . . . .   17 Fundamental and Related Chapters  . . . . . . . . . . .   17 Introduction  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   17 Surgical Indications and Contraindications  . . . .   17 Dynamic Voice Assessment with Flexible Laryngoscopy  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   18 Nasopharynx  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   19 Base of Tongue  . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   19 Larynx (Global)  . . . . . . . . . . . . . . . . . . . . . . . . . . . .   19 Vocal Fold (Focal)  . . . . . . . . . . . . . . . . . . . . . . . . . .   19 Recording of Laryngeal Examination  . . . . . . . . . .   19 Key Points  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   20 Selected Bibliography  . . . . . . . . . . . . . . . . . . . . . . .   20 Pathological Conditions of the Vocal Fold  . . . . .   21 Fundamental and Related Chapters  . . . . . . . . . . .   21 Introduction  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   21 Epithelial Pathology of the Vocal Folds  . . . . . . . .   21 Recurrent Respiratory Papillomatosis of the Larynx   . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   21 Leukoplakia of the Vocal Fold  . . . . . . . . . . . . . . . .   21 Dysplasia–Carcinoma in Situ of the Vocal Folds  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   22 Carcinoma of the Vocal Fold  . . . . . . . . . . . . . . . . .   22 Benign Diseases of the Vocal Fold Lamina Propria  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   23 Overview of Midmembranous Vocal Fold Lesions  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   23 Approach to Midmembranous Vocal Fold Lesions  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   23 Vocal Fold Nodules  . . . . . . . . . . . . . . . . . . . . . . . . .   23 Vocal Fold Cyst (Subepithelial)  . . . . . . . . . . . . . . .   23 Vocal Fold Cyst (Ligament)  . . . . . . . . . . . . . . . . . .   24 Vocal Fold Polyp  . . . . . . . . . . . . . . . . . . . . . . . . . . .   24 Fibrous Mass (Subepithelial)  . . . . . . . . . . . . . . . . .   24 Fibrous Mass (Ligament)  . . . . . . . . . . . . . . . . . . . .   24 Reactive Lesion  . . . . . . . . . . . . . . . . . . . . . . . . . . . .   25 Miscellaneous Disorders of the Vocal Fold  . . . . .   25 Polypoid Corditis (Reinke’s Edema)  . . . . . . . . . . .   25 Vocal Fold Granuloma  . . . . . . . . . . . . . . . . . . . . . .   25 Rheumatologic Lesions of the Vocal Folds  . . . . .   26 Vascular Lesions of the Vocal Folds  . . . . . . . . . . .   26 Vocal Fold Scar and Sulcus Vocalis  . . . . . . . . . . . .   27 Key Points  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   27 Selected Bibliography  . . . . . . . . . . . . . . . . . . . . . . .   27

XVIII

Contents

5 5.1 5.2 5.2.1 5.3 5.3.1 5.4 5.4.1 5.4.2 5.5 5.5.1 5.5.2 5.6 5.7 5.7.1 5.7.2 5.7.3 5.7.4 5.7.5 5.8 5.8.1 5.8.2 5.8.3

Glottic Insufficiency: Vocal Fold Paralysis, Paresis, and Atrophy  . . . . . . . . . . . . . . . . . . . . . . .   29 Introduction  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   29 Unilateral Vocal Fold Paralysis  . . . . . . . . . . . . . . .   29 Etiology  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   29 Surgical Indications and Contraindications  . . . .   30 Vocal Quality and Swallowing  . . . . . . . . . . . . . . . .   30 Unilateral Vocal Fold Paralysis: Physical Examination  . . . . . . . . . . . . . . . . . . . . . . .   31 General  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   31 Laryngeal  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   31 Unilateral Vocal Fold Paralysis: Workup  . . . . . . .   32 Serology  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   32 Imaging Studies  . . . . . . . . . . . . . . . . . . . . . . . . . . . .   32 Unilateral Vocal Fold Paralysis: Treatment  . . . . .   32 Unilateral/Bilateral Vocal Fold Paresis  . . . . . . . . .   33 Etiology  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   33 History  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   33 Physical Examination  . . . . . . . . . . . . . . . . . . . . . . .   33 Diagnostic Workup   . . . . . . . . . . . . . . . . . . . . . . . .   33 Treatment  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   33 Presbylaryngis/Age-Related Changes in the Larynx  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   34 General Considerations  . . . . . . . . . . . . . . . . . . . . .   34 Etiology, History, and Physical Findings  . . . . . . .   34 Workup  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   34 Key Points  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   34 Selected Bibliography  . . . . . . . . . . . . . . . . . . . . . . .   35

Glottic and Subglottic Stenosis: Evaluation and Surgical Planning  . . . . . . . . . . . . . . . . . . . . . .   37 6.1 Fundamental and Related Chapters  . . . . . . . . . . .   37 6.2 Introduction  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   37 6.3 Etiology of Glottic and Subglottic (Laryngotracheal) Narrowing  . . . . . . . . . . . . . . . .   37 6.3.1 Common Clinical Conditions and Associated Risk Factors  . . . . . . . . . . . . . . . . . .   37 6.4 Glottic and Subglottic Stenosis: History  . . . . . . . .   38 6.4.1 Symptoms/Time Course  . . . . . . . . . . . . . . . . . . . . .   38 6.4.2 Medical Comorbidities  . . . . . . . . . . . . . . . . . . . . . .   38 6.5 Glottic and Subglottic Stenosis: Physical Examination  . . . . . . . . . . . . . . . . . . . . . . .   38 6.5.1 Local Anesthesia Techniques for Examination  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   38 6.5.2 Documentation of Examination  . . . . . . . . . . . . . .   38 6.5.2.1 Flexible Laryngoscopy/Tracheoscopy Protocol  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   39 6.6 Additional Studies for the Evaluation of Glottic/Subglottic Stenosis  . . . . . . . . . . . . . . . . .   40 6.6.1 Voice Evaluation (VHI-10, Audio Recording)   . . . . . . . . . . . . . . . . .   40 6.6.2 Air-Flow Measures  . . . . . . . . . . . . . . . . . . . . . . . . .   40 6.6.3 Radiographic Studies  . . . . . . . . . . . . . . . . . . . . . . .   40 6.6.4 Laboratory Testing  . . . . . . . . . . . . . . . . . . . . . . . . .   40 6.7 Glottic and Subglottic Stenosis: Surgical Planning  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   41 6.7.1 Corrective Surgical Procedures for Glottic/ Subglottic Stenosis   . . . . . . . . . . . . . . . . . . . . . . . . .   41

 

6.7.2 6.7.3 6.7.4

Criteria for Endoscopic Treatment for Subglottic Stenosis  . . . . . . . . . . . . . . . . . . . . . . .   41 Criteria for T-Tube Stenting for Subglottic Stenosis  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   42 Criteria for External Treatment of Glottic/ Subglottic Stenosis  . . . . . . . . . . . . . . . . . . . . . . . . . .   42 Key Points  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   42 Selected Bibliography  . . . . . . . . . . . . . . . . . . . . . . .   42

7 7.1 7.2 7.3 7.4 7.5 7.6 7.6.1 7.6.2 7.6.3 7.6.4 7.6.5 7.6.6 7.7 7.8 7.9 7.10

Nonsurgical Treatment of Voice Disorders  . . . .   43 Fundamental and Related Chapters  . . . . . . . . . . .   43 Introduction  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   43 Surgical Indications and Contraindications  . . . .   43 Vocal Fold Granuloma  . . . . . . . . . . . . . . . . . . . . . .   43 Infectious and Inflammatory Disorders  . . . . . . . .   44 Neurologic Disorders  . . . . . . . . . . . . . . . . . . . . . . .   45 Spasmodic Dysphonia  . . . . . . . . . . . . . . . . . . . . . .   45 Essential Tremor  . . . . . . . . . . . . . . . . . . . . . . . . . . .   45 Parkinson’s Disease  . . . . . . . . . . . . . . . . . . . . . . . . .   45 Muscle Tension Dysphonia  . . . . . . . . . . . . . . . . . .   45 Paradoxical Vocal Fold Motion Disorder   . . . . . .   46 Postviral Vagal Neuropathy  . . . . . . . . . . . . . . . . . .   46 Allergy and Voice Disorders  . . . . . . . . . . . . . . . . .   46 Medications and Their Effects on Voice  . . . . . . . .   46 Vocal Hygiene   . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   47 Role of the Speech–Language Pathologist in Voice Therapy  . . . . . . . . . . . . . . . . . . . . . . . . . . .   47 Key Points  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   48 Selected Bibliography  . . . . . . . . . . . . . . . . . . . . . . .   48

8

Timing, Planning, and Decision Making in Phonosurgery  . . . . . . . . . . . . . . . . . . . . . . . . . . .   49 Fundamental and Related Chapters  . . . . . . . . . . .   49 Key Components to Successful Care of Patients with Voice Disorders  . . . . . . . . . . . . . .   49 Surgical Indications and Contraindications  . . . .   49 Timing of Phonomicrosurgery  . . . . . . . . . . . . . . .   49 Preoperative Considerations for Phonomicrosurgery  . . . . . . . . . . . . . . . . . . . . . . . .   49 Decision Making in Phonosurgery  . . . . . . . . . . . .   50 Informed Consent Regarding Phonosurgery   . . .   51 Key Points  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   51 Selected Bibliography   . . . . . . . . . . . . . . . . . . . . . . .   51

6

8.1 8.2 8.3 8.3.1 8.3.2 8.4 8.5

9 9.1 9.2 9.3 9.4 9.5 9.6

Anesthesia and Airway Management for Laryngeal Surgery  . . . . . . . . . . . . . . . . . . . . . .   53 Fundamental and Related Chapters  . . . . . . . . . . .   53 Equipment  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   53 Surgical Indications and Contraindications  . . . .   53 Principles of Airway Management: Subglottic and Tracheal Stenosis  . . . . . . . . . . . . . .   54 Special Circumstances: Difficult Exposure of the Larynx  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   55 Anesthesia for Laryngeal Framework Surgery  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   58 Key Points  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   58 Selected Bibliography  . . . . . . . . . . . . . . . . . . . . . . .   58

 

Contents

Part B Phonomicrosurgery for Benign Laryngeal Pathology

I Fundamentals of Phonomicrosurgery

10 10.1 10.2 10.3 10.4 10.5 10.5.1 10.5.2 10.5.3 10.5.4 10.5.5 10.5.6 10.5.7 10.5.8 10.6

11 11.1 11.2 11.3 11.4 11.5 11.6 11.7

12 12.1 12.2 12.3 12.4 12.5

13 13.1 13.2 13.2.1

Principles of Phonomicrosurgery  . . . . . . . . . . . .   63 Fundamental and Related Chapters  . . . . . . . . . . .   63 Introduction  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   63 Surgical Indications and Contraindications  . . . .   63 Equipment for Phonomicrosurgery  . . . . . . . . . . .   65 Phonomicrosurgery Procedures, Techniques, and Methods  . . . . . . . . . . . . . . . . . . .   67 Anesthesia   . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   67 Patient Position  . . . . . . . . . . . . . . . . . . . . . . . . . . . .   68 Laryngoscope Placement  . . . . . . . . . . . . . . . . . . . .   68 Suspension Device   . . . . . . . . . . . . . . . . . . . . . . . . .   70 External Counter-Pressure  . . . . . . . . . . . . . . . . . . .   71 Telescopic Evaluation of Vocal Fold Pathology  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   71 Operating Microscope and Surgeon Ergonomics  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   72 Microflap Approach to Submucosal Pathology  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   73 Postoperative Care and Complications  . . . . . . . .   75 Key Points  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   75 Selected Bibliography  . . . . . . . . . . . . . . . . . . . . . . .   75 Perioperative Care for Phonomicrosurgery  . . . .   77 Fundamental and Related Chapters  . . . . . . . . . . .   77 Timing of Phonomicrosurgery   . . . . . . . . . . . . . . .   77 Surgical Indications and Contraindications  . . . .   77 Considerations for the Day of Phonomicrosurgery   . . . . . . . . . . . . . . . . . . . . . . . .   78 Postoperative Voice Rest  . . . . . . . . . . . . . . . . . . . .   78 Postoperative Voice Care  . . . . . . . . . . . . . . . . . . . .   78 Intralaryngeal Steroid Injection to Soften Postoperative Scar in the Vocal Fold  . . . . . . . . . .   78 Key Points  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   79 Selected Bibliography  . . . . . . . . . . . . . . . . . . . . . . .   79 Management and Prevention of Complications Related to Phonomicrosurgery  . . . . . . . . . . . . . . . . . . . . .   81 Fundamental and Related Chapters  . . . . . . . . . . .   81 Overview of Management and Prevention of Complications Related to Phonomicrosurgery     81 Surgical Indications and Contraindications   . . . .   81 Postoperative Dysphonia   . . . . . . . . . . . . . . . . . . . .   81 Medical Complications Associated with Phonomicrosurgery   . . . . . . . . . . . . . . . . . . . . . . . .   82 Key Points  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   82 Selected Bibliography  . . . . . . . . . . . . . . . . . . . . . . .   83 Principles of Laser Microlaryngoscopy  . . . . . . . .   85 Fundamental and Related Chapters  . . . . . . . . . . .   85 Laser Physics  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   85 Wavelength  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   85

XIX

13.2.2 13.2.3 13.2.4 13.3 13.4 13.5 13.5.1 13.5.2 13.5.3 13.6 13.6.1 13.6.2

Tissue Interaction  . . . . . . . . . . . . . . . . . . . . . . . . . Delivery Systems  . . . . . . . . . . . . . . . . . . . . . . . . . . Types of Laser   . . . . . . . . . . . . . . . . . . . . . . . . . . . . Surgical Indications and Contraindications  . . . Equipment: Laser Microlaryngoscopy Setup  . . CO2 Laser Safety Guidelines  . . . . . . . . . . . . . . . . General Guidelines (Fig. 13.1)  . . . . . . . . . . . . . . . CO2 Laser Settings  . . . . . . . . . . . . . . . . . . . . . . . . . Safety Protocol  . . . . . . . . . . . . . . . . . . . . . . . . . . . . Surgical Principles   . . . . . . . . . . . . . . . . . . . . . . . . Smoke Evacuation  . . . . . . . . . . . . . . . . . . . . . . . . . Protecting Surrounding Tissue from Laser Damage  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 13.6.3 Maintenance of a Clean Surgical Field  . . . . . . . . 13.7 Complications and Their Treatments  . . . . . . . . . 13.7.1 Laser Fire  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 13.7.2 Tracheal Perforation  . . . . . . . . . . . . . . . . . . . . . . . Key Points  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Selected Bibliography  . . . . . . . . . . . . . . . . . . . . . .

  85   85   86   86   87   87   87   88   88   88   88

Principles of Vocal Fold Augmentation  . . . . . . Fundamental and Related Chapters  . . . . . . . . . . Vocal Fold Augmentation: Advantages, Disadvantages, and Clinical Utility   . . . . . . . . . . 14.3 Surgical Indications and Contraindications  . . . 14.4 Characteristics of Vocal Fold Augmentation Materials  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 14.4.1 Overview  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 14.4.2 Categories of Vocal Fold Augmentation Materials  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 14.4.3 Description of Vocal Fold Augmentation Materials Characteristics  . . . . . . . . . . . . . . . . . . . 14.5 General Principles of Vocal Fold Augmentation  . . . . . . . . . . . . . . . . . . . . . . . . . . . . Key Points  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Selected Bibliography  . . . . . . . . . . . . . . . . . . . . . .

  91   91

14 14.1 14.2

15 15.1 15.2 15.3 15.4 15.5 15.6

16 16.1 16.2 16.3 16.4 16.5

  88   88   89   89   89   89   89

  91   91   92   92   92   92   94   95   96

II Phonomicrosurgical Voice Procedures Vocal Fold Polyp  . . . . . . . . . . . . . . . . . . . . . . . . . .   99 Fundamental and Related Chapters  . . . . . . . . . .   99 Disease Characteristics and Differential Diagnosis  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   99 Surgical Indications and Contraindications  . . .   99 Surgical Equipment  . . . . . . . . . . . . . . . . . . . . . . . .   99 Surgical Procedures  . . . . . . . . . . . . . . . . . . . . . . .   100 Postoperative Care/Complications  . . . . . . . . . .   103 Key Points  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   103 Selected Bibliography  . . . . . . . . . . . . . . . . . . . . .   103 Vocal Fold Nodules  . . . . . . . . . . . . . . . . . . . . . . .   105 Fundamental and Related Chapters  . . . . . . . . .   105 Disease Characteristics and Differential Diagnosis  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   105 Surgical Indications and Contraindications  . .   105 Surgical Equipment  . . . . . . . . . . . . . . . . . . . . . . .   105 Surgical Procedure  . . . . . . . . . . . . . . . . . . . . . . .   106

XX

Contents

16.6

Postoperative Care and Complications  . . . . . .   107 Key Points  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   107 Selected Bibliography  . . . . . . . . . . . . . . . . . . . . .   107

17

Vocal Fold Cyst and Vocal Fold Fibrous Mass  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   109 Fundamental and Related Chapters  . . . . . . . . .   109 Diagnostic Characteristics and Differential Diagnosis   . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   109 Surgical Indications and Contraindications  . .   109 Surgical Equipment  . . . . . . . . . . . . . . . . . . . . . . .   109 Surgical Procedure  . . . . . . . . . . . . . . . . . . . . . . .   109 Postoperative Care and Complications   . . . . . .   111 Key Points  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   112 Selected Bibliography  . . . . . . . . . . . . . . . . . . . . .   112

17.1 17.2 17.3 17.4 17.5 17.6

18 18.1 18.2 18.3 18.4 18.5 18.6

Polypoid Corditis  . . . . . . . . . . . . . . . . . . . . . . . .   113 Fundamental and Related Chapters  . . . . . . . . .   113 Disease Characteristics  . . . . . . . . . . . . . . . . . . . .   113 Surgical Indications and Contraindications  . .   113 Surgical Equipment  . . . . . . . . . . . . . . . . . . . . . . .   114 Surgical Procedure  . . . . . . . . . . . . . . . . . . . . . . .   114 Postoperative Care and Complications  . . . . . .   116 Key Points  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   116 Selected Bibliography  . . . . . . . . . . . . . . . . . . . . .   117

19 19.1 19.2

Vocal Fold Granuloma  . . . . . . . . . . . . . . . . . . . .   119 Fundamental and Related Chapters  . . . . . . . . .   119 Disease Characteristics and Differential Diagnosis  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   119 Surgical Indications and Contraindications  . .   119 Surgical Equipment  . . . . . . . . . . . . . . . . . . . . . . .   119 Surgical Procedure  . . . . . . . . . . . . . . . . . . . . . . .   120 Postoperative Care and Complications  . . . . . .   121 Key Points  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   121 Selected Bibliography   . . . . . . . . . . . . . . . . . . . . .   121

19.3 19.4 19.5 19.6

20 20.1 20.2 20.3 20.4 20.5 20.6

21 21.1 21.2 21.3

Vocal Fold Leukoplakia and Hyperkeratosis    123 Fundamental and Related Chapters  . . . . . . . . .   123 Diagnostic Characteristics and Differential Diagnosis  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   123 Surgical Indications and Contraindications  . .   123 Surgical Equipment  . . . . . . . . . . . . . . . . . . . . . . .   123 Surgical Procedure  . . . . . . . . . . . . . . . . . . . . . . .   123 Postoperative Care and Complications  . . . . . .   126 Key Points  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   126 Selected Bibliography  . . . . . . . . . . . . . . . . . . . . .   127 Surgical Treatment of Recurrent Respiratory Papillomatosis of the Larynx  . . .   129 Fundamental and Related Chapters   . . . . . . . . .   129 Disease Characteristics and Differential Diagnosis  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   129 Surgical Indications and Contraindications  . .   129

 

21.4 21.5 21.6

Surgical Equipment  . . . . . . . . . . . . . . . . . . . . . . .   130 Surgical Procedure  . . . . . . . . . . . . . . . . . . . . . . .   130 Postoperative Care and Complications  . . . . . .   133 Key Points  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   134 Selected Bibliography  . . . . . . . . . . . . . . . . . . . . .   134

22

Surgical Management of Vocal Fold Vascular Lesions  . . . . . . . . . . . . . . . . . . . . . . . . .   135 Fundamental and Related Chapters  . . . . . . . . .   135 Diagnostic Characteristics and Differential Diagnosis of Vocal Fold Varicosities  . . . . . . . . .   135 Surgical Indications and Contraindications   . .   136 Surgical Equipment  . . . . . . . . . . . . . . . . . . . . . . .   136 Surgical Procedure   . . . . . . . . . . . . . . . . . . . . . . .   136 Postoperative Care and Complications   . . . . . .   138 Key Points  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   139 Selected Bibliography  . . . . . . . . . . . . . . . . . . . . .   139

22.1 22.2 22.3 22.4 22.5 22.6

23 23.1 23.2 23.3 23.4 23.5 23.6

24 24.1 24.2 24.3 24.4 24.5 24.6

25 25.1 25.2 25.3 25.4 25.5 25.6

26 26.1

Vocal Fold Scar and Sulcus Vocalis  . . . . . . . . .   141 Fundamental and Related Chapters  . . . . . . . . .   141 Disease Characteristics and Differential Diagnosis   . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   141 Surgical Indications and Contraindications  . .   142 Surgical Equipment  . . . . . . . . . . . . . . . . . . . . . . .   143 Surgical Procedure  . . . . . . . . . . . . . . . . . . . . . . .   143 Postoperative Care and Complications  . . . . . .   150 Key Points  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   150 Selected Bibliography  . . . . . . . . . . . . . . . . . . . . .   150 Endoscopic Management of Teflon Granuloma  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   151 Fundamental and Related Chapters  . . . . . . . . .   151 Disease Characteristics and Differential Diagnosis  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   151 Surgical Indications and Contraindications  . .   151 Surgical Equipment  . . . . . . . . . . . . . . . . . . . . . . .   151 Surgical Procedure  . . . . . . . . . . . . . . . . . . . . . . .   151 Postoperative Care and Complications  . . . . . .   153 Key Points  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   153 Selected Bibliography  . . . . . . . . . . . . . . . . . . . . .   154 Endoscopic Excision of Saccular Cyst  . . . . . . .   155 Fundamental and Related Chapters  . . . . . . . . .   155 Disease Characteristics and Differential Diagnosis  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   155 Surgical Indications and Contraindications  . .   156 Surgical Equipment  . . . . . . . . . . . . . . . . . . . . . . .   156 Surgical Procedure for Saccular Cyst   . . . . . . . .   156 Postoperative Care and Complications  . . . . . .   157 Key Points  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   158 Selected Bibliography  . . . . . . . . . . . . . . . . . . . . .   158 Anterior Glottic Web  . . . . . . . . . . . . . . . . . . . . .   159 Fundamental and Related Chapters  . . . . . . . . .   159

 

26.2 26.3 26.4 26.5 26.6



27 27.1 27.2 27.3 27.4 27.5 27.6

28 28.1 28.2 28.3 28.4 28.5 28.6

Contents

Disease Characteristics and Differential Diagnosis  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   159 Surgical Indications and Contraindications  . .   159 Surgical Equipment  . . . . . . . . . . . . . . . . . . . . . . .   159 Surgical Procedure  . . . . . . . . . . . . . . . . . . . . . . .   160 Postoperative Care and Complications  . . . . . .   164 Key Points  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   164 Selected Bibliography  . . . . . . . . . . . . . . . . . . . . .   164 III Laser Microlaryngeal Surgery (Airway/Neoplastic Conditions) Bilateral Vocal Fold Paralysis  . . . . . . . . . . . . . . .   167 Fundamental and Related Chapters  . . . . . . . . .   167 Disease Characteristics and Differential Diagnosis  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   167 Surgical Indication and Contraindications  . . .   167 Surgical Equipment  . . . . . . . . . . . . . . . . . . . . . . .   168 Surgical Procedure   . . . . . . . . . . . . . . . . . . . . . . .   168 Postoperative Care and Complications  . . . . . .   171 Key Points  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   173 Selected Bibliography  . . . . . . . . . . . . . . . . . . . . .   173 Posterior Glottic Stenosis: Endoscopic Approach  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   175 Fundamental and Related Chapters  . . . . . . . . .   175 Diagnostic Characteristics and Differential Diagnosis  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   175 Surgical Indications and Contraindications  . .   176 Surgical Equipment  . . . . . . . . . . . . . . . . . . . . . . .   176 Surgical Procedure  . . . . . . . . . . . . . . . . . . . . . . .   176 Postoperative Care  . . . . . . . . . . . . . . . . . . . . . . .   179 Key Points  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   179 Selected Bibliography  . . . . . . . . . . . . . . . . . . . . .   180

29

Subglottic/Tracheal Stenosis: Laser/ Endoscopic Management  . . . . . . . . . . . . . . . . .   181 29.1 Fundamental and Related Chapters  . . . . . . . . .   181 29.2 Disease Characteristics and Differential Diagnosis  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   181 29.3 Surgical Indications and Contraindications   . .   181 29.4 Surgical Equipment  . . . . . . . . . . . . . . . . . . . . . . .   182 29.5 Surgical Procedure  . . . . . . . . . . . . . . . . . . . . . . .   182 29.6 Postoperative Care and Complications   . . . . . .   185 29.7 T-Tube Stenting of SGS  . . . . . . . . . . . . . . . . . . .   185 29.8 Surgical Equipment  . . . . . . . . . . . . . . . . . . . . . . .   185 29.9 Surgical Procedure  . . . . . . . . . . . . . . . . . . . . . . .   185 29.10 Postoperative Care  . . . . . . . . . . . . . . . . . . . . . . .   189 29.11 Special Considerations in T-Tube Stenting  . . .   189 Key Points  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   189 Selected Bibliography  . . . . . . . . . . . . . . . . . . . . .   190

30 30.1

Carcinoma of the Vocal Fold  . . . . . . . . . . . . . . .   191 Fundamental and Related Chapters  . . . . . . . . .   191

30.2 30.3 30.4 30.5 30.6



IV Laryngeal Injection Techniques

31 31.1 31.2 31.2.1 31.3 31.4 31.5 31.5.1 31.5.2 31.5.3 31.5.4 31.6

32 32.1 32.2 32.3 32.4 32.5 32.6

33

Disease Characteristics and Differential Diagnosis  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   191 Surgical Indications and Contraindications  . .   191 Surgical Equipment  . . . . . . . . . . . . . . . . . . . . . . .   191 Surgical Procedure   . . . . . . . . . . . . . . . . . . . . . . .   192 Postoperative Care and Complications  . . . . . .   192 Key Points  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   193 Selected Bibliography   . . . . . . . . . . . . . . . . . . . . .   193

Vocal Fold Augmentation via Direct Microlaryngoscopy  . . . . . . . . . . . . . . . . . . . . . .   197 Fundamental and Related Chapters  . . . . . . . . .   197 Disease Characteristics   . . . . . . . . . . . . . . . . . . .   197 Material Selection  . . . . . . . . . . . . . . . . . . . . . . . .   197 Surgical Indications and Contraindications  . .   198 Surgical Equipment  . . . . . . . . . . . . . . . . . . . . . . .   198 Surgical Procedure   . . . . . . . . . . . . . . . . . . . . . . .   198 Principles of Deep Vocal Fold Augmentation  . . . . . . . . . . . . . . . . . . . . . . . . . . .   198 Vocal Fold Augmentation via Microlaryngoscopy  . . . . . . . . . . . . . . . . . . . . . . .   199 Endoscopic Vocal Fold Injection  . . . . . . . . . . . .   199 Lipoinjection of the Vocal Fold  . . . . . . . . . . . . .   200 Postoperative Care and Complications  . . . . . .   202 Key Points  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   203 Selected Bibliography  . . . . . . . . . . . . . . . . . . . . .   203 Superficial Vocal Fold Injection  . . . . . . . . . . . .   205 Fundamental and Related Chapters  . . . . . . . . .   205 Disease Characteristics and Differential Diagnosis   . . . . . . . . . . . . . . . .   205 Surgical Indications and Contraindications  . .   205 Surgical Equipment  . . . . . . . . . . . . . . . . . . . . . . .   205 Surgical Procedure  . . . . . . . . . . . . . . . . . . . . . . .   205 Postoperative Care and Complications  . . . . . .   206 Key Points  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   207 Selected Bibliography  . . . . . . . . . . . . . . . . . . . . .   207

Peroral Vocal Fold Augmentation in the Clinic Setting  . . . . . . . . . . . . . . . . . . . . . .   209 33.1 Fundamental and Related Chapters  . . . . . . . . .   209 33.2 Disease Characteristics and Differential Diagnosis  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   209 33.3 Surgical Indications and Contraindications  . .   209 33.3.1 Suitability for Peroral Vocal Fold Augmentation in the Clinic Setting  . . . . . . . . .   210 33.4 Surgical Equipment   . . . . . . . . . . . . . . . . . . . . . .   210 33.5 Surgical Procedure  . . . . . . . . . . . . . . . . . . . . . . .   210 33.6 Postoperative Care and Complications  . . . . . .   213 Key Points  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   213 Selected Bibliography  . . . . . . . . . . . . . . . . . . . . .   213

XXI

XXII

Contents

34

Percutaneous Vocal Fold Augmentation in the Clinic Setting  . . . . . . . . . . . . . . . . . . . . . .   215 34.1 Fundamentals and Related Chapters  . . . . . . . .   215 34.2 Disease Characteristics and Differential Diagnosis   . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   215 34.3 Surgical Indications and Contraindications  . .   215 34.3.1 Suitability for Percutaneous Vocal Fold Augmentation in the Clinic Setting  . . . . .   216 34.4 Surgical Equipment  . . . . . . . . . . . . . . . . . . . . . . .   216 34.5 Surgical Procedure  . . . . . . . . . . . . . . . . . . . . . . .   216 34.6 Postoperative Care and Complications  . . . . . .   219 Key Points  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   219 Selected Bibliography  . . . . . . . . . . . . . . . . . . . . .   220 Botulinum Toxin Injection of the Larynx  . . . .   221 Fundamental and Related Chapters  . . . . . . . . .   221 Disease Characteristics and Differential Diagnosis   . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   221 35.2.1 Botulinum Toxin Fundamentals  . . . . . . . . . . . .   221 35.2.2 Spasmodic Dysphonia and Essential Tremor    221 35.2.3 Different Botulinum Toxin Injection Approaches  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   222 35.3 Surgical Indications and Contraindications  . .   222 35.4 Equipment  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   223 35.5 Procedure  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   223 35.6 Postprocedure Care and Complications  . . . . . .   227 Key Points  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   227 Selected Bibliography  . . . . . . . . . . . . . . . . . . . . .   227

35 35.1 35.2

Part C Laryngeal Framework Surgery 36 36.1 36.2 36.3 36.3.1 36.3.2 36.3.3 36.4 36.5 36.6

Principles of Laryngeal Framework Surgery    231 Fundamental and Related Chapters  . . . . . . . . .   231 Introduction  . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   231 Surgical Indications and Contraindications  . .   231 Medialization Laryngoplasty  . . . . . . . . . . . . . . .   231 Arytenoid Adduction  . . . . . . . . . . . . . . . . . . . . .   231 Cricothyroid Subluxation  . . . . . . . . . . . . . . . . . .   232 Patient Selection for Laryngeal Framework Surgery  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   232 Timing of Medialization Laryngoplasty  . . . . . .   232 Technical Notes and Pertinent Anatomic Landmarks for Medialization Laryngoplasty    232 Key Points  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   234 Selected Bibliography  . . . . . . . . . . . . . . . . . . . . .   234

Perioperative Care for Laryngeal Framework Surgery  . . . . . . . . . . . . . . . . . . . . . .   235 37.1 Fundamental and Related Chapters  . . . . . . . . .   235 37.2 Perioperative Issues in Laryngeal Framework Surgery  . . . . . . . . . . . . . . . . . . . . . . .   235 37.3 Surgical Indications and Contraindications  . .   235 37.4 Suboptimal Results/Surgical Errors  . . . . . . . . .   236 37.4.1 Revision Surgery  . . . . . . . . . . . . . . . . . . . . . . . . .   237

 

37.5

Long-Term Surgical Issues  . . . . . . . . . . . . . . . . .   239 Key Points  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   239 Selected Bibliography  . . . . . . . . . . . . . . . . . . . . .   239

38

Silastic Medialization Laryngoplasty for Unilateral Vocal Fold Paralysis  . . . . . . . . . .   241 Fundamental and Related Chapters  . . . . . . . . .   241 Disease Characteristics and Differential Diagnosis  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   241 Surgery Indications and Contraindications  . . .   241 Surgical Equipment  . . . . . . . . . . . . . . . . . . . . . . .   241 Surgical Procedure  . . . . . . . . . . . . . . . . . . . . . . .   242 Postoperative Care and Complications  . . . . . .   250 Key Points  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   251 Selected Bibliography  . . . . . . . . . . . . . . . . . . . . .   251

38.1 38.2 38.3 38.4 38.5 38.6

39 39.1 39.2 39.3 39.4 39.5 39.6

GORE-TEX® Medialization Laryngoplasty  . . . .   253 Fundamental and Related Chapters  . . . . . . . . .   253 Disease Characteristics and Differential Diagnosis  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   253 Surgical Indications and Contraindications  . .   253 Surgical Equipment   . . . . . . . . . . . . . . . . . . . . . .   253 Surgical Procedure  . . . . . . . . . . . . . . . . . . . . . . .   254 Postoperative Care and Complications  . . . . . .   255 Key Points  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   256 Selected Bibliography  . . . . . . . . . . . . . . . . . . . . .   256

40 40.1 40.2 40.3 40.4 40.5 40.6

Arytenoid Adduction  . . . . . . . . . . . . . . . . . . . . .   257 Fundamental and Related Chapters  . . . . . . . . .   257 Fundamentals of Arytenoid Adduction  . . . . . .   257 Surgical Indications and Contraindications  . .   257 Surgical Equipment  . . . . . . . . . . . . . . . . . . . . . . .   257 Surgical Procedure  . . . . . . . . . . . . . . . . . . . . . . .   257 Postoperative Care and Complications  . . . . . .   262 Key Points   . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   262 Selected Bibliography  . . . . . . . . . . . . . . . . . . . . .   262

41 41.1 41.2

Cricothyroid Subluxation  . . . . . . . . . . . . . . . . .   263 Fundamental and Related Chapters  . . . . . . . . .   263 Disease Characteristics and Differential Diagnosis   . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   263 Surgical Indications and Contraindications  . .   263 Surgical Equipment  . . . . . . . . . . . . . . . . . . . . . . .   263 Surgical Procedure  . . . . . . . . . . . . . . . . . . . . . . .   263 Postoperative Care and Complications  . . . . . .   264 Key Points  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   265 Bibliography  . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   265

41.3 41.4 41.5 41.6

37

42 42.1 42.2

Translaryngeal Removal of Teflon Granuloma  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   267 Fundamental and Related Chapters  . . . . . . . . .   267 Disease Characteristics and Differential Diagnosis  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   267

 

42.3 42.4 42.5 42.6

Contents

Surgical Indications and Contraindications   . .   267 Surgical Equipment  . . . . . . . . . . . . . . . . . . . . . . .   268 Surgical Procedure  . . . . . . . . . . . . . . . . . . . . . . .   268 Postoperative Care and Complications  . . . . . .   271 Key Points  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   271 Selected Bibliography  . . . . . . . . . . . . . . . . . . . . .   271

46 46.1 46.2 46.3 46.4 46.5 46.6

Excision of Combined Laryngocele  . . . . . . . . .   273 Fundamental and Related Chapters  . . . . . . . . .   273 Disease Characteristics and Differential Diagnosis  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   273 43.2.1 Anatomy and Classification  . . . . . . . . . . . . . . . .   273 43.2.2 Clinical Presentation and Differential Diagnosis  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   274 43.3 Surgical Indications and Contraindications  . .   274 43.4 Surgical Equipment  . . . . . . . . . . . . . . . . . . . . . . .   275 43.5 Surgical Procedure   . . . . . . . . . . . . . . . . . . . . . . .   275 43.6 Postoperative Care and Complications  . . . . . .   277 Key Points  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   277 Selected Bibliography  . . . . . . . . . . . . . . . . . . . . .   277

47

44 44.1 44.2 44.3 44.4 44.5 44.6

Repair of Laryngeal Fracture  . . . . . . . . . . . . . .   279 Fundamental and Related Chapters   . . . . . . . . .   279 Disease Characteristics   . . . . . . . . . . . . . . . . . . .   279 Surgical Indications and Contraindications   . .   279 Surgical Equipment   . . . . . . . . . . . . . . . . . . . . . .   280 Surgical Procedure   . . . . . . . . . . . . . . . . . . . . . . .   280 Postoperative Care and Complications   . . . . . .   282 Key Points  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   282 Selected Bibliography   . . . . . . . . . . . . . . . . . . . . .   282

48

45

Glottic and Subglottic Stenosis: Laryngotracheal Reconstruction with Grafting  . . . . . . . . . . . . . . . . . . . . . . . . . . . .   283 Fundamental and Related Chapters  . . . . . . . . .   283 Disease Characteristics and Differential Diagnosis  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   283 Surgical Indications and Contraindications  . .   283 Surgical Equipment  . . . . . . . . . . . . . . . . . . . . . . .   283 Surgical Procedure  . . . . . . . . . . . . . . . . . . . . . . .   284 Postoperative Care and Complications  . . . . . .   287 Key Points  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   287 Selected Bibliography  . . . . . . . . . . . . . . . . . . . . .   288

43 43.1 43.2

45.1 45.2 45.3 45.4 45.5 45.6

47.1 47.2 47.3 47.4 47.5 47.6

48.1 48.2 48.3 48.4 48.5 48.6

Glottic and Subglottic Stenosis: Cricotracheal Resection with Primary Anastomosis  . . . . . . . . . . . . . . . . . . . . . . . . . . . .   289 Fundamental and Related Chapters  . . . . . . . . .   289 Diagnostic Characteristics for Open Treatment of Subglottic Stenosis  . . . . . . . . . . . .   289 Surgical Indications and Contraindications  . .   289 Surgical Equipment  . . . . . . . . . . . . . . . . . . . . . . .   289 Surgical Procedure   . . . . . . . . . . . . . . . . . . . . . . .   289 Postoperative Management  . . . . . . . . . . . . . . . .   292 Key Points  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   292 Selected Bibliography  . . . . . . . . . . . . . . . . . . . . .   293 Tracheal Stenosis: Tracheal Resection with Primary Anastomosis  . . . . . . . . . . . . . . . .   295 Fundamental and Related Chapters  . . . . . . . . .   295 Background Information and Diagnosis of Tracheal Stenosis  . . . . . . . . . . . . . . . . . . . . . . .   295 Surgical Indications and Contraindications  . .   295 Surgical Equipment  . . . . . . . . . . . . . . . . . . . . . . .   295 Surgical Procedure  . . . . . . . . . . . . . . . . . . . . . . .   295 Postoperative Care and Complications  . . . . . .   298 Key Points  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   298 Selected Bibliography  . . . . . . . . . . . . . . . . . . . . .   298 The Gray Minithyrotomy for Vocal Fold Scar/Sulcus Vocalis  . . . . . . . . . . . . . . . . . . . . . . .   299 Fundamental and Related Chapters  . . . . . . . . .   299 General Considerations  . . . . . . . . . . . . . . . . . . .   299 Surgical Indications and Contraindications  . .   299 Surgical Equipment  . . . . . . . . . . . . . . . . . . . . . . .   299 Surgical Procedure  . . . . . . . . . . . . . . . . . . . . . . .   299 Postoperative Care and Complications   . . . . . .   303 Key Points  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   304 Selected Bibliography  . . . . . . . . . . . . . . . . . . . . .   304

Subject Index  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   305

XXIII

 



Contributing Authors

Milan Amin, M.D. Chief, Division of Laryngology Department of Otolaryngology New York University School of Medicine 550 First Avenue, NBV 5E5 New York, NY 10016 USA Chapter 2: Principles of Clinical Evaluation for Voice Disorders Chapter 45: Subglottis Stenosis: Laryngotracheal Reconstruction with Grafting Michiel J. Bové, M.D. Searle Building Room 12-561 320 Superior Chicago, IL 60611 USA Chapter 2: Principles of Clinical Evaluation for Voice Disorders Mark Courey, M.D. UCSF Voice & Swallowing Center 2330 Post Street, 5th Floor San Francisco, CA 94115 USA Chapter 28: Posterior Glottis Stenosis—Endoscopic Approach (Laser Division with MMC) Jonathan R. Grant, M.D. Dept. of Otolaryngology and Communication Sciences Medical College of Wisconsin Milwaukee, IL USA Chapter 34: Percutaneous VF Augmentation in a Clinical Setting

Patrick J. Gullane, M.D. 7-242 Eaton Wing N Toronto General 200 Elizabeth Street, Room 3S438 Toronto, Ontario M5G 2CH Canada Chapter 46: Glottic and Subglottic Stenosic: Cricotracheal resection with primary anastamosis Rene Gupta, MD Department of Otolaryngology New York University School of Medicine 550 First Avenue, NBV 5E5 New York, NY 10016 USA Chapter 29: Subglottis Stenosis: Laryngotracheal Reconstruction with Grafting Michael Johns, M.D. Emory Health Care Dept. of Otolaryngology 550 Peachtree Street, Suite 9-4400 Atlanta, GA 30308 USA Chapter 1: Anatomy and Physiology of the Larynx Priya Krishna, M.D. University of Pittsburg Voice Center Department of Otolaryngology 200 Lothrop Street, Suite 500 Pittsburgh, PA 15213 USA Chapter 7: Medical Treatment of Voice Disorders

XXVI

Invited Authors

Albert Merati, M.D. University of Washington Department of Otolaryngology Box 356515 Health Sciences Building Suite BB1165 Seattle, WA 98195 Chapter 34: Percutaneous VF Augmentation in a Clinical Setting Chapter 47: Tracheal Resection with Primary Anastomosis Christine Novak PT 7-242 Eaton Wing N Toronto General 200 Elizabeth Street, Room 3S438 Toronto, Ontario M5G 2CH Canada Chapter 46: Glottic and Subglottic Stenosic: Cricotracheal resection with primary anastamosis Gregory Postma, M.D. Department of Otolaryngology Medical College of Georgia 1120 15th Street Augusta, GA 30912 USA Chapter 39: Goretex Medialization Laryngoplasty

 

Anthony Rider, MD Department of Otolaryngology and Communication Sciences Medical College of Wisconsin Milwaukee, WI USA Chapter 47: Tracheal Resection with Primary Anastomosis Robert T. Sataloff, M.D. 1721 Pine Street Philadelphia, PA 19103 USA Chapter 22: Vocal Fold Varix Lucian Sulica, M.D. 10 Union Square East, Suite 4J New York, NY 10003 USA Chapter 35: Botox Toxin Injection Chapter 37: Peri-Operative Care for Laryngeal Framework Surgery Chapter 38: Principles of Laryngeal Framework Surgery Chapter 48: Mini-Thyrotomy for Vocal Fold Scar

Part A Clinical Evaluation of Laryngeal Disorders

Chapter 1

Anatomy and Physiology of the Larynx

1.1

Anatomy

1.1.1

Laryngeal Cartilages

1.1.1.1 Thyroid The laryngeal skeleton consists of several cartilaginous structures (Fig. 1.1), the largest of which is the thyroid cartilage. The thyroid cartilage is composed of two rectangular laminae that are fused anteriorly in the midline. The incomplete fusion of the two laminae superiorly forms the thyroid notch. Attached to each lamina posteriorly are the superior and inferior cornua. The superior cornua articulate with the greater horns of the hyoid bone, while the inferior cornua form a synovial joint with the cricoid cartilage (the cricothyroid joint). At the junction of each superior cornu with its respective thyroid ala is a cartilaginous prominence, the superior tubercle. The superior tubercle is of significance because it marks the point 1 cm below which the superior laryngeal artery and nerve cross over the lamina from laterally to pierce the thyrohyoid membrane. The sternothyroid and the thyrohyoid strap muscles attach to

1

the anterior surface of the thyroid laminae at the oblique line. The inferior pharyngeal constrictor muscles insert on the posterior edge of each thyroid lamina. The relationship of the internal laryngeal structures to the surface anatomy of the thyroid cartilage is important in surgical planning, particularly in planning the placement of the window for thyroplasty. The level of the vocal fold lies closer to the lower border of the thyroid cartilage lamina than to the upper, and not at its midpoint, as is frequently (and erroneously) stated. Correct placement of the window is necessary to avoid medialization of the false vocal folds or ventricular mucosa.

1.1.1.2 Cricoid This signet ring-shaped cartilage is the only laryngeal cartilage to encircle completely the airway. The cricoid cartilage articulates with the thyroid cartilage’s inferior cornua on the cricothyroid joint facets. It joins the first tracheal ring inferiorly via membranous attachments. The face of the cricoid cartilage has a vertical height of only about 3–4 mm, while the lamina posteriorly stands about 20–30 mm high. There is a steep incline from anterior to posterior of the superior margin of the cricoid cartilage. This incline leaves an anterior window where the cricothyroid membrane lies.

1.1.1.3 Arytenoid The arytenoid cartilages are paired, pyramidal cartilages that articulate with the posterior lamina of the cricoid cartilage at the cricoarytenoid joint. Each arytenoid has both a vocal process medially and a muscular process laterally. These processes act as the attachment sites for the vocal ligament and the major intrinsic muscles of vocal fold movement respectively.

1.1.1.4 Accessory Cartilages: Cuneiform and Corniculate

Fig. 1.1  Cartilaginous and fibroelastic structures of the larynx

The cuneiform cartilages are crico-arytenoid joint paired elastic cartilages that sit on top of, and move with, the corresponding arytenoid. The soft tissue of the aryepiglottic folds covers these cartilages. The corniculates are small, paired, fibroelastic cartilages that sit laterally to each of the arytenoids, and are completely embedded within the aryepiglottic folds. These



1

Anatomy and Physiology of the Larynx

likely serve to provide additional structural support to the aryepiglottic folds.

 

1.1.2

Laryngeal Joints

1.1.2.1 Cricothyroid Joint 1.1.1.5 Epiglottis The epiglottis is an oblong, feather-shaped fibroelastic cartilage that is attached, at its inferior end, to the inner surface of the thyroid cartilage laminae just above the anterior commissure. The major function of the epiglottis is to help prevent aspiration during swallowing. The epiglottis is displaced posteriorly by tongue base contraction and laryngeal elevation. This causes the superior free edge of the epiglottis to fall over the laryngeal inlet, which, in conjunction with sphincteric closure of the larynx at the glottic and supraglottic level, closes off the laryngeal vestibule.

The cricothyroid joint is a synovial joint formed from the articulation of the inferior cornua of the thyroid cartilage with facets on the cricoid lamina. The two major actions at this joint are anteroposterior sliding and rotation of the inferior thyroid cornu upon the cricoid cartilage. Cricothyroid muscle contraction pulls the thyroid ala anteriorly with respect to the cricoid cartilage and closes the anterior visor angle between the thyroid and the cricoid cartilage. This motion increases the distance between the anterior commisure and the vocal processes and serves to lengthen and tense the vocal folds. This joint can be manipulated to assist in pitch control in cases of paralytic dysphonia. Cricothyroid joint subluxation, resulting in an exaggerated decrease in the anterior cricothyroid angle, can assist in traditional medialization procedures to provide vocal fold tightening.

1.1.2.2 Cricoarytenoid Joint

Fig. 1.2  Cricoarytenoid joint action in abduction (left) and adduction

(right). Note the lowering of the vocal process as adduction occurs

The cricoarytenoid joint is the primary moving structure of the intrinsic larynx (Fig. 1.2). The arytenoids articulate with the cricoid cartilage forming multiaxial joints. The action of movement at the cricoarytenoid joints changes the distance between the vocal processes of the two arytenoids and between each vocal process and the anterior commissure. The combined action of the intrinsic laryngeal muscles on the arytenoid cartilages alters the position and shape of the vocal folds. Each cricoarytenoid joint sits at a surprisingly steep 45° angle with the horizontal plane on the cricoid cartilage and permits motion in a sliding, rocking, and twisting fashion.

1.1.3

Laryngeal Musculature

1.1.3.1 Intrinsic Laryngeal Muscles The intrinsic muscles of the larynx are responsible for altering the length, tension, shape, and spatial position of the vocal folds by changing the orientation of the muscular and vocal processes of the arytenoids with the fixed anterior commissure (Fig. 1.3). Traditionally, the muscles are categorized into the following scheme: three major vocal fold adductors, one abductor, and one tensor muscle. Adductor Muscles The Lateral Cricoarytenoid Muscle (LCA)

Fig. 1.3  Neuromuscular structures of the larynx

This paired laryngeal muscle is attached to the anterior part of the muscular process medially and to the superior border of the cricoid cartilage laterally. Contraction of this muscle results in movement of the muscular process anterolaterally,

 

while simultaneously forcing the vocal process downward and medially. The result is adduction and lengthening of the vocal folds. This muscle runs lateral and in large part parallel with the thyroarytenoid muscle. Thyroarytenoid Muscle (TA) The thyroarytenoid muscle consists of two main muscle bellies, the internus and the externus. The thyroarytenoid externus inserts anteriorly at the anterior commissure (Broyles’ ligament), and posterolaterally on the lateral surface of the arytenoid. During contraction of this portion of the muscle, the vocal process is brought closer to the anterior commissure and the vocal folds are shortened and adducted. The thyroarytenoid internus arises from the anterior commissure and inserts onto the vocal process of the arytenoid cartilage. During contraction, the vocal folds are shortened and thickened. This portion of the thyroarytenoid is also known as the vocalis muscle. In isolation, this action serves to lower the resonant frequency of the vocal folds. In most cases, there is a significant superior extension of the TA muscle into the false vocal folds, often referred to as the ventricularis muscle.

Chapter 1

noids “upright” and has a major role in vocal fold length and tension. The PCA muscle anatomy serves as a key landmark for arytenoid adduction surgery. Tensor Muscle Cricothyroid Muscle The cricothyroid muscle is a laryngeal tensor, composed of two separate muscle bellies, located on the external surface of the laryngeal cartilages. The pars recta, the more vertical component, arises laterally from the superior rim of the cricoid cartilage and inserts on the inferior rim of the thyroid cartilage, while the pars obliqua, runs obliquely from the superior arch of the cricoid to insert on the inferior cornu. Contraction of the cricothyroid muscle bellies affects motion at the cricothyroid joint. During contraction, the cricothyroid space is narrowed anteriorly, while the posterior cricoid lamina and cricoarytenoid joints are forced caudally, resulting in lengthening, tightening and thinning of the vocal folds and as well as increasing their resonant frequency. This action also results in vocal fold adduction.

Interarytenoid Muscle (IA) This nonpaired muscle consists of both transverse fibers and oblique fibers. The transverse fibers insert on the posterior face of each arytenoid and run horizontally, while the oblique fibers attach to each arytenoid apex and run obliquely to attach to the posterior face on the opposite side. Contraction of this muscle leads to arytenoid adduction, closure of the posterior glottis, and narrowing of the laryngeal inlet. Some oblique fibers extend to travel along the quadrangular membrane and are referred to as the aryepiglottic muscle Abductor Muscle Posterior Cricoarytenoid Muscle (PCA) The posterior cricoarytenoid muscle arises from the posterior face of the cricoid lamina. Its fibers run diagonally to insert on the muscular process of the arytenoid. Contraction displaces the muscular process posteriorly and caudally, while the vocal process moves upward and laterally. The result is vocal fold abduction. The posterior cricoarytenoid is the only abductor of the vocal folds and is principally responsible for control of the glottic airway. The posterior cricoarytenoid muscle affects motion at the cricoarytenoid joint in two planes by its two separate muscle bellies. The medial portion of the posterior cricoarytenoid (horizontal belly) arises from the posterior cricoid lamina and courses obliquely in a superiolateral fashion to insert on the medial aspect of the muscular process. The lateral portion (vertical belly) runs in a more vertical fashion to insert on the lateral side of the muscular process. Because of slightly different positions and orientations, contraction of each muscle belly in isolation causes cricoarytenoid joint motion about a different oblique axis. The horizontal belly has been shown, in cadaver studies, to cause motion in a more vertical axis (true vocal fold abduction), while the vertical belly keeps the aryte-

1.1.3.2 Extrinsic Laryngeal Muscles The infrahyoid strap muscles (the sternothyroid, the sternohyoid, and the thyrohyoid), the mylohyoid, digastric, geniohyoid, and stylopharyngeus muscles all act in concert to provide laryngeal stabilization, and indirectly may affect vocal fold position.

1.1.4

Fibroelastic Tissue of the Larynx

1.1.4.1 Quadrangular Membrane The quadrangular membrane is an accessory elastic support structure of the supraglottic larynx. It attaches anteriorly to the lateral edges of the epiglottis, and wraps around posteriorly to attach to the arytenoids. The superior free edge of the quadrangular membrane is the mucosa-covered aryepiglottic fold. As the quadrangular membrane extends inferiorly, it becomes the medial wall of the piriform sinus. At its inferior extent, it is continuous with the vestibular ligament.

1.1.4.2 Conus Elasticus The thick fibroelastic support structure of the glottis and subglottis originates inferiorly along the superior border of the cricoid cartilage. Is extends superiorly to attach to the anterior commissure and vocal processes. The conus elasticus rolls medially within the substance of the vocal fold; its medial extent is the vocal ligament. Anteriorly, the conus elasticus is continuous with the cricothyroid membrane.





1

Anatomy and Physiology of the Larynx

1.1.5

Microanatomy of the Vocal Fold

The complex microanatomy of the true vocal fold allows the loose and pliable superficial mucosal layers to vibrate freely over the stiffer structural underlayers (Fig. 1.4). The true vocal fold can be divided into three major layers: the mucosa, the vocal ligament, and the underlying muscle. The mucosa of the vocal fold is highly specialized for its vibratory function; it can also be divided into layers. The most superficial layer is the squamous epithelium. Deep to the epithelium are three layers of lamina propria, each of increasing rigidity. The most superficial layer (superficial layer of the lamina propria, or SLP) is mostly acellular and composed of extracellualar matrix proteins, water, and loosely arranged fibers of collagen and elastin. The SLP is gelatinous in nature. The potential space between the SLP and the intermediate layer of lamina propria is Reinke’s space. The intermediate and deep layers of the lamina propria (ILP and DLP) are composed mostly of elastin and collagen; the deepest and most dense layer (DLP) is composed of tightly arranged collagen fibers. The ILP and DLP together form the vocal ligament. The gelatinous superficial layer of the lamina propria, together with the squamous epithelium, moves freely over the underlying vocal ligament and muscle to form the vibrations that produce sound. The vocal fold mucosa and vocal ligament cover the vocalis muscle and extend from the anterior commissure to the vocal processes of the arytenoids. The mucosa and vocal ligament extend posteriorly to cover the entirety of the vocal process. The posterior third of the endoscopically visualized true vocal fold, then, is the aphonatory (respiratory), or cartilaginous portion, while the anterior two thirds of the endoscopically visualized vocal fold is the phonatory, or membranous portion.

1.1.6

 

Vasculature

The arterial supply to the larynx comes from the superior and inferior laryngeal arteries; the venous supply mirrors the arterial supply. The superior laryngeal artery is a branch of the superior thyroid artery, which arises directly from the external carotid. The superior laryngeal artery branches from the superior thyroid artery at the level of the hyoid bone. This artery then courses medially with the internal branch of the superior laryngeal nerve and enters the thyrohyoid membrane 1 cm anterior and superior to the superior tubercle. The cricothyroid artery, one of the major branches of the superior laryngeal artery, runs along the inferior surface of the thyroid cartilage to supply its similarly named muscle and joint. Branches of this artery pierce the cricothyroid membrane and ascend on the internal surface of the thyroid cartilage, making them possible targets during the creation of a thyroplasty window. The second major arterial supply to the larynx comes from the inferior laryngeal artery, a branch of the inferior thyroid artery. This artery enters the larynx between fibers of the inferior constrictor muscle and anastomoses with branches of the superior laryngeal artery.

Fig. 1.4  Coronal section through the free edge of the vocal fold, dem-

onstrating the layered microanatomical structures that allow vibration

1.1.7

Innervation

Corticobulbar fibers from the cerebral cortex descend through the internal capsule and synapse on the motor neurons in the nucleus ambiguus. The nucleus ambiguus is the area within the brainstem (medulla) from which the fibers that will contribute to the vagus nerve arise. Lower motor neurons leave the nucleus ambiguus and travel laterally, exiting the medulla between the olive and the pyramid as a series of eight to ten rootlets. These rootlets coalesce into a single nerve root, known as the vagus nerve, which then exits the skull base via the jugular foramen. The vagus nerve descends in the carotid sheath, giving off three major branches: the pharyngeal branch, the superior laryngeal nerve (SLN), and the recurrent laryngeal nerve (RLN). The SLN supplies sensation to the glottic and supraglottic larynx, as well as motor input to the cricothyroid muscle, which controls vocal fold lengthening and pitch. There are some recent anatomic studies that suggest that the superior aspect of the TA muscle (the ventricularis muscle in the false vocal fold) may have SLN innervation, which could explain the presence of false vocal fold muscular contraction in cases of RLN transection. The RLN arises from the vagus nerve in the upper chest and loops under the aortic arch (left) or subclavian artery (right), and ascends back into the neck, traveling in the tracheoesophageal groove. The nerve enters the larynx posteriorly, adjacent to the cricothyroid joint (Fig. 1.3). The RLN innervates the ipsilateral posterior cricoarytenoid (PCA), the interarytenoid (IA) (an unpaired muscle), and the lateral cricoarytenoid (LCA), and terminates in the thyroarytenoid (TA). Thus, the RLN supplies all of the intrinsic laryngeal muscles with the exception of the cricothyroid muscle (and possibly the ventricularis muscle, as indicated above). Ipsilateral RLN transection typically results in vocal fold immobility (the ipsilateral CT does not contribute to vocal fold adduction or abduction). It is important to remember, however, that the interarytenoid muscle is unpaired,

 

Chapter 1

and contralateral RLN input to the IA may lead to some adduction of the vocal fold on the paralyzed side. The RLN also supplies the glottic and subglottic mucosa and the myotatic receptors of the laryngeal musculature.

1.2

Physiology

1.2.1

Major Laryngeal Functions: Lower Airway Protection, Respiration, and Phonation

interarytenoid muscle, on the other hand, has been shown to have increased latency of contraction, but regular sustained tonicity during prolonged sound production. The cricothyroid seems to have the greatest measurable action with increases in pitch and volume, while the posterior cricoarytenoid shows its greatest degree of activation with voluntary deep inhalation and sniff functions. Actual phonation is a complex and specialized process that involves not only brainstem reflexes and the muscular actions described above, but high-level cortical control as well. Accessory effects such as lung capacity, chest wall compliance, pha-

The most primitive of the laryngeal functions is protection of the airway. In humans, the larynx has evolved into a highly complex and specialized organ not only for airway protection and control of respiration, but also for sound and speech production. Precise control of all of these mechanisms, as well as exact anatomic structure, is required for normal laryngeal functioning. The larynx has evolved several important reflexes for the purpose of airway protection against external stimuli and foreign bodies. These reflex mechanisms are relayed by the mucosal (sensory afferent), myotatic, and articular receptors of the larynx via both the superior and recurrent laryngeal nerves (Fig. 1.3). The strongest of the laryngeal reflexes is that of laryngospasm—a response to mechanical stimulation. The larynx has also evolved reflexes that produce cough, apnea, bradycardia, and hypotension.

1.2.1.1 Phonation The most complex and highly specialized of the laryngeal functions is sound production. The ability to couple phonation with articulation and resonance allows for human speech. Phonation and precisely how it relates to laryngeal vibration has undergone many evolving theories over the years. Sound production requires that several mechanical properties be met. There must be adequate breath support to produce sufficient subglottic pressure. There also must be adequate control of the laryngeal musculature to produce not only glottic closure, but also the proper length and tension of the vocal folds. Finally, there must be favorable pliability and vibratory capacity of the tissues of the vocal folds. Once these conditions are met, sound is generated from vocal fold vibration. The detailed contribution, timing, and recruitment of each of the above-described laryngeal muscles in the production of sound have been studied. In a fine-wire electromyographic study of human larynges, it was found that the intrinsic laryngeal muscles are not only highly specialized for their particular vector of action, but they are also controlled for the timing of onset of contraction, and the degree of recruitment and fade during phonation. The thyroarytenoid and the lateral cricoarytenoid muscles have been shown to exhibit burst-like activity at the onset of phonation (as well as pre-phonatory), with a measurable degree of fade during sustained phonation. The

Fig. 1.5  Schematic coronal section through the vocal folds, demon-

strating mucosal wave propagation. 1 Vocal folds are completely closed as subglottal pressure (arrow) builds up. 2 Lower lips separate due to rising subglottal pressure. 3 Only the upper lips are in contact. 4 A puff of air is released as the vocal folds separate completely. 5, 6 As airflow continues, the elastic recoil of the vocal folds, as well as Bernoulli’s forces, result in the lower lips of the vocal folds drawing inward. At the same time, the mucosal wave is propagated superiolaterally. 7 Airflow is reduced, and the lower lips are completely approximated. 8 In a zipper-like closure, the free edge of the vocal folds come into contact from inferiorly to superiorly





1

Anatomy and Physiology of the Larynx

ryngeal, nasal, and oral anatomy, and subsequent mental status also play a role. The process begins with inhalation and subsequent glottal closure. An increase in subglottic pressure follows until the pressure overcomes the glottal closure force and air is allowed to escape between the vocal folds. Once air passes between the vocal folds, the body-cover concept of phonation takes effect. The body-cover theory describes the wave-like motion of the loose mucosa of the vocal folds over the stiffer, more densely organized vocal ligament and vocalis muscle. This motion is known as the mucosal wave. The wave begins infraglottically and is propagated upward to the free edge of the vocal fold and then laterally over the superior surface (Fig. 1.5). Eventually, the inferior edges become reapproximated due both to a drop in pressure at the open glottis, and to the elastic recoil of the tissues themselves. The closure phase is also propagated rostrally. With the vocal folds fully approximated, subglottic pressure may again build and the cycle is repeated (Fig. 1.5).

 

Selected Bibliography 1 2 3

4

5

6

7

Key Points 8

1. The relationship of the surface anatomy of the thyroid and arytenoid cartilages to the internal laryngeal structures are critical to surgical planning for laryngeal framework surgery and in-office procedures (i. e., percutaneous laryngeal injections). 2. The primary adductor muscles of the larynx consist of: ■ Lateral cricoarytenoid (LCA) ■ Thyroarytenoid (TA) ■ Interarytenoid (IA) 3. The main abductor muscle of the larynx is the posterior cricoarytenoid (PCA). 4. The cricothyroid and the TA/LCA muscles control vocal fold length, tension, and vocal frequency. 5. The microanatomy of the vocal folds is complex and consists of the following layers, from superficial to deep: ■ Epithelium ■ Superficial lamina propria ■ Intermediate lamina propria ■ Deep lamina propria ■ Vocalis muscle 6. Reinke’s space is a potential space between the superficial and intermediate layer of the lamina propria. The intermediate and deep layers of the lamina propria together are referred to as the vocal ligament.

9

10 11

12

13

14 15

16

17

Bielamowicza S (2004) Perspectives on medialization laryngoplasty. Otolaryngol Clin N Am 37:139–160 Schwenzer V, Dorfl J (1997) The anatomy of the inferior laryngeal nerve. Clin Otolaryngol Allied Sci 22:362–369 Zeitels SM (2000) New procedures for paralytic dysphonia: adduction arytenopexy, Gortex medialization laryngoplasty, and cricothyroid subluxation. Otolaryngol Clin N Am 33:841–854 Ludlow C (2004) Recent advances in laryngeal sensorimotor control for voice, speech, and swallowing. Curr Opinion in Otolaryngol 12:160–165 Hillel A (2001) The study of laryngeal muscle activity in normal human subjects and in patients with laryngeal dystonia using multiple fine-wire electromyography. Laryngoscope 111:1–47 Hirano M (1977) Structure and vibratory behavior of the vocal fold. In: Sawashima M, Cooper F (eds) Dynamic aspects of speech production. University of Tokyo, Tokyo, Japan, pp 13–30 Jones-Bryant N, Woodsen GE, Kaufman K et al (1996) Human posterior cricoarytenoid muscle compartments: anatomy and mechanics. Arch Otolaryngol Head Neck Surg 122:1331–1336 Armstrong WB, Netterville JL (1995) Anatomy of the larynx, trachea, and bronchi. Otolaryngol Clin N Am 28:685 Mathew OP, Abu-Osba YK, Thach BT (1982) Influence of upper airway pressure changes in respiratory frequency. Resp Physiol 29:223 Hirano M, Kakita Y (1985) Cover-body theory of vocal fold vibration. Speech science. College-Hill Press, San Diego Bryant NJ et al (1996) Human posterior cricoarytenoid muscle compartments: anatomy and mechanics. Arch Otolaryngol 122:1331 Kempster GB, Larson CR, Distler MK (1988) Effects of electrical stimulation of cricothyroid and thyroarytenoid muscles on voice fundamental frequency. J Voice 2:221 Buchthal F, Faaborg-Anderson K (1964) Electromyography of laryngeal and respiratory muscles: correlation with respiration and phonation. Ann Otol Rhino Laryngol 73:118 Gay T et al (1972) Electromyography of intrinsic laryngeal muscles during phonation. Ann Otol 81:401 Kotby MN, Kirchner JA, Kahane JC, Basiouny SE, el-Samaa M (1991) Histo-anatomical structure of the human laryngeal ventricle. Acta Otolaryngol 111:396–402 Sanud, JR, Maranillo E, Leon X et al (1999) An anatomical study of anastomoses between the laryngeal nerves. Laryngoscope 109:983–87 Platzer W (ed) Atlas of topographic and applied human anatomy: head and neck, (Pernkopf Anatomy, vol 1, 3rd edn.). Urban & Schwarzenberg, Vienna

Chapter 2

Principles of Clinical Evaluation for Voice Disorders

2.1

Fundamental and Related Chapters

Please see Chaps. 1, 3, 4, and 5 for further information.

2.2

Introduction

Many processes resulting in dysphonia affect the vocal folds in subtle ways. Objective evidence of vocal pathology is not always easily discernable on physical examination, even when aided with sophisticated diagnostic instruments. It is, therefore, essential that the laryngologic exam be supported by a careful review of the patient’s medical and vocal history. Perhaps more than any other aspect of otolaryngology, the information derived from a careful review of the patient’s complaints provides an invaluable context within which to interpret the findings on physical exam and objective voice testing.

2.3

Gathering a Patient History

A detailed and directed questionnaire mailed to patients before their office visits can have multiple advantages. First, it enables patients to record accurately the symptoms they are experiencing and to chronicle the history of their problems. It also allows them to document comprehensively and accurately all their medications and dosages. Addresses and telephone numbers of primary care and referring physicians can also be obtained. This strategy not only increases the efficiency of an office consultation, but it may also allow preliminary differential diagnosis to be formulated in certain patients. To this aim, Sataloff has developed a pair of questionnaires, one directed at the singer, another at the professional voice user. Standardized, patientbased, voice-related quality of life instruments should also be given to the patient prior to the start of the patient evaluation (see Sect. 2.9, “Listening to the Voice”). Although useful, the questionnaire cannot substitute for a thoughtful and thorough face-to-face interview with the patient. The classic template of history of present illness, past medical history, past surgical history, review of systems, medications, and social history provides a reliable framework for achieving a thorough medical and voice history.

2.4

2

History of Present Illness

The exact nature of the voice patient’s chief complaint should be reviewed with care. The term hoarseness, for instance, is often used to describe a variety of symptoms, including loss of upper register, roughness, pitch instability, difficulty in transition between singing registers, breathiness, and early vocal fatigue. Each of these symptoms can have distinct implications. A rough voice is often associated with abnormalities of the free edge of the vocal fold, as seen in laryngitis or mass lesions. Breathiness, on the other hand, results from any condition preventing full approximation of the vocal folds leading to excessive loss of air during vocalization. Conditions that may cause breathiness include vocal fold paralysis/paresis, ankylosis of the cricoarytenoid joint, arytenoid dislocation, vocal fold scar, vocal fold lesions, and presbylarynx. Raspiness refers to a disruption of the vocal harmony that usually reflects perturbation of normal mucosal wave, resulting in instability of the fundamental frequency. A strained voice is often the result of hyperfunctional glottal closure. Although primary glottal hyperfunction may be the result of neurological impairment or poor vocal technique, this hyperfunction may also represent a supraglottic compensation for glottal insufficiency. Early vocal fatigue can similarly result from glottal incompetence secondary to vocal fold atrophy, vocal fold scar, vocal fold lesions, or paresis. Inadequate airflow production from the lungs due to pulmonary or neuromuscular pathologies can also present with vocal fatigue and/or decreased volume. Determining the duration of each voice complaint will distinguish acute processes from chronic dysfunction. An acute process, such as an upper respiratory infection, for instance, may unmask or exacerbate a separate and potentially more consequential chronic process such as a vocal lesion or a pattern of vocal misuse. In addition, upper respiratory infection (URI) symptoms frequently precede the onset of a viral vagal neuropathy. Careful attention to the duration of each of a patient’s symptoms will thereby allow a complex symptom picture to be segregated into its component pathologies. The exact time course of the ailment can be particularly helpful in the evaluation of rapid onset dysphonia. Sudden development of hoarseness (occurring over seconds or minutes) should, in fact, always raise suspicion of vocal fold hemorrhage or psychogenic etiologies.

10

Principles of Clinical Evaluation for Voice Disorders

2.5

2

Past Medical History

Salient points regarding the patient’s history include any condition or medications potentially affecting pulmonary status, posture, and hydration. Chronic obstructive pulmonary disease (COPD) will adversely affect the power supply for the patient’s voice. Various rheumatological and musculoskeletal ailments can alter posture, impairing voice quality. Any underlying acute or chronic inflammatory conditions can significantly affect voice. Allergic disease manifesting as persistent postnasal drip, for instance, will lead to chronic laryngeal inflammation and vocal fold trauma. Anticholinergic effects of prescription, as well as over the counter medications, can affect mucosal hydration and lubrication, and have an adverse effect on vocal fold vibration. It has been estimated that approximately half of patients presenting with laryngeal and voice disorders have laryngopharyngeal reflux (LPR) as the primary cause, or as a significant etiologic factor. Typical symptoms include chronic or intermittent dysphonia (especially in the morning), halitosis, globus, excessive throat mucous, frequent throat clearing, and chronic cough. A frequent complaint of patients with LPR is morning hoarseness that improves as the day progresses. This pattern is not seen in most other conditions causing dysphonia. Surprisingly, most patients with LPR do not present with heartburn, indigestion, or belching—the cardinal symptoms of gastroesophageal reflux disease. Consequently, LPR is often referred to as silent reflux. The pervasive but often overlooked nature of LPR demands that the physician evaluating the dysphonic patient consider this diagnosis in almost every case. The reflux symptom index (RSI) is a nine-item, patient-based outcome instrument that is useful in predicting the likelihood of LPR (Table 2.1) It is easily administered, and highly reproducible. Some degree of reflux is present in normal individuals, and an RSI of greater than 10 is considered abnormal. Endocrinologic changes can have profound effects on the voice. Many of these changes are reflected in alterations of the

 

lamina propria. An increase in acid mucopolysaccharides in the submucosal tissues of the vocal fold has been demonstrated in an animal model of induced hypothyroidism. This increase draws fluid into Reinke’s space osmotically, resulting in edema. The patient may complain of dysphonia, vocal fatigue, muffling of the voice, loss of range, and globus. Some women report vocal changes associated with the normal menstrual cycle. Most of the adverse effects occur in the premenstrual phase, a phenomenon known as laryngopathia premenstrualis. Slight hoarseness and muffling, vocal fatigue, and loss of the highest notes in the voice characterize this vocal dysfunction. While relatively uncommon in women without formal vocal training, as many as a third of singers report menstrual related dysphonia. In addition, vocal fold varices often increase in size before and during menstruation and have been associated with an increased incidence of submucosal vocal fold hemorrhages. A few important generalized neurological disorders are characterized by specific patterns of dysphonia. Neurologic disorders resulting in hypoadduction of the vocal folds will present with a weak, breathy voice, vocal fatigue, and an ineffective cough. Such diseases include myasthenia gravis, muscular dystrophy, Parkinson’s disease, Shy-Drager syndrome, postpolio syndrome, traumatic brain injury, and abductor spasmodic dysphonia. Hyperfunctional neurologic disorders are associated with a staccato or strained voice. These disorders include adductor spasmodic dysphonia, pseudobulbar palsy, and Huntington’s disease. Other neurologic disorders present with mixed ad- and abductor components, making the dysphonia more difficult to diagnose. These disorders include multiple sclerosis, ataxic (cerebellar) dysphonia, and amyotrophic lateral sclerosis. Lastly, vocal tremor can be associated with Parkinson’s disease, benign essential tremor, spasmodic dysphonia, and palatopharyngeal myoclonus. Table 2.2 provides an overview of the historical elements of particular importance when obtaining a voice history. Table 2.3 demonstrates symptoms suggestive of specific voice disorders.

Table 2.1  Reflux Symptom Index

Within the last month, how did the following problems affect you?

0 = No problem 5 = Severe problem

1. Hoarseness or a problem with your voice.

012345

2. Clearing your throat.

012345

3. Excess throat mucus or postnasal drip.

012345

4. Difficulty swallowing food, liquids or pills.

012345

5. Coughing after you ate or after lying down.

012345

6. Breathing difficulties or choking episodes.

012345

7. Troublesome or annoying cough.

012345

8. Sensations of something sticking in your throat or a lump in your throat.

012345

9. Heartburn, chest pain, indigestion, or stomach acid coming up.

012345

From: Belafsky PC, Postma G, Koufman JC (2002) Validity and reliability of the Reflux Symptom Index (RSI). J Voice 16:274–277

 

2.6

Chapter 2

Past Surgical History

A history of prior surgery is important to elicit with laryngeal dysfunction. In addition to questions concerning otolaryngologic procedures, any procedure requiring general anesthesia and endotracheal intubation—even briefly—should be identified. Injuries associated with endotracheal intubation include arytenoid dislocation, vocal process granuloma, vocal fold paralysis/ paresis from cuff pressure on the recurrent laryngeal nerves, posterior glottic stenosis, and interarytenoid adhesions.

2.7

Social History

The voice patient’s personal habits should be detailed. Even moderate consumption of alcohol is detrimental to the voice, through dehydration and effects on judgment. Caffeine, a diuretic, can affect the voice by thickening secretions and deTable 2.2  Special topics to include within a voice history

Upper respiratory infection Endotracheal intubation Time course Trauma Voice usage/demands Profession Vocal abuse Tobacco, alcohol, and drug use Dietary habits Foods precipitating reflux esophagitis Hydration Allergy history Environmental history Climate Heating and cooling units

creasing the efficiency of vocal fold vibration. Certain foods and alcohol predispose to gastroesophageal reflux. The deleterious effects of tobacco smoke on vocal fold are well documented. Both smoke and the heat produced by burning tobacco appear to contribute. Other fumes, such as stage smoke—particularly oil-based ones—can be of significance to vocal performance, especially stage actors.

2.8

Occupational History

Voice disorders affecting vocal professionals have considerably greater impact on function than those affecting nonprofessional voice users. Koufman and Isaacson describe four levels of vocal usage based on occupation. Level I refers to the elite vocal performer such as singers and actors. Level II describes professional voice users such as lecturers and clergy. Level III patients are nonvocal professionals such as teachers and lawyers and level IV users are nonvocal nonprofessionals. Vocal needs and function vary widely among these groups. Although the description of vocal usage is useful as a general categorization, evaluation and therapy must be individually tailored to a person’s specific voice use setting and demands.

2.9

Listening to the Voice

A critical part of the clinical evaluation is a careful subjective assessment of the patient’s voice. While taking the history, one should evaluate the quality of the patient’s speaking voice. The pitch of the voice and the rate and rhythm of speech should be noted. Posture and respiratory rate are important and should be noted during the encounter. Facial movements, especially around the mouth, as well as neck and shoulder movements should be examined for evidence of excess tension, tremors, or spasms. Consideration should be given to efficiency of breath support during speech. Evidence of excess rate, volume, or ten-

Table 2.3  Symptoms suggestive of specific voice disorders

Symptoms

Associated diagnoses

Breathiness

Vocal fold paralysis (unilateral), vocal fold mass lesion

Vocal fatigue

Vocal fold atrophy or paralysis, neurogenic dysphonia

Choking

Vocal fold paralysis, CVA

Odynophonia

Vocal fold granuloma, MTD

Paralaryngeal pain or tension

Muscular tension dysphonia (primary or secondary)

Laryngospasm

LPR, gastroesophageal reflux disease, nerve injury

Stridor

Bilateral vocal fold paralysis, laryngeal stenosis, paradoxical vocal fold motion

Vocal tremor

Parkinson’s disease, spasmodic dysphonia, benign essential tremor, myoclonus

Velopharyngeal insufficiency

Myasthenia gravis, ALS, vagal paralysis

Globus

LPR, neurologic disease, MTD

CVA cerebrovascular accident, MTD muscle tension dysphonia, ALS amyotrophic lateral sclerosis, LPR laryngopharyngeal reflux

11

12

2

Principles of Clinical Evaluation for Voice Disorders

sion during speech may indicate vocal abuse, which is highly prevalent in the dysphonic population. After careful patient observation, formal vocal testing may proceed by having the patient perform several different vocal tasks. After hearing normal speech, the patient may be asked to alter his or her type of vocal output, such as hum, sing, whisper, or yell. Also, the patient should alter pitch, perform glissando, and use rapid alternating speech. Such vocal tasks will help the listener gain insight into how the vocal pathology is affecting the different aspects of the patient’s speech, and may provide insight into the nature of the vocal dysfunction. Additionally, various words or sounds call upon the coordination of different phonatory elements. Asking the patient to recite certain phrases will assist the clinician in characterizing the disorder. For instance, the word “taxi” can be used to elicit signs of abductor spasmodic dysphonia. The phoneme “kaa” requires good palatal lift and closure and “maa” requires mouth closure. The /m/ and /n/ phonemes require good nasal resonance and are useful for testing hyper- and hyponasality. The rainbow passage (Table 2.4), which is composed of every phoneme in the English language, is used as a standardized method of recording voice in order to track clinical progress.

2.10

Perceptual Analysis

To evaluate the voice, the “trained” ear remains the most discerning instrument. Nonetheless, a standardized objective, instrument to characterize voice remains an important goal of voice science. To this end, Hirano proposed the GRBAS scale—a widely used perceptual rating instrument used by speech pathologists and laryngologists for the evaluation of voice quality in clinical settings. This scale is a subjective perceptual evaluation of five vocal characteristics assigned a value between 0 to 3, where 0 is normal, and 3 is extreme. The five elements are grade (G), a description of the degree of hoarseness, roughness (R), the perceptual irregularity of vocal fold vibrations, usually the result of a change in fundamental frequency or amplitude of vibration. Breathiness (B), or the assessment of air leakage through the glottis, is the third component of the scale. Aesthenic (A) voice denotes weakness and lack of power. Strain (S) reflects a perception of vocal hyperfunction. Another widely used auditory-perceptual evaluation of dysphonia is the Consensus Auditory-Perceptual Evaluation-Voice (CAPE-V) (Table 2.5). This rating scale was recently created by

 

Special Interest Division 3 of the American Speech-LanguageHearing Association as a standardized tool for assessment of auditory–perceptual attributes of voice. Six salient features— overall dysphonia severity, roughness, breathiness, strain, pitch, and loudness—are rated by trained listeners (SLPs and laryngologists) using a 100-mm visual analogue scale for each parameter, with the option for additional user-defined parameters.

2.11

Quality-of-Life Questionnaires

Much work has been performed to codify and measure patient self-perception of vocal dysfunction in the form of standardized questionnaires and other metrics. The voice handicap index (VHI) is a quality-of-life questionnaire specific to voice disorders, which has excellent reliability and reproducibility. The VHI assessment is a subjective patient-based questionnaire composed of 30 questions. Rosen et al. have introduced an abridged version composed of ten questions, the VHI-10 (Table 2.6). This instrument is both easily self-administered and scored quickly at the time of evaluation while preserving the original VHI’s utility and validity. Because vocal pathologies have different levels of handicap to different individuals, these questionnaires are extremely important in understanding the personal impact of these disorders on daily activities. For instance, vocal nodules that are devastating to a professional voice user may only be a minor inconvenience to a non-professional. The Voice-related Quality of Life (VRQOL) instrument has been validated and found to be useful (see Bibliography). Voice-related, patient-based surveys are helpful in judging quickly and accurately the patient’s perception of their degree of voice handicap.

2.12

Professional Speaking/Singing Voice

A comprehensive and somewhat adapted historical background is necessary in the evaluation of the singing voice. The date of the next important performance, for instance, will determine whether management of the voice problem can be conservative—designed to assure the long-term protection of the larynx—or, rather, whether more urgent intervention is needed in view of a impending important engagement. The length

Table 2.4  Rainbow passage

When the sunlight strikes raindrops in the air, they act like a prism and form a rainbow. The rainbow is a division of white light into many beautiful colors. These take the shape of a long round arch, with its path high above, and its two ends apparently beyond the horizon. There is, according to legend, a boiling pot of gold at one end. People look, but no one ever finds it. When a man looks for something beyond his reach, his friends say he is looking for the pot of gold at the end of the rainbow.

Passage reprinted from: Fairbanks G (1960) Voice and articulation handbook, p 127. Copyright 1960 by Harper Collins Publishers, Inc.

 

Chapter 2

Table 2.5  Consensus Auditory-Perceptual Evaluation of Voice (CAPE-V)

of time a singer has been performing is also important, especially if his or her performance career predates their formal vocal training. Undesirable singing techniques developed by amateur singers are particularly difficult to modify. Moreover, intermittent training, or training at the hand of multiple teachers/coaches can often result in an incompatible amalgamation of techniques requiring significant time and expert instruction to rectify. The settings in which the singer performs are of importance. Allergies to dust and mold can become major factors in older concert halls where curtains, backstage trappings, and cramped dressing room quarters are rarely cleaned.

This is especially true if stage construction is underway during rehearsals. A history of recent or frequent airplane travel suggests an alternate source of mucosal irritation. Cabin air is dry, usually at 5% or less humidity. Singers must therefore take care to maintain adequate laryngeal moisture by maintaining nasal breathing and constant hydration. Finally, exposure to stage smoke presents a unique problem, most prevalent among stage actors. Most stage smoke preparations, especially oilbased ones, can result in mucosal irritation, allergy, and bronchospasm resulting in the commonly encountered complex of hoarseness, vocal “tickle,” and vocal fatigue.

13

14

Principles of Clinical Evaluation for Voice Disorders

 

Table 2.6  Voice Handicap Index 10

2

My voice makes it difficult for people to hear me.

01234

People have difficulty understanding me in a noisy room.

01234

My voice difficulties restrict personal and social life.

01234

I feel left out of conversations because of my voice.

01234

My voice problem causes me to lose income.

01234

I feel as though I have to strain to produce voice.

01234

The clarity of my voice is unpredictable.

01234

My voice problem upsets me.

01234

My voice makes me feel handicapped.

01234

People ask, “What’s wrong with your voice?”

01234

From: Rosen CA, Lee AS, Osborne J, Zullo T, Murry T (2004) Development and validation of the voice handicap index-10 (VHI-10) Laryngoscope 114:1549–1556

Key Points

6 7

■ A successful surgical outcome is dependent upon proper clinical evaluation of the patient’s voice disorder. It therefore behooves the serious practitioner of laryngology to focus not only on his or her surgical skills, but also on evaluative and perceptual skills. This will ensure proper patient selection and make for improved surgical outcomes. ■ Careful history taking and clinical evaluation are important tools in the diagnostic evaluation of the voice patient. ■ When caring for patients with voice disorders, the clinician should pay particular attention to the level of voice use, the importance of the voice to the patient, and the impact of the voice disorder on their quality of life. ■ Clinical outcome instruments such as the Reflux Symptom Index (RSI) and the Voice Handicap Index 10 (VHI-10) are extremely useful tools for the evaluation of vocal complaints.

Selected Bibliography 1 2

3 4 5

Sataloff RT (1997) Professional voice—the science and art of clinical care, 2nd edn. Singular, San Diego Koufman JA, Amin MR, Panetti M, Prevalence of reflux in 113 consecutive patients with laryngeal and voice disorders (2000) Otolaryngol Head Neck Surg 123:385–8. Erratum in: Otolaryngol Head Neck Surg 124:104 Koufman JA (1991) The otolaryngologic manifestations of gastroesophageal reflux disease. Laryngoscope 101(Suppl.)53:1–78 Belafsky PC, Postma GN, Koufman JA (2002) Validity and reliability of the reflux symptom index (RSI). J Voice 16:274–277 Ritter FN (1973) Endocrinology. In: Paparella M, Shumrick D (eds) Otolaryngology. Saunders, Philadelphia, pp 727–734

8 9

10 11 12

13 14

15 16

17 18

19

20

Silverman EM, Zimmer CH (1978) Effect of the menstrual cycle on voice quality. Arch Otolaryngol Head Neck Surg 104:7–10 Courey MS, Postma GN (1996) Microvascular lesions of the true vocal folds. Curr Opin Otolaryngol Head Neck Surg 4:134 Sataloff RT (1995) Vocal fold hemorrhage: diagnosis and treatment. NATS J May/June:45 Smith ME, Ramig LO (1995) Neurological disorders and the voice. In: Rubin JS, Sataloff RT, Korovin GS et al (eds) Diagnosis and treatment of voice disorders. Igaku-Shoin, New York, pp 203–219 Koufman JA, Isaacson G (1991) The spectrum of vocal dysfunction. Otolaryngol Clin North Am 24:985–988 Cooper M (1973) Modern trends in voice rehabilitation. Charles C. Thomas Springfield, Ill. Bassich CJ, Ludlow DL (1986) The use of perceptual methods by new clinicians for assessing voice quality. J Speech Hear Dis 51:125 Dejonckere PH et al (1993) Perceptual evaluation of dysphonia: reliability and relevance, Folia Phoniatr (Base1) 45:76 Kreiman J et al (1993) Perceptual evaluation of voice quality: review, tutorial, and a framework for future research, J Speech Hear Res 36:21 Hirano M (1981) Clinical examination of the voice. Springer, Berlin, Heidelberg, New York Voice disorders: Consensus Auditory-Perceptual Evaluation of Voice (CAPE-V). American Speech-Language-Hearing Association Special Interest Division 3: Voice and Voice Disorders. 2003. Available at: http://www.asha.org Benninger MS, Ahuja AS, Gardner G, Grywalski C (1998) Assessing outcomes for dysphonic patients. J Voice 12:540–550 Jacobson GH, Johnson A, Grywalski C et al (1997) The Voice handicap index (VHI): development and validation. Am J Speech Lang Pathol 6:66–70 Hogikyan ND, Sethuraman G (1999) Validation of an instrument to measure voice-related quality of life (V-RQOL). J Voice 13:557–569 Ma EP-M, Yiu EM-L (2001) Voice activity and participation profile: assessing the impact of voice disorders on daily living. J Speech Lang Hear Res 44:511–524

  21 Carding PN, Horsley IA, Docherty GD (1999) Measuring the effectiveness of voice therapy in a group of forty-five patients with non-organic dysphonia. J Voice 13:76–113 22 Deary IJ, Wilson JA, Carding PN et al (2003) VoiSS, a patientderived voice symptom scale. J Psychosometr Res 54:483–489 23 Hogikyan ND, Rosen CA (2002) A review of outcome measurements for voice disorders. Otol Head Neck Surg 126:562–572

Chapter 2 24 Jacobson BH, Johnson A, Grywalsky C et al (1997) The Voice Handicap Index (VHI): development and validation. Am J Speech Lang Pathol 6:66–70 25 Rosen CA, Lee AS, Osborne J, Zullo T, Murray T (2004) Development and validation of the Voice Handicap Index-10. Laryngoscope 114:1549–1556

15

Chapter 3

Videostroboscopy and Dynamic Voice Evaluation with Flexible Laryngoscopy

3.1

Fundamental and Related Chapters

Please see Chaps. 1, 2, 4, and 5 for further information.

3.2

Introduction

Visualization of the larynx and specifically the vocal folds is paramount for the evaluation and care of patients with voice disorders. There are a variety of methods used for this visualization, ranging from indirect mirror laryngoscopy to high-speed photography. The most common and relevant clinical tools for modern-day voice evaluation and care include stroboscopic visualization of vocal fold vibration and dynamic voice evaluation with flexible laryngoscopy. These two techniques when used in a complimentary fashion can provide the clinician with detailed information on intricate vocal fold vibratory activity and phonatory and functional use of the entire vocal tract. This chapter focuses on these two main clinical methods.

3.3

Surgical Indications and Contraindications

Stroboscopy utilizes a method of “shuttering,” or synchronized illumination of the vocal folds during vocal fold vibration (Fig. 3.1). This provides “pseudo” slow motion visualization of vocal fold vibration. Real-time vocal fold vibration is too rapid to visualize with the unaided eye. The stroboscopic light source illumination provides representative images from the entire vibratory cycle. A periodic or nearly periodic vocal fold vibratory activity is required for stroboscopy to be successful. It is important to note that stroboscopy can be done through any type of visualization instrument including flexible laryngoscopy and rigid perioral laryngoscopy. Stroboscopy is strictly the light source and not the actual equipment used for visualization of the vocal folds. (i. e., flexible laryngoscopy or rigid telescope). The most common vocal fold vibratory characteristics that stroboscopy allows one to view are: ■ ■ ■ ■ ■

Vocal fold closure (pattern and duration) Mucosal wave movement (propagation) Symmetry of vibration Amplitude of vocal fold vibration Periodicity

3

Stroboscopy helps elucidate specific lesions of the vocal folds, especially as they relate to closure pattern for exophytic lesions and defects of the lamina propria such as seen in adynamic segments of the vocal fold, vocal fold scar, and sulcus vocalis. Vocal fold closure pattern is typically described as the global overall pattern of vocal fold closure, as seen during the majority of the examination specifically at modal pitch and intensity of vowel prolongation. The most commonly cited and utilized closure patterns include complete, incomplete, hourglass, anterior glottic gap, and excessive posterior glottic gap (Fig. 3.2). Mucosal wave as seen during stroboscopy refers to a rippling motion traveling over the vocal fold and within the vocal fold mucosa. The wave is propagated from the subglottic area and travels from underneath the vocal fold along the free edge, then over the superior surface of the vocal fold and is dampened in the area of the ventricle. This mucosal wave activity is crucial for assessing the pliability and functional characteristics of the lamina propria of the vocal folds. Areas of diminished mucosal wave represent loss of pliability or viscoelasticity of the vocal fold lamina propria and are an important aspect of voice evaluation. Mucosal wave activity should be assessed at a variety of phonatory tasks, specifically at low, medium, and high pitch and different levels of intensity. The duration of vocal fold closure is also an important clinical assessment parameter. At modal pitch and intensity, vocal fold vibratory closure should occur approximately half of the vibratory cycle. This can be measured in a detailed fashion us-

Fig. 3.1  “Representative” set of images from stroboscopy depicting

“one” vibratory cycle

18

3

Videostroboscopy – Flexible Laryngoscopy

ing electroglottography but can also be estimated using frameby-frame review of the recorded stroboscopic images. Vocal fold vibration symmetry during stroboscopy is judged by comparing the vocal folds’ vibratory activity to one another. The vibration of one vocal fold should be a mirror image of the contralateral fold. The degree of vocal fold amplitude (horizontal excursion from midline) during vocal fold vibration as seen during stroboscopy is an important assessment tool and involves both the comparative as well as overall subjective assessment of the amount of amplitude of each vocal fold during vocal fold vibration (Fig. 3.3). Of course, amplitude and closure are two stroboscopy parameters that are directly affected by the voice intensity and pitch during the stroboscopic examination and these factors must be constantly monitored and taken into consideration when assessing these parameters. For example, at high pitches both the amplitude and mucosal wave decrease as compared to lower pitches. Periodicity describes the regularity of vocal fold vibration. Periodicity is based on the regularity of successive cycles of vibration. Even though symmetry and periodicity may be thought to assess similar behavior, in fact, vocal folds can have distinctly different amplitude and symmetrical activity and still be quite periodic. The converse is also true where vocal folds can demonstrate aperiodic activity with normal and symmetric amplitude (as often seen with vocal fold paresis). Stroboscopy of the vocal folds is helpful for visualization of a variety of vocal fold lesions, which are discussed in detail in Chap. 4, “Pathological Conditions of the Vocal Cords.” Stroboscopy is also extremely important for visualization of seg-

 

ments of the vocal fold with poor vibratory characteristics due to scar, subtle lesions, loss of lamina propria tissue or sulcus vocalis (see Chap. 23, “Sulcus Vocalis and Vocal Fold Scar”). Stroboscopy to assess vocal fold vibratory activity should be done using a fairly consistent assessment protocol. First, it is essential to identify that the patient has a periodic or nearly periodic signal. A typical stroboscopy examination protocol includes: ■ Modal voice (most comfortable pitch and intensity) ■ Low pitch (soft and loud to assess maximum pliability) ■ High pitch, soft intensity phonatory task The latter is extremely helpful for identifying subtle lesions of the vocal fold as well as assessing abnormalities associated with vocal fold pliability and vocal fold vibratory activities. The low pitch-loud task is helpful not only for assessing overall pliability, but also for patients with the most aperiodic voice. When performing stroboscopy, the vocal fold vibratory activity and characteristics should be first compared internally (to each other), and then compared to the examiners experiential database and most importantly correlated with the amount and nature of dysphonia of the patient. There should be a good correlation from an auditory and visual perceptual basis. If this is not the case, then a repeat examination or careful examination of other factors should be undertaken.

3.4

Dynamic Voice Assessment with Flexible Laryngoscopy

Flexible laryngoscopy is an essential evaluation technique for voice disorders-related “functional” problems such as muscle tension dysphonia, paradoxical vocal fold motion disorder and

Fig. 3.2  Different vocal fold closure patterns

Fig. 3.3  Vocal fold amplitude

 

Chapter 3

functional aphonia, neurologic voice disorders (spasmodic dysphonia, essential tremor, etc.), and vocal fold paresis. Dynamic voice assessment with flexible laryngoscopy evaluates multiple parameters associated with phonation done in a dynamic and “most natural” setting. Equipment required includes nasal speculum, decongestant and anesthetic for the nasal cavity, flexible laryngoscopy, and illumination light source(s) (continuous halogen and preferably stroboscopy). This examination is done in a stepwise fashion, examining each section of the vocal tract which is outlined below from an anatomic and a physiologic perspective (at rest and then in activation). The specific areas of activation include vegetative functions and phonation. The subregions of the dynamic voice assessment include nasopharynx, base of tongue, larynx (global), and the vocal folds. At each one of these specific subportions of the dynamic voice assessment, specific tasks are elicited from the patient to look for different pathologies in the area and confirm or rule out a variety of disorders (Table 3.1).

3.4.1

Table 3.1  DVA tasks, findings, and correlated diagnoses: examination

protocol—tasks

Velum Sustained /ee/ /koka kola/ Base of tongue Evaluation of symmetry and mucosa Larynx Quiet respiration Sustained /ee/—comfortable pitch Sustained /ee/—low and high pitch /ee/ /ee/ /ee/ (with a breath between each “hee”) “We were away a year ago.” “We were away a year ago.”—comfortable pitch Example of connected speech (Ask, “What did you do yesterday?”) Sing “Happy Birthday” Cough Laugh

Nasopharynx

1. Patient task: rest, sustained phonation (/ee/) and speech

(/koka kola/) and prolonged fricative /s/

2. Parameters of evaluation: nasal disease, masses of the naso-

pharynx, tremor of the soft palate (rest and activation) and velopharyngeal incompetence (VPI) 3. Pathology: velopharyngeal incompetence, vocal tremor, sinonasal disease, (infectious or allergic) nasopharyngeal neoplasms

3.4.4

Vocal Fold (Focal)

1. Patient task: respiration, sustained phonation and alternat-

ing speech and respiration (see Table 3.1)

2. Parameters of evaluation: vocal fold lesions, glottal insuf-

ficiency and tremor

3. Pathology: focal vocal fold lesions (polyp, nodules, etc.)

3.4.2

Base of Tongue

1. Patient task: rest and tongue protrusion 2. Parameters of evaluation: tremor, fasciculations (ALS), tu-

mors, infections 3. Pathology: essential tremor of the vocal tract, amyotrophic lateral sclerosis (ALS), neoplasm (benign and malignant) and infection

3.4.3

Larynx (Global)

1. Patient task: quiet respiration, alternating sustained phona-

tion and respiration (hee-hee-hee, with a breath between each “hee”) and connected speech (“We were away a year ago.”) 2. Parameters of evaluation: vocal fold mobility and synchrony of mobility Paradoxical vocal fold motion, supraglottic constriction associated with phonation, and global laryngeal tremor 3. Pathology: paradoxical vocal fold motion disorder, primary muscle tension dysphonia, secondary muscle tension dysphonia, vocal tremor, vocal fold paralysis, vocal fold paresis, as well as pyriform/vallecular lesions, LPR

cancer, vocal fold atrophy, vocal field paralysis and vocal fold paresis

3.5

Recording of Laryngeal Examination

It is highly recommended but not absolutely necessary that the stroboscopy and/or dynamic voice evaluation be recorded. The two most common methods of recording portions or all of these examinations are with either still photography or video recording. The advantages of recording all or portions of the laryngeal examinations include: ■ ■ ■ ■

Longitudinal comparison Preoperative planning Patient education Medical/legal uses

Further justification and use of a video recording include the ability to record an audio track in conjunction with the video examination. Both audio and video examination can be extremely helpful for all of the above-mentioned reasons; especially in a court of law. It is essential to have a baseline or preoperative audio and/or voice recording prior to and after

19

20

3

Videostroboscopy – Flexible Laryngoscopy

elective surgical procedures. This is analogous to the documentation procedures for cosmetic surgical procedures. Video recordings of the vibratory parameters of the vocal fold are also very helpful to refer to when surgically resecting a lesion.

Key Points ■ Stroboscopy and dynamic voice assessment (DVA) with flexible laryngoscopy are essential aspects of a voice evaluation and care. ■ Strobe and DVA are complementary and should not be viewed in isolation. ■ The dynamic voice assessment and evaluation allows for a natural in vivo evaluation of the entire vocal tract during rest, vegetative activities, and phonation (connected and sustained), and stroboscopy allows the examiner insight into key vocal fold vibratory activity, specifically the physiologic and pathophysiologic activities related to the patient’s dysphonia.

 

■ The combination of stroboscopy and dynamic voice assessment with flexible laryngoscopy allows the clinician to correlate the patient’s voice symptoms, related physical exam abnormal findings, craft an accurate diagnosis and form a successful treatment plan.

Selected Bibliography 1 2 3 4 5

Hirano M, Bless DM (1993) Videostroboscopic examination of the larynx. Singular, San Diego Stasney CR (1996) Atlas of dynamic laryngeal pathology. Singular, San Diego Cornut G, Bouchayer M. Assessing dysphonia: the role of videostroboscopy. Five videocassettes, 254 min Rosen CA (2005) Stroboscopy as a research instrument: development of a perceptual evaluation tool. Laryngoscope 115:423–428 Roehm PC, Rosen C (2004) Dynamic voice assessment using flexible laryngoscopy—how I do it: a targeted problem and its solution. Am J Otolaryngol 25:138–141

Chapter 4

4

Pathological Conditions of the Vocal Fold

4.1

Fundamental and Related Chapters

Please see Chaps. 2 and 3 for further information.

4.2

Introduction

The variety of pathologic conditions that occur within the vocal fold can be separated into categories based on their anatomical location. The chapter is divided among epithelial pathology of the vocal folds, benign midmembranous lesions, and miscellaneous vocal fold pathology. A brief overview and discussion of the key points of each of these vocal fold lesions, especially as they relate to the surgical treatment is included. It should be stressed that with the exclusion of carcinoma and recurrent respiratory papilloma of the vocal folds, most of the vocal fold lesions are benign and in general should be managed with a conservative approach that involves maximizing all nonsurgical treatment methods first, and then only proceeding with surgical treatment if key functional issues (i. e., voice quality and vocal function) are still persistent.

4.3

Epithelial Pathology of the Vocal Folds

4.3.1

Recurrent Respiratory Papillomatosis of the Larynx

Recurrent respiratory papillomatosis of the larynx is an epithelial growth of the larynx most commonly seen at the level of the vocal folds (Fig. 4.1). These growths are a direct response to a human papilloma virus infection and tend to be recurrent in nature. The most common human papilloma virus types involved with RRP of the larynx are HPV types 6 and 11. These recurrent benign lesions grow most significantly at epithelial transition sites, such as where pseudostratified columnar and stratified squamous are juxtaposed. Any time a new epithelial transition site is created in a patient who is infected with the human papilloma virus, there is a high risk of a new papillomatous disease growth at that site. This is frequently demonstrated when a tracheotomy is performed on a patient with recurrent respiratory papillomatosis. Malignant transformation of these types of HPV infection are extremely rare, and historical experience has demonstrated that external beam radiation therapy, tobacco exposure, pul-

monary involvement, and alcohol exposure increase the risk of RRP malignant transformation. It cannot be overemphasized that the chance of curing patients with RRP using surgical excision alone is low; likewise, there is no evidence that a more aggressive operation will increase the patient’s long-term control of his or her disease. The surgical philosophical approach for RRP should be to: (1) maintain a patent airway without using a tracheotomy, (2) optimize functional results with respect to voice and swallowing, and (3) minimize chance of operative complications and sequelae such as glottic webbing and vocal fold scar formation.

4.3.2

Leukoplakia of the Vocal Fold

Abnormal epithelial hypertrophy or dysplasia of the vocal folds can be manifested as redundancy of the epithelial or keratotic layers of the vocal folds resulting in hyperkeratosis, parakeratosis, and is clinically referred to as leukoplakia (Fig. 4.2). An important differentiation of this pathology relates to the anatomic structure of the cells involved in the abnormal epithelium. Often these cells can become dysplastic and are thought to be a precursor for malignancy. However, many patients who suffer from keratosis of the vocal fold show no dysplasia of these lesions and are strictly burdened by the repetitive regrowth of a hyperkeratotic epithelial covering at various locations of the

Fig. 4.1  Recurrent respiratory papillomatosis, bilateral

22

Pathological Conditions of the Vocal Fold

 

vocal folds. These lesions can be singular in nature or they can be multiple and diffuse throughout the vocal folds and arytenoid cartilages. Given that the risk of transformation of this leukoplakic biologic activity into a malignancy is present (statistically < 10%), these patients require careful monitoring and a complete surgical excision of any suspicious leukoplakic lesion. Suspected risk factors for keratosis include viral infection, LPR, and vocal fold phonotrauma (primary or secondary to glottal insufficiency). It is equally important to remember that the majority of patients with keratosis of the vocal folds will not develop a malignancy and most likely will have recurrent lesions in the future; thus, principles of conservative excision and patient observation with longitudinal photo documentation are essential to the care of this patient group. There is no role for external beam radiation for these patients.

4

Fig. 4.2  Keratosis of the left vocal fold

4.3.3

Dysplasia–Carcinoma in Situ of the Vocal Folds

Dysplasia or carcinoma in situ of the vocal folds represents a demonstrable change of the normal epithelial cellular structure and is thought to be a precursor toward development of malignancy of the vocal folds (Fig. 4.3). Specifically, dysplasia is graded on the severity of the abnormal morphology of the epithelial cells. Carcinoma in situ refers to carcinomatous transformation without basal membrane penetration. Once abnormal epithelial cells have breached the basement membrane of the epithelium, the condition is then defined as a carcinoma or microinvasive carcinoma of the vocal folds. Complete excision of dysplasia and/or carcinoma in situ of the vocal folds is crucial to preventing more serious and significant problems of carcinoma of the vocal folds.

4.3.4 Fig. 4.3  Dysplasia–carcinoma in situ of the right vocal fold

Fig. 4.4  Carcinoma of the left vocal fold

Carcinoma of the Vocal Fold

Carcinoma of the vocal fold represents a malignant invasion of the epithelial cells into the vocal fold, lamina propria, and beyond, depending on the severity of the invasion. (Fig. 4.4) Staging of vocal fold cancer is based on the location(s) of the disease as well as the degree of invasion and subsequent limitation of vocal fold motion due to the cancer invasion. Early T1 and T2 stage cancer of the vocal folds can be successfully treated with surgical excision and/or radiation therapy. T1 vocal cord carcinoma has a 5-year survival of 90–98% when treated with either one of these modalities (see Chap. 30, “Carcinoma of the Vocal Fold”).

 

Chapter 4

4.4

Benign Diseases of the Vocal Fold Lamina Propria

4.4.1

Overview of Midmembranous Vocal Fold Lesions

Midmembranous lesions of the vocal fold are abnormalities of lamina propria of the vocal fold, with minimal or no changes of the overlying epithelium. These lesions are extremely common causes of voice disorders and often require surgical therapy. Significant confusion and debate exists regarding the nomenclature and classification of these lesions. Unfortunately, visualization alone of these lesions does not properly stratify and classify these lesions, and thus a multidimensional system has been developed and is required to classify properly the midmembranous vocal fold lesions. It is important for this classification to be exact, given that clinical outcomes and patient prognosis, and surgical treatment with different midmembranous vocal fold lesions differ significantly. This book uses a classification system utilizing four commonly used clinical modalities to differentiate seven distinct benign midmembranous vocal fold lesions. These classification methods include (1) morphology (midmembranous vocal fold lesion), (2) characteristics of the mucosa wave of the lesion and surrounding areas as seen on stroboscopy (minimal–normal versus significant impairment), (3) response of the lesion in the form of resolution or reduction in size to voice rest/voice therapy, and (4) intraoperative findings. The latter includes location of the pathology (subepithelial or near the vocal ligament) and the physical characteristics of the lesion, presence or absence of a capsule wall, physical features, and nature of the pathology.

4.4.2

Approach to Midmembranous Vocal Fold Lesions

In most instances, patients with midmembranous vocal fold lesions have relatively normal epithelium overlying their pathologic process, and thus, the concern for cancer is extremely low. Often these lesions respond extremely well to nonsurgical treatment methods such as voice therapy and treatment of comorbid medical problems. This approach should be taken for most patients with midmembranous vocal fold lesions causing significant dysphonia (see Chap. 7, “Medical Treatment of Voice Disorders”). After the implementation and adequate treatment time of these nonsurgical treatment methods, the patient should have a repeat comprehensive voice evaluation to determine the amount of improvement and to determine if there are any residual functional limitations to their voice use and demands. If these functional limitations are significant to the patient and can be reasonably projected to improve with surgical excision of the vocal fold lesion(s), then phonomicrosurgery is indicated. The decision making on initial treatment(s), duration and timing of surgery is complex and does not lend to formulaic approaches. In general, patients should be treated with nonsurgical therapy before surgery. Exceptions include distinct lesions that are hightly unlikely to

improve without surgery (i. e., a large, pedunculated polyp). In these instances, a short period of both reduced voice use and voice therapy is implemented (2–3 weeks), followed by a reevaluation of the lesion(s) and patient’s vocal functional abilities (see Chap. 8, “Timing, Planning, and Decision Making for Laryngeal Surgery”).

4.4.3

Vocal Fold Nodules

Vocal fold nodules are benign, midmembranous vocal fold lesions involving most likely the most superficial aspect of the lamina propria as well as the basement membrane zone of the vocal fold epithelium (Fig. 4.5). They are thought to be “calluses” of the vocal folds and are always bilateral and fairly symmetric. Vocal fold nodules are seen almost exclusively in females in adults, and both genders in children. These lesions by definition respond to a combination of voice rest and voice therapy, when the patient is compliant and the voice therapy is done in an appropriate fashion. Stroboscopic behavior of vocal fold nodules typically demonstrates an hourglass closure pattern and normal or minimally reduced mucosal wave vibratory activity (see Chap. 16, “Vocal Cord Nodules”).

4.4.4

Vocal Fold Cyst (Subepithelial)

A subepithelial vocal fold cyst represents an encapsulated lesion within the superficial aspect of the lamina propria, typically found in the midmembranous vocal fold (Fig. 4.6). The stroboscopic pattern of a subepithelial vocal fold cyst is an hourglass closure pattern, with normal to minimal disruption of the mucosal wave vibratory activity (depending on

Fig. 4.5  Vocal fold nodules (bilateral)

23

24

Pathological Conditions of the Vocal Fold

 

rest or voice therapy, and the prognosis for prompt recovery of the voice after surgical excision is less when compared with a vocal fold polyp or subepithelial cyst. The surgical approach to this lesion involves a microflap (see Chaps. 10 and 17).

4

4.4.6

Fig. 4.6  Cyst (subepithelial) of left vocal fold

A vocal fold polyp is a pathologic process of the lamina propria that involves typically an exophytic or pedunculated lesion of the midmembranous vocal fold that can be unilateral or bilateral (Fig. 4.8). The stroboscopic pattern of a vocal fold polyp shows an hourglass closure pattern with normal or minimal reduction of the vibratory activity of the mucosa. A vocal fold polyp does not respond to voice therapy and rest (by definition), and intraoperative exploration reveals a focal accumulation of a gelatinous material, often under a severely thin and atrophic epithelium. Surgical excision of the vocal fold lesion can be done through a microflap approach or truncation of the vocal fold lesion (see Chap. 10, “Principles of Phonomicrosurgery” and 15, “Vocal Fold Polyp”).

4.4.7

Fig. 4.7  Cyst (ligament) of left vocal fold

size). Subepithelial vocal fold cysts typically do not respond or change in any appreciable fashion to voice rest or voice therapy. Surgical excision when indicated of a vocal fold subepithelial cyst is done through a microflap approach to the vocal fold (see Chaps. 10, “Principles of Phonomicrosurgery” and 17, “Vocal Fold Cyst and Fibrous Mass”).

4.4.5

Vocal Fold Cyst (Ligament)

A vocal fold cyst found in the area near the vocal ligament is an encapsulated, benign pathologic process that typically involves significant reduction of mucosal wave vibratory wave activity as seen on stroboscopy as well as an hourglass closure pattern (Fig. 4.7). It is located in the deep aspect of the lamina propria and often better visualized within the vocal fold in abduction compared to adduction. This lesion does not respond to voice

Vocal Fold Polyp

Fibrous Mass (Subepithelial)

A subepithelial fibrous mass represents an accumulation of fibrous tissue within the subepithelial aspect of the midmembranous vocal fold (Fig. 4.9). This material is typically amorphous in nature and often has thin extensions anteriorly and posteriorly within the vocal fold, giving it a fusiform shape. Stroboscopic pattern of fibrous mass in the subepithelium demonstrates an hourglass closure pattern, with significant reduction of the mucosal wave vibratory activity as seen on stroboscopy. This pathology does not respond to nonsurgical treatment methods, and the surgical approach for this lesion is through a microflap. The surgical approach to these lesions is similar to a subepithelial vocal fold cyst, but the vocal recovery is more delayed and overall prognosis reduced comparatively (see Chaps. 10, “Principles of Phonomicrosurgery” and 17, “Vocal Fold Cyst and Fibrous Mass”).

4.4.8

Fibrous Mass (Ligament)

A ligamentous fibrous mass represents fibrous tissue accumulation in the midmembranous vocal fold near the vocal ligament (Fig. 4.10). Often this tissue is amorphous and has extensions anteriorly and posteriorly in the vocal fold. This lesion does not respond to nonsurgical treatment methods. The stroboscopic pattern of fibrous mass and ligament reveals hourglass closure pattern and significant reduction of the mucosal wave vibratory activity. The surgical approach is similar to a ligamentous vocal fold cyst, via a microflap. The speed of vocal recovery is reduced compared with a vocal fold cyst, and the overall vocal function prognosis is worse than other midmembranous vocal fold lesions (see Chaps. 10, “Principles of Phonomicrosurgery” and 17, “Vocal Fold Cyst and Fibrous Mass”).

 

Chapter 4

4.4.9

Reactive Lesion

A reactive lesion is a submucosal, pathologic process of the vocal fold in response to a contralateral vocal fold lesion (i. e., vocal fold cyst, vocal fold polyp, fibrous mass) (Fig. 4.11). This lesion typically has a hourglass closure pattern seen on stroboscopy and has minimally reduced or normal mucosal wave vibratory activity on stroboscopy. This lesion responds quite favorably to voice rest and voice therapy and typically will reduce in size with this treatment modality. Surgical excision of the lesion can be done if the contralateral lesion requires surgery. The surgical approach is similar to a vocal fold polyp (see Chaps. 10, “Principles of Phonomicrosurgery” and 15, “Vocal Fold Polyp”). One may also elect not to operate on the reactive lesion, to remove the risk of an adverse surgical outcome (scar) at the operative site.

4.5

Miscellaneous Disorders of the Vocal Fold

4.5.1

Polypoid Corditis (Reinke’s Edema)

Fig. 4.8  Polyp, left vocal fold

Fig. 4.9  Fibrous mass (subepithelial), right vocal fold

Reinke’s edema is a pathologic condition of the vocal fold that involves an accumulation of a gelatinous type of fluid throughout the superficial aspect of the lamina propria (Fig. 4.12). Often these accumulations can be quite severe, and it may become asymmetric; however, in general the process occurs throughout the entire vocal fold and is also exclusively found bilaterally. Reinke’s edema involves a demonstrable increase in size of the mass and volume of the vocal fold, which typically lowers the pitch of the voice and causes increased vocal effort and instability. The most common etiologic factors of Reinke’s edema involve tobacco abuse (97%), laryngopharyngeal reflux disease, and phonotrauma. Each of these potential etiologic factors should be addressed in a strict and thorough fashion prior to proceeding with surgical treatment of the Reinke’s edema (see Chaps. 10, “Principles of Phonomicrosurgery” and 18, “Polyp Corditis [Reinke’s Edema]”).

4.5.2

Fig. 4.10  Fibrous mass (ligament), left vocal fold

Vocal Fold Granuloma

A vocal fold granuloma is inflammatory tissue arising from the perichondrium of the arytenoid cartilage (Fig. 4.13). This is a response to trauma of the arytenoid perichondrium, often found after orotracheal intubation, or excessive hyperadduction of the arytenoid cartilage (found in some phonatory behaviors and chronic cough). LPR is thought to contribute to further inflammation and propagation of granulomatous formation. Once the etiologic trauma and irritants that initiated the vocal fold granuloma are removed, vocal fold granuloma disease will often spontaneously resolve over a matter of several months. Surgical excision of vocal fold granuloma should only be performed if there is an acute airway obstruction, a suspicion of malignancy or after all etiologic factors have been thoroughly addressed (see Chap. 19, “Vocal Process Granuloma”).

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Pathological Conditions of the Vocal Fold

 

4.5.3

4

Fig. 4.11  Reactive lesion of the right vocal fold (asterisk)

Rheumatologic Lesions of the Vocal Folds

A variety of rheumatological disorders (e. g., rheumatoid arthritis, systemic lupus) can cause an unusual inflammatory process and deposition of abnormal tissue within the lamina propria of the vocal fold. This tissue typically results in severe reduction of the vibratory activity of the vocal folds, as seen in stroboscopy. These lesions are often adjacent to the vocal fold ligament or can occupy the entire width of the lamina propria. They have been known to form several distinct lesions within a single vocal fold, resulting in a “bamboo” appearance of the vocal fold; thus, these lesions are often called bamboo lesions of the vocal fold (Fig. 4.14). Microflap approach to surgical excision of these lesions is warranted when there is significant dysphonia, and all attempts to control the rheumatological disease have been implemented (see Chap. 10, “Principles of Phonomicrosurgery”). Given the intense fibrotic nature of this lesion(s), the surgical dissection can be difficult and tedious, and postoperative vocal fold stiffness is common.

4.5.4

Vascular Lesions of the Vocal Folds

A variety of vascular lesions of the vocal fold can occur, most commonly associated with repeated phonotrauma of the vocal folds. This involves an abnormal vascular structure formation and vessel diameter of the subepithelial blood vessels of the vocal fold (Fig. 4.15). By convention, the normal subepithelial vocal fold vasculature runs parallel to the longitudinal axis of the vocal fold. Vascular abnormalities of the vocal fold typically run perpendicular to the longitudinal axis of the vocal fold and are significantly greater than one millimeter in diameter. They can present and develop in a variety of different patterns, such as vascular lakes, ectasias, and varices. The management and Fig. 4.12  Reinke’s edema of the vocal folds, bilateral

Fig. 4.13  Arytenoid granuloma

Fig. 4.14  Rheumatological lesions of the right vocal fold (asterisks)

 

Chapter 4

mation of the vocal fold epithelium onto the vocal fold ligament. Sulcus vocalis presents typically as a furrow along the free edge of the vocal fold in varying lengths and varying severity with respect to the degree of loss of the lamina propria (Fig. 4.16). Sulcus vocalis can often also have associated vocal fold pathologic entities, such as vocal fold lesions (e. g., cysts, fibrous mass, etc.) and mucosal bridges. The medical and surgical approaches to vocal fold scar and sulcus vocalis are discussed in Chaps. 23, “Sulcus Vocalis and Vocal Fold Scar,” and 48, “Gray’s Minithyrotomy for Vocal Fold Scar/Sulcus Vocalis,” respectively.

Key Points

Fig. 4.15  Vascular lesions of the vocal fold

■ Most pathological conditions of the vocal folds are benign and occur within the epithelium or the lamina propria. ■ Recurrent respiratory papillomatosis of the larynx occurs from a viral (HPV) infection of the epithelium (most commonly the epithelium of the vocal folds). The diffuse infection of the virus and the recurrent nature of the disease demand a conservative surgical approach. ■ Premalignant changes of the epithelium and cancer of the vocal fold require careful observation/treatment to maximize treatment success and voice preservation. ■ Benign midmembranous vocal fold lesions typically occur from vocal misuse/overuse. These lesions cannot be accurately diagnosed by viewing alone. Using morphology, response to voice therapy and surgical findings, seven distinct lesions can be strictly defined: vocal nodules, fibrous mass (subepithelial or ligament), cyst (subepithelial or ligament), polyp, and reactive lesion. ■ Vocal fold scar and sulcus vocalis represent severe derangement or loss of the vocal fold lamina propria (respectively).

Fig. 4.16  Sulcus vocalis

Selected Bibliography surgical approach to these lesions are discussed in Chap. 22, “Surgical Management of Vocal Fold Vascular Lesions”.

1

2

4.5.5

Vocal Fold Scar and Sulcus Vocalis

Vocal fold scar and sulcus vocalis represent severe abnormalities of the lamina propria of the vocal fold. The former involves replacement of the normal extracellular matrix proteins of the lamina propria with abnormal scar tissue and an altered collagen matrix structure. Sulcus vocalis is a loss or absence of the vocal fold lamina propria, resulting in a direct approxi-

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4

Rosen CA et al (2003) Benign midmembranous vocal fold lesion nomenclature paradigm. AAO-HNS annual meeting, Orlando, Fla., 23 September 2003 Derkay CS, Hester RP, Burke B, Carron J, Lawson L (2004) Analysis of a staging assessment system for prediction of surgical interval in recurrent respiratory papillomatosis. Int J Pediatr Otorhinolaryngol 68:1493–1498 Schweinfurth JM, Powitzky E, Ossoff RH (2001) Regression of laryngeal dysplasia after serial microflap excision. Ann Otol Rhinol Laryngol 110:811–814 Thekdi, AA, Rosen CA (2003) Surgical treatment of benign vocal fold lesions. Curr Opin Otolaryngol Head Neck Surg 10:492–496

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Pathological Conditions of the Vocal Fold 5

6

4

Zeitels SM, Hillman RE, Bunting GW, Vaughn T (1997) Reinke's edema: phonatory mechanisms and management strategies. Ann Otol Rhinol Laryngol 106:533–543 Hochman I, Sataloff RT, Hillman RE, Zeitels SM (1999) Ectasias and varices of the vocal fold: clearing the striking zone. Ann Otol Rhinol Laryngol 108:10–16

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Welham NV, Rousseau B, Ford CN, Bless DM (2003) Tracking outcomes after phonosurgery for sulcus vocalis: a case report. J Voice 17:571–578 Rosen CA (2000) Vocal fold scar: evaluation and treatment. Otolaryngol Clin North Am 33:1081–1086 Verdolini K, Rosen CA, Branski R. (2005) Classification Manual of Voice Disorders. Lawrence Erlbaum Associates, Mahwah, NJ

Chapter 5

Glottic Insufficiency: Vocal Fold Paralysis, Paresis, and Atrophy

5.1

Introduction

Glottic insufficiency is one of the most common contributing factors in patients who present with dysphonia. It is also one of the easiest findings to overlook in the clinical evaluation (Fig. 5.1). Causes of glottal insufficiency include: ■ Vocal fold immobility/partial immobility from one or a combination of: ■ Vocal fold paralysis ■ Vocal fold paresis ■ Cricoarytenoid joint derangements (e. g., fixation or subluxation) ■ Vocal fold atrophy/soft tissue deficiency due to: ■ Deinnervation (vocal fold paralysis/paresis) ■ Age-related changes (presbylaryngis) ■ Tissue loss from ablative/destructive vocal fold procedures ■ Vocal fold scar ■ Sulcus vocalis deformity ■ Myopathic disease (rare) In clear-cut clinical settings such as unilateral vocal fold paralysis, the diagnosis of glottic insufficiency can is made through flexible laryngoscopy alone. However, videostroboscopy is essential to evaluate for glottal insufficiency when both vocal folds appear mobile, as is frequently the case with subtle vocal fold weakness, vocal fold scar and sulcus vocalis (Chap. 3, “Videostroboscopy and Dynamic Voice Evaluation with Flexible Laryngoscopy”). The most common causes of symptomatic glottic insufficiency and the focus of this chapter are: 1. Unilateral vocal fold paralysis (UVFP) 2. Presbylaryngis/age-related changes of the larynx 3. Vocal fold paresis (unilateral and bilateral)

5.2

Unilateral Vocal Fold Paralysis

5.2.1

Etiology

The etiology of UVFP involves dysfunction of the brainstem nuclei, the vagus nerve, or the recurrent laryngeal nerve (RLN) supplying the involved side of the larynx. The vagus nerve exits the skull base via the jugular foramen and descends in the carotid sheath, giving off three major branches: the pharyngeal branch, the superior laryngeal nerve (SLN), and the re-

5

current laryngeal nerve (RLN). The SLN supplies sensation to the glottic and supraglottic larynx, as well as motor input to the cricothyroid muscle, which controls vocal fold lengthening and pitch. The RLN arises from the vagus nerve in the upper chest and loops under the aortic arch (left) or subclavian artery (right), and ascends back into the neck, traveling in the tracheoesophageal groove. The nerve enters the larynx posteriorly, adjacent to the cricothyroid joint. The RLN innervates the ipsilateral posterior cricoarytenoid (PCA), the interarytenoid (IA) (an unpaired muscle), and the lateral cricoarytenoid (LCA), and terminates in the thyroarytenoid (TA). Thus, the RLN supplies all of the intrinsic laryngeal muscles with the exception of the cricothyroid muscle. Ipsilateral RLN transection usually results in complete unilateral vocal fold immobility (the ipsilateral CT does not contribute to vocal fold adduction or abduction). It is important to remember, however, that the interarytenoid muscle is unpaired, and contralateral RLN input to the IA may lead to some adduction of the vocal fold on the paralyzed side (Fig. 5.2) The causes of unilateral VFP are myriad, but can be broken down into categories to highlight the relevant pathophysiology. These are shown in Table 5.1. Iatrogenic nerve injury likely represents the most common cause for otolaryngologic referral. Common iatrogenic surgical causes of UVFP include thyroidectomy/parathyroidectomy, anterior cervical disc surgery, esophagectomy, thymectomy, neck dissection, carotid endarterectomy, mediastinoscopy, and cardiothoracic surgery, including aortic surgery, coronary ar-

Fig. 5.1  Videostroboscopy image of glottic insufficiency due to a right

vocal fold paralysis. The right vocal fold is lateralized and a visible glottic gap is present during phonation

30

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Glottic Insufficiency

tery bypass grafting, and pulmonary lobar resection. Endotracheal intubation, prolonged nasogastric tube placement, and even esophageal stethoscope placement have been implicated as occasional causes of VFP. Nonlaryngeal malignancies are another common cause of unilateral VFP. The most common scenario involves bronchiogenic carcinoma of the lung associated with a left RLN paralysis. The cause in these cases is usually due to mediastinal spread of the malignancy into the aortopulmonary window. These paralyses rarely resolve spontaneously, and deserve early intervention. Other nonlaryngeal malignancies include thyroid, esophageal, and skull base (i. e., paraganglioma) tumors. The neurologic event most commonly associated with unilateral VFP is stroke, usually of the brainstem. However, in these patients, other neurologic symptoms (such as paraplegia) or additional cranial nerve involvement are the rule, and isolated UVFP in this setting is highly unlikely. Many of these patients have severe dysphagia and aspiration due to ipsilateral laryngopharyngeal sensory and motor deficits. Idiopathic UVFP is also seen frequently. A small number of case reports suggest that “idiopathic” UVFP may be due to her-

Fig. 5.2  Diagram depicting the dual innervation (from both the right

and left RLN) of the interarytenoid muscle

Table 5.1  Unilateral vocal fold immobility: causes

Cause (%) Malignancy—nonlaryngeal (24.7) Iatrogenic—surgical trauma (23.9) Idiopathic (19.6) Nonsurgical trauma (11.1) Intubation (7.5) Neurologic (7.9) Thoracic aortic aneurysm (4.3) Pulmonary or mediastinal TB (1.1)

Adapted from: Benninger MS, Gillen JB, Altman JS (1998) Changing etiology of vocal fold immobility. Laryngoscope 108:1346–1349

 

pes simplex infection (HSV1) of the vagus nerve or its branches. The injury is presumed to be an inflammatory neuropathy, similar to the cranial neuritis observed with Bell’s palsy. Although this theory is widely regarded as true, little scientific data have been published to demonstrate that HSV neuritis is the causative agent in “idiopathic” UVFP. In addition, no studies exist that evaluate the benefit of systemic corticosteroids and/or antivirals in the treatment of this condition. Idiopathic UVFP is a diagnosis of exclusion, only after a detailed history and appropriate imaging studies fail to demonstrate a cause. Medications such as the vinca alkaloids (vincristine and vinblastine), and cisplatinum, are known to cause neurotoxicity of the RLN (unilateral or bilateral). Fortunately, the VFP associated with the vinca alkaloids is dose related, and usually resolves over a 4- to 6-week period after stopping or adjusting the dose of the medication Systemic diseases can (rarely) cause vocal fold immobility, due to either paralysis or joint fixation. Such diseases include gout, sarcoidosis, tuberculosis, rheumatoid arthritis, and hypothyroidism (only in cases of myxedema). These systemic diseases would be expected to have myriad symptoms in addition to unilateral vocal fold immobility, and these conditions should not be suspected in cases of isolated VFP. In the case of endotracheal intubation leading to unilateral vocal fold mobility, one must be careful to rule out the possibility of arytenoid dislocation or subluxation as the true cause of an immobile vocal fold, although this scenario is probably quite rare. Laryngeal electromyography is helpful in these situations, as indicated below. Other traumatic causes of VFP include blunt or penetrating injuries to the neck.

5.3

Surgical Indications and Contraindications

5.3.1

Vocal Quality and Swallowing

The primary symptom of UVFP is dysphonia. The voice can vary from simple vocal fatigue in mild or well-compensated cases, to almost complete aphonia in severe cases. Much of the quality of the voice is determined by the muscular tone and position of the affected vocal fold and each patient’s unique laryngeal compensatory strategy. An atrophic and poorly compensated vocal fold paralysis typically presents with a breathy, weak voice due to air escape. The voice may also have a watery or “gurgle-y” quality to it if secretions are retained in the pyriform sinus, as is typical in high vagal injuries. With time, some patients will eventually progress to a stronger voice, using various compensatory strategies. Supraglottic hyperfunctional compensation is common. These patients constrict the supraglottic tract either laterally, apposing the false folds, and/ or in an anterior posterior dimension, apposing the epiglottis to the arytenoids. This hyperfunctional muscular contraction leads to a characteristic rough, pitch-locked, low-frequency voice. This voice can sound quite similar to a patient with primary muscular tension dysphonia, and the diagnosis of vocal fold paralysis may not be suspected. “Unloading” of the voice, as described later in this chapter, is used to help analyze these patients. In contrast, other patients, often females, may

 

Chapter 5

develop an unnaturally high-pitched voice that is breathy in quality. This has been referred to as a “paralytic falsetto,” and is characterized by a mean increase in fundamental frequency 85 Hz above “natural” pitch. This condition is thought caused by compensatory contraction of the ipsilateral cricothyroid (CT) muscle, which remains innervated in isolated RLN paralysis. Swallowing difficulties are often encountered, specifically aspiration of liquids, along with a weak and ineffective cough. Some dysphagia for solids may also be present, especially in brainstem or high vagal injuries, due to the concomitant denervation of the pharyngeal constrictors. Risk of aspiration is heightened in these instances as well, due to the loss of ipsilateral laryngeal sensation from SLN involvement. It is important to obtain a vocal inventory of the patient’s voice responsibilities (both work related and social). Vocal professionals rely on a serviceable voice for their livelihood, and these patients should be questioned regarding their upcoming work schedule to help determine the urgency of early surgical intervention. Most professional voice users will opt for temporizing vocal augmentation (Chap. 14, “Principles of Vocal Fold Augmentation”) so that they may return to work as soon as possible. A validated instrument, such as the VHI-10 is very useful for understanding the perceived severity of the patient’s vocal disability.

5.4

Unilateral Vocal Fold Paralysis: Physical Examination

5.4.1

General

Examination of the neck for adenopathy and thyroid masses should be performed. Cranial nerve X neural compression and infiltration by a neck or thyroid neoplastic process can lead to VFP in advanced cases. Palatal movement when phonating /a/ should be observed. Palatal paralysis in combination with ipsilateral VFP may indicate a “high” vagal lesion. In the case of palatal paralysis, the palate retracts toward the uninvolved “good” side (e. g., in a left vagal paralysis, the palate retracts to the right). A complete cranial nerve exam should evaluate for other involved nerves, especially CN XI and XII due to the close proximity these have to CN X at the skull base. Involvement of these adjacent cranial nerves warrants a thorough radiographic evaluation of the base of the skull.

5.4.2

Laryngeal

The appropriate evaluation for VFP starts with the recognition of unilateral vocal fold immobility on examination. Indirect (mirror) laryngoscopy and rigid 70 or 90° laryngoscopy are helpful but do not replace flexible laryngoscopy. It is important to obtain an unencumbered, extended viewing period of the vocal folds during a variety of tasks. Flexible laryngoscopy is the only method to view vocal fold mobility in its natural state (refer to Chap. 3, “Videostroboscopy and Dynamic Voice Evaluation with Flexible Laryngoscopy”). When evaluating for suspected UVF paralysis/paresis, a useful task is to ask the

patient to perform an “ee-sniff ” maneuver, where the patient alternates between phonating an “e” vowel and sniffing vigorously. This causes the vocal folds to alternately adduct and abduct maximally and is an excellent way to judge the degree of paresis/paralysis. Any purposeful and appropriate abduction of the affected vocal fold suggests incomplete paralysis (paresis). It is important not to falsely attribute a small amount of adduction of the affected vocal fold as representing evidence of partial innervation. RLN sectioning leads to paralysis of the ipsilateral thyroarytenoid, posterior cricoarytenoid, and lateral cricoarytenoid, but not the interarytenoid. The interarytenoid is a midline muscle, and has dual innervation from both RLNs; therefore, some residual adduction may be present in complete unilateral VFP, due to innervation from the contralateral RLN. A paralyzed vocal fold can occupy a variety of positions, including lateral (cadaveric), paramedian, and median. It was once thought that the position of the paralyzed vocal fold had some topognostic significance (for example, that lateral vocal fold position indicated complete CN X paralysis due to RLN and SLN involvement). This theory was later disproven by both Woodson and Koufman. The final position of the vocal fold after nerve injury is now thought to be due entirely to the degree of reinnervation and synkinesis present. It is important to focus on the vocal fold movement itself, rather than the arytenoid position, in determining vocal fold immobility. In some cases of vocal fold immobility, however, an overhanging arytenoid obscures the observation of the underlying vocal fold, making it impossible to ignore its position. This overhanging, anteriorly displaced arytenoid is sometimes mistaken for an arytenoid dislocation; however, this finding is usually caused by complete denervation or poor reinnervation of the PCA muscle In some patients with UVFP, compensatory supraglottic contractions (i. e., “plica ventricularis”) obscure vocal fold movement. In these cases, the author advocates that the patient phonate with an easy onset such as a “sigh,” or be instructed to “hum through the nose.” This technique, described by Koufman as “unloading,” is useful for removing unwanted compensatory supraglottic hyperfunction that obscures vocal fold visualization. This technique is invaluable in many cases of longstanding VFP that have been misdiagnosed as primary muscle tension dysphonia, or plica ventricularis. Videostroboscopy is a helpful part of the workup of vocal fold movement abnormalities, demonstrating the degree of incomplete closure present. In many cases of VFP, however, the paralyzed vocal fold shows increased amplitude of vibration due to the atrophic, “floppy” nature of the denervated vocalis muscle. In cases of mild or moderate vocal fold paresis, the increased amplitude seen on stroboscopy, or an asynchronous “chasing wave” may be the only signs of vocal fold weakness. Stroboscopy may also provide information regarding vocal fold height differences and the status of vocal process contact during phonation. These parameters help determine the need for arytenoid adduction, when evaluating patients for laryngeal framework surgery. A simple test to evaluate the degree of vocal disability and glottic incompetence is measuring the patient’s maximal phonation time (MPT). This is done by simply instructing the patient to take a deep breath and phonate an “ee” vowel for as long as possible. Normal MPT for a healthy adult is approx-

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Glottic Insufficiency

imately 25 seconds. In cases of VFP, the MPT is reduced to 10 seconds or less, typically. Shorter MPT values indicate more severe glottic incompetence, worse voice, and increased vocal fatigue. MPT values of 5 seconds or less indicate severe, uncompensated VFP that may need arytenoid adduction in addition to medialization laryngoplasty. Poor pulmonary reserve from asthma or chronic obstructive pulmonary disease may reduce MPT significantly, so results need to be taken in context of the patient’s pulmonary status. MPT should be expected to improve (i. e., increase) after successful medialization surgery for VFP.

5.5

Unilateral Vocal Fold Paralysis: Workup

It should be noted that unilateral vocal fold immobility is a physical finding, and not a diagnosis. One must determine the cause of the immobility. In the vast majority of cases of unilateral vocal fold immobility, VFP is the cause. Therefore, the bulk of the evaluation pertains to UVFP. In a small number of cases, the etiology may be cricoarytenoid (CA) joint arthritis (rheumatoid arthritis, gout), cricoarytenoid joint effusion/subluxation/dislocation (external trauma/ traumatic endotracheal intubation), or neoplastic infiltration (“occult” carcinoma in the ventricle/paraglottic space). In general, the history will suggest whether CA joint derangements are the culprit, and careful flexible laryngoscopy combined with CT scan will reveal neoplastic infiltration as the cause of vocal fold immobility. In cases where one cannot confidently exclude the CA joint involvement or neoplasm as the cause of unilateral vocal fold immobility, laryngeal electromyography and a laryngoscopy with palpation for passive mobility of the vocal folds is warranted.

5.5.1

Serology

There is little yield from ordering screening laboratory tests such as chemistry panel, complete blood count, urinalysis, VDRL/FTA-ABS, thyroid function tests, autoimmune panels, or erythrocyte sedimentation rate. If additional elements of the history and physical exam point towards a systemic process as the cause of unilateral vocal fold immobility, directed serology tests may be indicated. However, in general, a “shotgun” approach to the workup of uncomplicated UVFP is unnecessary and wasteful.

5.5.2

Imaging Studies

As screening tools, barium swallow and thyroid scans have virtually no yield in determining the etiology of VFP and are not advocated in the diagnostic workup. In contrast, a modified barium swallow or functional endoscopic evaluation of swallowing to evaluate swallowing and aspiration risk is frequently helpful in managing patients with dysphagia in the workup of VFP.

 

In cases where a clear-cut temporal relation exists between surgical iatrogenic trauma and VFP, no additional radiologic workup is necessary. In cases where no cause can be found for the VFP, imaging studies are essential. Most investigators agree that a CT (with contrast) or MRI encompassing the base of skull through the upper chest is adequate. Laryngeal electromyography (LEMG) undoubtedly has a place in the work up of unilateral vocal fold immobility; its role is still yet to be determined. LEMG can provide definitive diagnosis and prognostic information on the possibility for spontaneous recovery of VFP. Useful information from LEMG is obtained between 1 and 6 months after the onset of VFP. Evaluation outside of these parameters can render the information misleading (early), or of limited usefulness (late).

5.6

Unilateral Vocal Fold Paralysis: Treatment

The treatment of VFP can be broken into three management strategies: 1. Observation for 9–12 months, reserving treatment for patients with continued dysphonia 2. Referral to speech pathology for voice strengthening or swallow therapy, as indicated 3. Early surgical intervention: a) Temporary: injection augmentation b) Permanent: laryngeal framework surgery, injection augmentation Obviously, these treatment strategies may overlap or may be employed simultaneously, but a management plan should be developed and followed as soon as all of the important diagnostic information is gathered. Several factors should be considered when determining the best course of action, and treatment must be individualized for each patient. A treatment algorithm is not advocated, as each patient’s expectations and vocal needs are unique. Classical teaching for the treatment of VFP advocates a watchful waiting period of 9–12 months before surgical intervention is considered. This management strategy was developed in the 1970s, when the only viable treatment option for VFP was injection augmentation with Teflon. As Teflon injection is irreversible and sometimes associated with an unfavorable vocal outcome, early surgical intervention was ill advised during this era. LEMG and laryngeal framework techniques, along with an arsenal of injectable substances, have made early surgical intervention an excellent option in the treatment of VFP. In patients with clear-cut aspiration due to VFP, early surgical intervention is indicated, either with injection augmentation of the vocal fold, or medialization laryngoplasty (ML). Evidence of severe denervation injury on LEMG may also lead to early surgical intervention. Clinical experience has shown that RLN paralysis due to carcinoma (lung, esophagus, thyroid, …) rarely recovers, and patients are counseled to consider early surgical intervention in these cases. Patients with VFP and high-level vocal demands (salespersons, clergy, teachers,

 

Chapter 5

attorneys) often have difficulty continuing their work-related duties. In these cases, it may be necessary to intervene early (prior to 9 or 12 months) to get the patient back on the job. Temporary surgical procedures such as injection augmentation of the vocal fold should be considered in this population. The medical health of the patient occasionally comes into play. Patients with significant cardiopulmonary and other medical comorbidities may not be candidates for a general anesthetic (i. e., for microlaryngoscopy with vocal fold injection augmentation), yet may be perfectly suitable for ML or injection augmentation performed under local anesthesia. In most cases, the patient should be counseled regarding the different treatment options, including the advantages and disadvantages of the three main strategies of treatment. In this way, the patient can actively participate in the decision-making process. When LEMG is available, it can serve as a crucial guide to the patient and surgeon regarding (1) treatment or observation and (2) temporary versus permanent treatment.

5.7

Unilateral/Bilateral Vocal Fold Paresis

5.7.1

Etiology

As is the case with vocal fold paralysis, incomplete paralysis or paresis can be due to iatrogenic, neoplastic, neurologic, and idiopathic causes outlined in section 5.2. Idiopathic causes are much more common with vocal fold paresis, and may represent a viral neuropathic process. A high index of suspicion for an underlying progressive neurologic disease (e. g., amyotrophic lateral sclerosis, postpolio syndrome) must be maintained as well.

5.7.2

History

In contrast to patients presenting with UVFP, the presenting symptoms of a patient with vocal fold paresis can be very subtle. While the patient may complain of a breathy, weak voice, more subtle forms of dysphonia are often present. These symptoms include: ■ ■ ■ ■ ■

Loss of volume/projection Vocal fatigue Loss of voice after extended use Odynophonia Loss of a portion of the vocal range (especially upper end of the register) ■ Problems with stamina/quality of the singing voice Vocal fatigue is usually present in patients with vocal fold paresis, and is a cardinal symptom of glottic insufficiency. The temporal course of the presenting vocal complaints can vary from sudden in onset, to gradually progressive, and even in some cases intermittent in nature.

5.7.3

Physical Examination

Flexible laryngoscopy and videostroboscopy, as outlined for UVFP in the previous sections is essential in the examination of the patient with suspected vocal fold paresis. The “ee-sniff ” maneuver should be performed, using slow-motion review to evaluate for motion asymmetries in abduction and adduction of the vocal folds. Compensatory muscle tension disorders are common with vocal fold paresis; therefore, “unloading” techniques are useful as described previously. ■ Videostroboscopy plays a pivotal role in the evaluation of suspected paresis. Subtle clues include: ■ Mild bowing of the vocal fold(s) ■ Incomplete glottic closure ■ Prolonged “open phase” of vibratory cycle ■ Increased vibratory amplitude in the paretic vocal fold (see Chap. 3, Fig 3.3) ■ “Chasing”/asynchronous mucosal wave propagation

5.7.4

Diagnostic Workup

Is the same as for UVFP, with the following notable exceptions: ■ LEMG is critical to confirming the diagnosis, and establishing the “sidedness” of the vocal fold paresis (left, right, or bilateral). Findings are typically limited to reduced recruitment of motor units in the RLN or SLN distribution. ■ Imaging studies are not generally obtained to evaluate the course of the vagus/RLN in cases of long-standing, stable vocal fold paresis. If vocal fold paresis progressively worsens or the affected vocal fold becomes immobile, then radiologic evaluation is indicated. ■ Some consideration should be given to the possibility that the paretic vocal fold is a manifestation of a progressive neurological disorder (if no clear etiology is identified). Neurologic consultation may be indicated. Possible conditions include: ■ ALS ■ Postpolio syndrome ■ Pseudobulbar palsy

5.7.5

Treatment

As with UVFP, treatment options include observation, voice therapy with a speech language pathologist, or surgical management either with injection augmentation of the vocal fold(s) or laryngeal framework surgery. In general, a less aggressive approach is used in the treatment of vocal fold paresis, as compared to UVFP. Voice therapy is more likely to be successful, and injection augmentation (lipoinjection, Radiesse) may be preferred over laryngeal framework surgery. If the diagnosis of vocal fold paresis is suspected, but cannot be confirmed, then

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Glottic Insufficiency

a “diagnostic” injection augmentation using a temporary filler can be done. Improvement in the voice after injection augmentation suggests that glottic insufficiency is present. Long-term strategies can then be employed after the effects of the injection wear off.

5

5.8

Presbylaryngis/Age-Related Changes in the Larynx

5.8.1

General Considerations

It is a common misconception to use the term vocal fold bowing synonymously with presbylaryngis. Vocal fold bowing is not a diagnosis, but a physical finding indicating an elliptical or scalloped contour to the membranous vocal fold (Fig. 5.3). Bowing can be due to vocal fold atrophy, vocal fold paresis/ paralysis, age-related changes (presbylaryngis), vocal fold softtissue loss/scarring, and sulcus vocalis.

5.8.2

Etiology, History, and Physical Findings

Presbylaryngis is the condition caused by senescent changes in the larynx, which generally present in the fifth decade of life or later. Typically, the patient complains of mild/moderate dysphonia, lack of volume/projection, and vocal fatigue, especially at the end of the day. Bilateral vocal fold bowing is the typical laryngoscopic feature on physical examination. Videostroboscopic exam often reveals mild/moderate degrees of glottal insufficiency/incomplete closure. However, unlike vo-

Fig. 5.3  Videostroboscopy image of bilateral vocal fold bowing due to

presbylaryngis

 

cal fold muscular atrophy due to deinnervation, presbylaryngis is a more global process that involves not only loss of muscle bulk, but also degeneration/loss of the layers of the lamina propria, as well as CA joint changes. For this reason, the vocal dysfunction related to presbylaryngis is usually addressed incompletely when “medialization” framework surgery is used to correct the glottal gap.

5.8.3

Workup

A diagnostic workup for suspected presbylaryngis is usually not necessary in most cases of elderly patients with a finding of vocal fold bowing on laryngeal examination. However, it should be noted that Parkinson’s disease (PD) often has an identical clinical presentation to that of presbylaryngis. Patients with PD, however, are more likely to have vocal tremor and monotone pitch in addition. The clinical distinction is important, as PD patients are generally poor surgical candidates for treatment of glottic insufficiency, due to the global bradykinetic nature of their vocal dysfunction. Lee-Silverman voice therapy (see Chap. 7, “Medical Treatment of Voice Disorders”) is the preferred primary method of treatment for dysphonia due to PD. Injection augmentation and laryngeal framework surgery are reserved as an adjunctive treatment in select cases.

Key Points ■ Glottic insufficiency is one of the most common contributing factors in patients who present with dysphonia and one of the easiest findings to overlook in the clinical evaluation. ■ The most common causes of symptomatic glottic insufficiency are unilateral vocal fold paralysis, unilateral or bilateral vocal fold paresis, and presbylaryngis. ■ Treatment of “early” unilateral vocal fold paralysis is individualized for each patient, and takes into account the patient’s risk of aspiration, vocal demands, nature of neural injury, and LEMG findings. ■ Videostroboscopy plays a pivotal role in the evaluation of suspected vocal fold paresis. Subtle clues include: ■ Mild bowing of the vocal fold(s) ■ Incomplete glottic closure ■ Prolonged “open phase” of vibratory cycle (see Chap. 2, “Principles of Clinical Evaluation for Voice Disorders”) ■ Increased vibratory amplitude in the paretic vocal fold ■ Chasing/asynchronous mucosal wave propagation ■ Loss of vocal projection and voice fatigue with extended use are classic symptoms of vocal fold paresis and can easily be missed in the history.

 

Chapter 5

■ All unexplained vocal fold paralysis should be investigated with imaging studies (CT or MRI), tracing the entire RLN from skull base to upper chest. ■ Parkinson’ s Disease (PD) often presents with dysphonia and vocal fold bowing and can be confused with presbylaryngis. The clinical distinction is important, as PD patients are generally poor surgical candidates, and should instead undergo voice therapy as primary treatment for their dysphonia.

6

Selected Bibliography

10

1

2 3 4

5

Benninger MS, Crumley RL, Ford CN et al (1994) Evaluation and treatment of the unilateral paralyzed vocal fold. Otolaryngol Head Neck Surg 111:497–508 Benninger MS, Gillen JB, Altman JS (1998) Changing etiology of vocal fold immobility. Laryngoscope 108:1346–1349 Blitzer A, Brin MF, Sasaki CT et al (eds) (1992) Neurologic disorders of the larynx. Thieme, Stuttgart Blitzer A, Jahn AF, Keider A (1996) Semon’s law revisited: an electromyographic analysis of laryngeal synkinesis. Ann Otol Rhinol Laryngol 105:764–769 Flowers RH, Kernodle DS (1990) Vagal mononeuritis caused by herpes simplex virus: association with unilateral vocal cord paralysis. Am J Med 1990; 88:686–688

7

8

9

11

12

13

14

15

Glazer HS, Aronberg DJ, Lee JKT, Sagel SS (1983) Extralaryngeal causes of vocal cord paralysis: CT evaluation. Am J Radiol 141:527–531 Koufman JA (1995) Evaluation of laryngeal biomechanics by flexible laryngoscopy. In: Rubin JS, Sataloff RT, Korovin GS, Gould WJ (eds) Diagnosis and treatment of voice disorders. Igaku-Shoin, New York, pp 122–134 Koufman JA, Walker FO, Joharji GM (1995) The cricothyroid muscle does not influence vocal fold position in laryngeal paralysis. Laryngoscope 105:368–372 Koufman JA, Walker FO (1998) Laryngeal electromyography in clinical practice indications, techniques, and interpretation. Phonoscope 1:57–70 Munin MC, Murry T, Rosen CA (2000) Laryngeal electromyography. Otolaryngol Clin North Am 33:759–770 Netterville JL, Koriwchak MJ, Winkle M et al (1996) Vocal fold paralysis following the anterior approach to the cervical spine. Ann Otol Rhinol Laryngol 105:85–91 Phillips TG, Green GE (1987) Left recurrent laryngeal nerve injury following internal mammary artery bypass. Ann Thoracic Surg 3:440 Shin-ichi I kKenji K, Ken I, Oshima K (2003) Hoarseness after cardiac surgery: possible contribution of low temperature to the recurrent nerve paralysis. Laryngoscope 113:1088–1089 Terris DJ, Arnstein DP, Nguyen HH (1992) Contemporary evaluation of unilateral vocal cord paralysis. Otolaryngol Head Neck Surg 107:84–90 Woodson GE (1993) Configuration of the glottis in laryngeal paralysis. I: Clinical study. Laryngoscope 103:1227–1234

35

Chapter 6

Glottic and Subglottic Stenosis: Evaluation and Surgical Planning

6.1

6

Fundamental and Related Chapters

Please see Chaps. 9, 13, 26, 28, 29, 45, 46, and 47 for further information.

6.2

Introduction

Evaluation of airway stenosis must be performed in a systematic and thorough manner to ensure accurate diagnosis and treatment planning. In the case of a patient with stridor and acute airway distress, the medical evaluation may be limited initially. However, once a secure airway is obtained, a more detailed evaluation (as outlined in this chapter) can be obtained. Fig. 6.1  Subglottic stenosis

6.3

■ ■ ■ ■ ■ ■ ■ ■

■

Etiology of Glottic and Subglottic (Laryngotracheal) Narrowing

Prolonged endotracheal intubation Complications related to tracheostomy tube placement External laryngeal trauma Thermal inhalation (burn) and caustic ingestion Autoimmune disease ■ Wegener’s granulomatosis ■ Relapsing polychondritis Amyloidosis Laryngopharyngeal reflux disease Malignancy ■ External tracheal compression (mediastinal tumor) ■ Intratracheal tumor (carcinoid, metastatic tumor) ■ Primary tumor of airway (e. g., chondrosarcoma of cricoid) Idiopathic

The vast majority of patients with glottic and subglottic airway narrowing (Fig. 6.1) are due to prolonged (at least 48–72 h or more) endotracheal intubation and complications related to tracheostomy tube placement. The endotracheal tube itself can lead to posterior glottic stenosis (PGS) from interarytenoid ulceration, pressure necrosis, and cicatricial formation in the posterior glottic space. The balloon and/or distal tip of the endotracheal tube (ETT) can likewise lead to subglottic and proximal tracheal stenosis from pressure-related effects during prolonged intubation. The risk of PGS increases markedly

after 10 days of endotracheal intubation. Additional medical factors may increase the risk of stenosis, including hypoxia, diabetes, LPR, vascular disease, localized infection, and other conditions. Tracheostomy tube placement (especially percutaneous dilational techniques) may narrow the airway through displacement of tracheal cartilage into the airway. Necrosis of tracheal cartilaginous flaps (e. g., the Björk flap) may also lead to delayed contracture and collapse of the supporting tracheal framework (see Chap. 29, Fig. 29.3). The other etiologies listed are much less common, but must be considered in non-traumatic airway stenosis, as described below.

6.3.1

Common Clinical Conditions and Associated Risk Factors

■ History of prolonged mechanical ventilation ■ Posterior glottic stenosis ■ Subglottic/tracheal stenosis ■ History of prior tracheostomy ■ Tracheal collapse, typically second or third ring ■ Suprastomal granulation tissue ■ History of radiation to neck ■ Laryngeal edema ■ Glottic stenosis/fibrosis, especially in advanced T3/T4 squamous cell carcinoma (SCCa)

38

6

Glottic and Subglottic Stenosis

 

■ Nontraumatic subglottic narrowing (CRAWLS) ■ Chondrosarcoma ■ Relapsing polychondritis ■ Amyloidosis ■ Wegener’s granulomatosis ■ Laryngopharyngeal reflux disease ■ Sarcoidosis

■ ■ ■ ■

6.4

Glottic and Subglottic Stenosis: History

6.5

Glottic and Subglottic Stenosis: Physical Examination

6.4.1

Symptoms/Time Course

6.5.1

Local Anesthesia Techniques for Examination

The patient with glottic or subglottic/tracheal stenosis typically presents with shortness of breath. They may have been previously misdiagnosed with asthma or “reactive airway disease,” and in many cases, they are using bronchodilators or inhaled steroids for their presumed condition. It is important to inquire specifically what level of activity the patient can tolerate before breathing difficulties are encountered (e. g., climbing up a flight of stairs, ambulating across the room, or simply at rest); this provides insight into the severity of the obstruction. In addition, one should specifically inquire whether the patient’s dyspnea is accompanied by an audible noise during inspiration. Given the strong association between prolonged endotracheal intubation and the development of airway stenosis, one should inquire about previous intubations in the past medical history especially if they extend beyond 2–3 days. Although the risk of airway stenosis increases markedly after 10 days of intubation, it can occur occasionally with shorter exposures. In addition, caustic ingestions, thermal inhalational injuries (smoke inhalation/burns), and laryngeal trauma are also important risk factors for the development of upper airway stenosis. In many patients with airway stenosis, there is a history of tracheostomy placement and decannulation 2–3 months prior to the development of airway obstruction. In some patients, the latency to onset of airway symptoms is due to gradual maturation of scar formation in the glottis/subglottis. However, the tracheostomy can be the direct cause of the airway obstruction due to tracheal granulation tissue proliferation or cartilage resorption/collapse after decannulation.

6.4.2

Medical Comorbidities

Medical comorbidities should be noted which can have a profound effect on determining if the patient is a surgical candidate for treatment of their airway stenosis. The following conditions are not absolute contraindications to surgical treatment; however, they may reduce the chances of success and/or decannulation: ■ Severe restrictive or obstructive pulmonary disease (especially if oxygen dependant) ■ Severe kyphoscoliosis

Diabetes mellitus History of radiation therapy of the larynx Severe aspiration/PEG tube dependence Morbid obesity with severe obstructive sleep apnea (OSA) ■ Autoimmune disease, especially if steroid dependent

Careful flexible laryngoscopic exam of the larynx and trachea in the clinic setting is the most important step in the evaluation of suspected glottic/subglottic stenosis. This can be achieved only if the patient’s upper airway is properly anesthetized. These methods of anesthesia include: ■ Topical lidocaine (4%) drip delivered through the side channel of the endoscope or an Abraham cannula ■ Nebulized lidocaine ■ Cricothyroid (or transtracheal) puncture, with instillation of 4% lidocaine To begin the exam, the nose is anesthetized in the standard fashion for nasolaryngoscopy (lidocaine and Neosynephrine sprays). After this, the flexible endoscope is passed transnasally, and positioned over the laryngeal inlet. When properly positioned, approximately 2–3 ml of lidocaine 4% is delivered through a side channel of the scope while the patient is phonating /ē/. This may have to be repeated until the patient demonstrates little or no response to the presence of the lidocaine in the laryngeal inlet. The endoscope is then advanced through the glottis, and additional topical lidocaine is applied as needed only. An alternative is the use of an Abraham cannula, which can deliver lidocaine through a peroral technique (Fig. 6.2). The maximum recommended adult dose of lidocaine is typically 300–400 mg (7–10 ml of lidocaine 4% in a 70-kg patient). In patients with a tracheotomy or a permanent tracheal stoma, the tracheostomy tube is removed and 2–5 ml of 4% lidocaine is dripped into the stoma. The patient’s stoma should be briefly occluded manually on anesthetic instillation so that the cough will distribute the anesthetic throughout the subglottis and trachea. With proper anesthesia, the entire laryngotracheal airway can be examined with a standard flexible endoscope in the clinic setting.

6.5.2

Documentation of Examination

It is helpful to capture the flexible endoscopic airway evaluation on videotape (or digital storage device) so that a more detailed review of the airway anatomy can be carried out after the

 

Fig. 6.2  Abraham cannula for peroral delivery of topical lidocaine to

the laryngotracheal region

Chapter 6

Fig. 6.3  Normal laryngeal exam during maximal abduction (sniffing).

Note the general shape of an equilateral triangle within the boundaries of the glottal aperture

examination. This is especially true those patients where only a brief examination can be performed (due to poor respiratory status or inability to tolerate the procedure). In these cases, the video can be reviewed in slow motion or freeze frame to insure accuracy of the examination.

6.5.2.1 Flexible Laryngoscopy/ Tracheoscopy Protocol The following information should be obtained during the flexible laryngoscopic airway examination: 1. Vocal fold mobility testing Having the patient alternate between phonating /ee/ and sniffing will test for vocal fold adduction and abduction. In general, during sniffing, maximal abduction occurs, and the glottic aperture has the general configuration of an equilateral triangle. Reduced abduction and narrowed glottic inlet can be due to posterior glottic stenosis and/or bilateral vocal fold paralysis/paresis (Figs. 6.3, 6.4). Patients with paradoxical vocal fold mobility disorder may be confused with these conditions; however, these patients will generally have full vocal fold abduction immediately after cough or other involuntary glottic closure task (see Chap. 3, “Videostroboscopy and Dynamic Voice Evaluation with Flexible Laryngoscopy”). 2. Examination of the posterior glottic space for scar The flexible scope should be advanced into the interarytenoid space at the level of the vocal folds to evaluate for the presence of scar within the posterior glottis. 3. Scope advancement past the vocal folds, into the subglottis and trachea, including the main-stem bronchi 4. Documentation of airway measurements If a stenosis is identified the approximate location should be noted (distance in mm distal to the vocal folds), then the length of the stenotic segment, and the estimated airway

Fig. 6.4  Laryngeal examination in a patient with posterior glottic ste-

nosis during maximal abduction. Note the limited space in the posterior glottis due to interarytenoid scarring, which results in a glottic aperture of a more narrowed isosceles triangle

diameter in mm. The presence of tracheomalacia/cartilage collapse or suspected external compression of the airway should be also noted. 5. Retrograde flexible examination of the subglottic airway through the tracheal stoma (if present) This perspective gives an unparalleled view of vocal fold mobility and posterior glottic configuration from below. The posterior glottic space can be clearly examined for scar formation.

39

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Glottic and Subglottic Stenosis

 

6

Fig. 6.5  Normal flow-volume loop

6.6

Additional Studies for the Evaluation of Glottic/Subglottic Stenosis

6.6.1

Voice Evaluation (VHI-10, Audio Recording)

Patients with glottic and subglottic stenosis often have varying degrees of dysphonia preoperatively and may develop worsening of their voice after surgery. For this reason, preoperative documentation of the voice is essential.

6.6.2

Air-Flow Measures

Pulmonary function testing with a flow-volume loop can help establish the presence of upper airway obstruction. A test that is consistent with “extrathoracic airway obstruction” is typically seen in patients with glottic or subglottic/tracheal airway narrowing (Figs. 6.5, 6.6).

Fig. 6.6  Flow-volume loop of patient with

subglottic stenosis, demonstrating “flattening” of the inspiratory limb. This is commonly referred to as a “fixed extrathoracic obstructive pattern”

6.6.3

Radiographic Studies

A fine-cut (1 mm) CT scan of the airway (neck and chest) with contrast is helpful in the evaluation of suspected airway obstruction. This is especially true in cases of suspected external compression or cartilage collapse (Fig. 6.7). Both of these conditions are contraindications for an endoscopic laser approach. It is important to remember that radiographic studies of the airway only provide a static view of the airway. Dynamic collapse of the airway (e. g., tracheomalacia) can only be ruled out with a flexible endoscopic examination of the entire upper airway.

6.6.4

Laboratory Testing

In a small handful of patients, there is no obvious traumatic/ iatrogenic cause of the patient’s subglottic/tracheal narrowing. In these cases, one must have a high degree of suspicion for an underlying inflammatory/autoimmune, or neoplastic cause.

 

Chapter 6

6.7.1

Corrective Surgical Procedures for Glottic/Subglottic Stenosis

These procedures are listed in order from least invasive to most invasive approach.

Fig. 6.7  Computerized tomography of the trachea (axial), demon-

strating collapse of the cartilaginous tracheal walls, resulting in airway narrowing. There is no evidence of intraluminal scar or soft tissue obstruction

The mnemonic for this condition (nontraumatic subglottic narrowing) is CRAWLS (see above). In these cases, the following protocol may be used: ■ c-ANCA, auto-immune profile, angiotensin-converting enzyme (ACE) level serum testing ■ Biopsies of the involved tissue (histopathology and culture) ■ Selective pH probe testing for LPR

6.7

Glottic and Subglottic Stenosis: Surgical Planning

In most cases, the initial microlaryngoscopy/ tracheobronchoscopy is planned as a therapeutic surgery. In certain instances, however, it may be appropriate to perform an airway endoscopy in the operating room strictly for diagnostic purposes. Examples include: ■ Incomplete office/radiographic evaluation of the airway—in this case, additional information (via operative endoscopy) needs to be obtained before a definitive treatment plan can be implemented ■ Suspicion of malignancy, or systemic disease—these cases should be evaluated with biopsy in the operating room. Definitive treatment may need to be delayed until histologic and/or microbiologic diagnosis is obtained, or the systemic disease is treated medically. ■ Evaluation and mapping of stenosis as an aid to planning an external procedure—in this instance the patient is known to have a stenosis that is not amendable to endoscopic treatment; however, anatomic mapping of the stenosis and tracheostomy location are obtained to aid in selection of the appropriate external surgical approach. (See Chap. 29, “Subglottic Stenosis,” for details in mapping the extent of the stenosis.)

■ Endoscopic (microlaryngoscopy, laser excision, rigid dilation) ■ Endoscopic with indwelling stent placement ■ T-tube stent with external limb (long term) ■ Intraluminal stent (short term, palliative) Dumon, Wall, Ultraflex, etc. ■ External procedures ■ Laryngotracheoplasty with cartilage grafting (airway expansion) ■ Cricotracheal resection with primary anastomosis In general, the least invasive procedures are attempted first (unless contraindicated), saving external procedures for those cases that fail to respond to an endoscopic approach. Airway stenting is a “middle ground” between endoscopic and external procedures; however, it is not widely practiced and requires experience to achieve consistent results. T-tube stenting is generally more successful for long-term stenosis treatment than are intraluminal stents, which have a tendency to migrate and incite granulation tissue formation. In general, intraluminal stents are not appropriate for long-term treatment of stenosis. These stents are better suited for palliative airway obstruction from metastatic tumor infiltration of the airway, and patients with terminal disease. External procedures are indicated when endoscopic treatments are contraindicated or are unsuccessful. In general, the morbidity and mortality of these procedures are significantly higher than for endoscopic treatments. Patients with significant comorbidities and advanced age may not be candidates for external stenosis treatment. Tracheostomy, although not a “corrective” procedure for airway stenosis, may be the appropriate treatment for extensive stenosis in patients with poor medical health, or when all treatments fail.

6.7.2

Criteria for Endoscopic Treatment for Subglottic Stenosis

Criteria include: ■ No external compression, tracheomalacia, or significant cartilage collapse ■ Length of stenosis no more than 2–3 cm ■ Identifiable airway lumen ■ If present, tracheostomy entry point not involving/adjacent to the stenotic site

 Repetitive mechanical trauma from the tracheostomy tube postoperatively has an adverse effect on healing of airway stenosis. Thus, if a tracheostomy tube is present, the stenotic region ideally should not extend down to the entry point of the tracheotomy.

41

42

Glottic and Subglottic Stenosis

6.7.3

6

Criteria for T-Tube Stenting for Subglottic Stenosis

■ Tracheotomized patients with subglottic/tracheal narrowing (from any cause) who have failed serial CO2 radial incisions/dilation treatment ■ Proximal subglottic/infraglottic region free of stenosis ■ 5- to 8-mm length of “normal” airway below vocal folds ■ Accommodates proximal limb of T-tube, without impingement on vocal fold

6.7.4

Criteria for External Treatment of Glottic/Subglottic Stenosis

Criteria include: ■ Failure of endoscopic and/or T-tube stent treatments ■ Extensive stenosis (no identifiable lumen, length greater than 3 cm) ■ Tracheomalacia, cartilage collapse It should be noted that the above recommendations are not absolute criteria for selecting external treatment approaches; they simply represent general guidelines. Certainly patients with lesser degrees of stenosis have failed endoscopic management, while conversely, those with more extensive stenosis have occasionally responded favorably to endoscopic treatment. The surgeon should use his/her judgment in determining suitability for endoscopic approach.

 

■ Nontraumatic subglottic narrowing should be investigated thoroughly to rule out associated inflammatory and neoplastic conditions, such as Wegener’s granulomatosis and laryngopharyngeal reflux disease. ■ Physical examination of a patient with suspected laryngotracheal stenosis should include a flexible laryngoscopy and tracheoscopy (down to the carina) in the clinic setting, using topical lidocaine for endolaryngeal/tracheal anesthesia. ■ Radiographic airway studies are essential if external compression is suspected, but do not replace a laryngoscopic airway evaluation. ■ Corrective surgical procedures for laryngotracheal stenosis include endoscopic management (microlaryngoscopy with laser radial incisions with dilation), indwelling stent placement, and external treatments (cartilage expansion grafts vs. segmental resection and primary anastomosis). ■ In patients with laryngotracheal stenosis, the least invasive surgical procedures are attempted first (unless contraindicated), reserving external procedures for those cases that fail to respond to an endoscopic approach. ■ Medical comorbidities (diabetes mellitus, restrictive or obstructive pulmonary disease, and obstructive sleep apnea) may have a significant negative impact on the surgical outcome and should be carefully considered prior to undertaking these treatments.

Selected Bibliography

Key Points

1

■ Laryngotracheal airway obstruction is generally caused by trauma to the upper airway from prolonged endotracheal intubation, which leads to pressure necrosis, granulation tissue, localized infection, and cicatrix formation. The risk of airway stenosis increases markedly after 10 days of intubation. ■ Tracheostomy can lead to delayed tracheal stenosis (typically 1–3 months after decannulation) and is typically due to collapse/contraction of the cartilaginous support.

2 3

4 5 6

Benjamin B (1993) Prolonged intubation injuries of the larynx: endoscopic diagnosis, classification, and treatment. Ann Otol Rhinol Laryngol 160(Suppl):1–15 Amin MR, Simpson CB (2004) Office evaluation of the tracheobronchial tree. Ear Nose Throat J 83(Suppl.):10–12 Shapshay SM, Beamis JF, Hybels RL et al (1987) Endoscopic treatment for subglottic and tracheal stenosis by radial laser incision and dilation. Ann Otol Rhinol Laryngol 96:661–664 McCaffrey TV (1991) Management of subglottic stenosis in the adult. Ann Otol Rhinol Laryngol 100:90–94 Gardner GM, Courey MS, Ossoff RH (1995) Operative evaluation of airway obstruction. Otolaryngol Clin North Am 28:737–750 Lano CF Jr, Duncavage JA, Reinisch L, Ossoff RH, Courey MS, Netterville JL (1998) Laryngotracheal reconstruction in the adult: a ten-year experience. Ann Otol Rhinol Laryngol 107:92–97

Chapter 7

7

Nonsurgical Treatment of Voice Disorders

7.1

Fundamental and Related Chapters

Please see Chaps. 2, 4, 5 and 8 for further information.

7.2

Introduction

Many voice problems do not require surgery if properly identified and treated. Though phonosurgical management of certain vocal pathologies is critical, many voice disorders are treated effectively by non-surgical means. This chapter gives a brief overview of several categories of voice disorders that are primarily treated without surgery.

7.3

Surgical Indications and Contraindications

Four to 10% of otolaryngologic visits are related to gastroesophageal reflux disease-related laryngeal complaints. Up to 50% of voice disorder patients may have coexisting laryngopharyngeal reflux (LPR). LPR manifests in many ways: sore throat, globus, hoarseness, throat clearing, dysphagia, chronic cough, and postnasal drip. The diagnosis of LPR is based on patient history and laryngeal signs noted during laryngoscopy. These include edema and erythema of the larynx, pseudosulcus (infraglottic edema), Reinke’s edema, interarytenoid mucosal changes, contact ulcers, granulomas, and posterior pharyngeal mucosal cobblestoning. It has been associated as well with paradoxical vocal fold motion disorder and asthma. It has also been linked to the development of leukoplakia and potentially, laryngeal cancer. Studies have alluded to the frequent association of LPR and/or gastroesophageal reflux disease (GERD) with subglottic stenosis in adults and children. It is critical to treat LPR after any type of airway reconstruction. Symptoms can be quantified by means of the Reflux Symptom Index and findings by the Reflux Finding Score. It is felt that both the acid and pepsin contribute to the inflammation associated with LPR and/or GERD. The gold standard in diagnosis remains the 24-h doubleprobe (esophageal and pharyngeal) pH study. With this study, a reflux event is defined as a 5 second drop in the intraluminal pH below 4.0. The standard of care for the treatment of LPR is the proton pump inhibitor (PPI), which works to irreversibly inhibit the proton pumps of the gastric parietal cell. Recent

studies have shown that twice-a-day therapy appears to result in the highest symptom resolution. Most clinicians and studies support duration of treatment of at least 4–6 months. It takes several months for affects to be noted by the patient, so patients typically need encouragement to remain compliant with their medication. Several controversies in the treatment of LPR include the strength of association between cough and LPR and duration of treatment. An additional point of contention is the use of histamine type 2 (H2RA) receptor antagonists in combination with PPIs. A few studies have confirmed that the H2RAs do not add any additional efficacy to treatment; however, many clinicians have noted significant improvement in LPR control with H2RAs, especially when given at night for the treatment of nocturnal acid breakthrough.

7.4

Vocal Fold Granuloma

Vocal fold granulomas (specifically nonintubation related) are notoriously recalcitrant to surgical therapy when underlying causative factors (such as LPR) are not controlled. Most vocal fold granulomas are located in the posterior third of the vocal fold either unilaterally or bilaterally. When granulomas occur postsurgically, they can occur anywhere an operative site exists. LPR plays an important role in the development of granulomas as do phonotrauma and trauma secondary to endotracheal intubation. Intubation granulomas are more common in women, presumably because their smaller larynx is more prone to trauma from the endotracheal tube. One study found that of patients with LPR, up to 75% responded to clinical treatment with PPIs; however, 21% demonstrated recurrence. The other treatment options for granulomas are voice therapy and botulinum toxin type A injection to the thyroarytenoid muscle. The latter causes a temporary paresis of the vocal fold to reduce extensive interarytenoid contact. Vocal fold granulomas also often occur (and recur) due to an underlying glottal insufficiency that may not be recognized by the treating physician. Excessive vocal fold closure pressure is applied to the arytenoids in an attempt to compensate for the glottal insufficiency, resulting in vocal fold granuloma formation or recurrence. Treatment for vocal fold granuloma due to glottal insufficiency involves vocal fold augmentation and/or medialization (see Chaps. 31, ”Vocal Fold Augmentation via Direct Laryngoscopy”; 38, “Silastic Medialization Laryngoplasty for Unilateral Vocal Fold Paralysis”; and 39, “GORE-TEX® Medialization Laryngoplasty”).

44

Nonsurgical Treatment of Voice Disorders

7.5

7

Infectious and Inflammatory Disorders

Fungal laryngitis is increasingly recognized as a cause of laryngitis. The widespread use of steroid based inhalers for the treatment of obstructive pulmonary disease has been a major contributor to the increase in fungal laryngitis incidence. Fungal laryngitis may be mistaken for leukoplakia. Clinical appearance of whitish plaques surrounded by erythematous mucosa is characteristic. Predisposing factors apart from inhaler use include radiotherapy, prolonged antibiotic use, smoking, and immunosuppression. Dysphonia may occur in 5–50% of patients using inhaled steroids. There appears to be a dose-dependent dysphonia in 34% of patients treated with beclomethasone dipropionate or budesonide when administered via pressured metered dose inhalers. The most common organism implicated is Candida, but the presence of Aspergillus, Blastomyces, Histoplasma, and Coccidioides has also been documented in cases of fungal laryngitis. Diagnosis is based on demonstration of fungal spores, hyphae, and/or pseudohyphae within upper epithelial layers of the laryngeal mucosa by culture or biopsy, both of which are done via laryngoscopy or office endoscopy. However, often the disease is treated clinically based on the characteristic findings. Inhalers used with a spacer decrease laryngeal deposition of the medication and can help with reduction or complete elimination of the offending agent. Treatment of fungal laryngitis rests on removal of the offending steroid when possible and antifungal medication. If the organism persists, then treatment with an oral conazole agent for 3–4 weeks is commenced. Current standard of care, however, is use of an oral conazole medication as initial treatment especially in the immunocompromised patient. Chemical laryngitis—specifically steroid inhaler laryngitis—is another common cause of dysphonia in the inhalerusing patient. Hoarseness is the most frequent local side effect of steroid inhalers. Several factors may contribute to this chemical irritation: the steroid “its preparation, the drug carrier” the type of inhaler device, mechanical irritation due to cough, inflammation of the upper airways and surrounding irritating triggers such as smoke. One study noted the following mucosal changes in patients with inhaler-related dysphonia: vascular lesions such as dilated blood vessels, capillary ectasias and varices, and “areas of thickening, irregularity, and leukoplakia.” These changes appear to improve after cessation of the steroid inhaler. In addition, some have attributed dysphonia secondary to steroid inhaler use to steroid myopathy, as both vocal folds appear atrophic and glottal closure is incomplete. Actual muscle bulk change due to steroid inhalers is controversial and not supported by scientific evidence. Some findings can overlap with those of LPR; therefore, LPR should be optimally controlled in conjunction with reduction or discontinuation, when possible, of the inhaler. Autoimmune disorders are relatively rare but several of these have effects on the vocal folds and subglottis. Rheumatoid arthritis (RA) affects 2–3% of the adult population, and 25–53% of patients have involvement of the larynx. The main two manifestations of RA at the level of the vocal folds are cri-

 

coarytenoid arthritis and rheumatoid lesions of the vocal fold. Systemic treatment of RA is favored to treat rheumatoid nodules; if they persist and cause a functional voice problem, then surgery is indicated. Vocal fold hypomobility associated with cricoarytenoid (CA) arthritis has resolved in some reports with systemic treatment and possibly steroid injection into or near the CA joint. Systemic lupus erythematosus (SLE) infrequently manifests itself in the larynx but can be associated with laryngeal edema in up to 28% of patients and vocal cord paralysis in 11% of patients with SLE. Wegener’s granulomatosis (WG) is a rare disease that involves principally three anatomical areas: the head and neck, lower respiratory tract, and the renal system. The cause of WG is unknown, but the disease is pathologically described by three findings: necrosis, granulomatous inflammation, and vasculitis. Signs associated with laryngeal involvement include wheezing or stridor, dyspnea, and dysphonia. Diagnosis is based on a blood test for the identification of antinuclear cytoplasmic antibody (ANCA) and specifically c-ANCA, which is found in 90% or more of patients with active WG. Subglottic stenosis is a major concern; the vocal folds proper are usually not involved. Systemic treatment incorporates use of corticosteroids and other immunosuppressive drugs, especially cyclophosphamide. If the stenosis is critical however, patients go on to either endoscopic or open surgical treatment, with or without tracheostomy depending on severity of the disease (see Chaps. 6, “Glottic and Subglottic Stenosis: Evaluation of Upper Airway Disorders”; 29, “Subglottic Stenosis”; 45, “Glottic and Subglottic Stenosis: Laryngotracheal Reconstruction with Grafting”; and 46, “Glottic and Subglottic Stenosis: Cricotracheal Resection with Primary Anastomosis”). The disease state should be under good medical control before performing surgical procedures for airway stenosis. Laryngeal amyloidosis is a rare and benign idiopathic disease, which presents as a primary disease or secondary with other disease processes. It comprises 0.2–1.2% of all benign tumors. The disease is indolent and when found in the larynx, can cause slowly progressive dysphonia and dyspnea; airway symptoms in general appear to predominate. When present in a secondary form, it can be associated with multiple myeloma, medullary thyroid carcinoma, and small cell carcinoma. Amyloid deposits or lesions are described typically as “firm, nonulcerating, orange-yellow, to gray epithelial nodules.” Definitive diagnosis is based on histopathologic presence of amyloid fibrils in a twisted β-pleated sheet patter with affinity for Congo red dye. The underlying condition in the secondary form requires treatment; however, systemic treatment frequently may not eliminate the amyloid deposits. When the airway or voice is compromised, surgical intervention is warranted. Serial laser laryngoscopy is often effective at controlling symptoms. More advanced disease may require laryngofissure with partial or total laryngectomy. Primary (localized) and secondary (systemic) amyloidosis are distinguished based on physical exam (for tender bones, heart failure, hepatosplenomegaly, lymphadenopathy), blood/serum and urine testing, chest and bone radiography, abdominal subcutaneous fat aspiration, CT exam of suspicious parts of the body, and rectal biopsy.

 

Chapter 7

7.6

Neurologic Disorders

7.6.1

Spasmodic Dysphonia

Spasmodic dysphonia (SD) is a focal dystonia characterized by vocal task specific action or intention induced spasms. Dystonias in general are disorders of central motor processing, and SD can be found in conjunction with other disorders, such as Meige’s syndrome, although typically it is isolated to the larynx. There are three classic types of SD. Adductor SD (1) comprises 80% of patients with the disorder. Abductor SD (2) and patients with both adductor and abductor activity, mixed SD (3), comprise the rest of disease population. Adductor SD is marked by a “strained-strangled” speech pattern caused by premature and excessive glottal closure, whereas abductor SD is marked by breathy speech breaks and an overall hypophonia due to inappropriate glottal opening during speech. SD typically presents in a female patient in her mid-30s, and if it has been present for some time, many patients develop compensatory changes, which may mask the true diagnosis. Patients may not demonstrate speech breaks during singing or laughing tasks, and patients find worsening of symptoms when under psychological stress. Diagnosis rests primarily on auditory-perceptual evaluation of connected speech supplemented by flexible nasopharyngolaryngeal examination. Diagnosis can be difficult, as patients may have associated essential tremor or actually have muscle-tension dysphonia; both disorders can cause voice breaks. Few if any medications have been successful in ameliorating symptoms of SD. Some patients find that alcohol or benzodiazepines are helpful to reduce the stress that may be the trigger for SD. The standard of care in the treatment of SD is injection of the affected muscle(s) with botulinum toxin (BTX), which causes a temporary chemical denervation of the thyroarytenoid–lateral cricoarytenoid muscle complex in adductor SD and the posterior cricoarytenoid muscle in abductor SD (see Chap. 35, “Botulinum Toxin Injection”). Prior to this, recurrent laryngeal nerve section was performed; however, recurrence of symptoms was typical (despite complete nerve section) and the overall voice quality worsened. Voice therapy can be used as adjunctive therapy to treat compensatory behaviors or assist in differentiating SD from muscle-tension dysphonia. Some newer surgical techniques have been developed but no long term data is available and thus are presently experimental and not validated.

of the voice is seen in 12–30% of patients with essential tremor, and a head tremor in 50%. Essential tremor of the voice is marked by a regular 4- to 12-kHz frequency oscillation of the affected muscles. Several drugs have also been associated with tremor production, and Parkinson’s disease is also considered in the differential diagnosis. Pharmacotherapy, specifically with primidone and propranolol, is employed as first-line treatment but is more effective for limb-based tremor than voice. Recently, some work has emerged concerning botulinum toxin A injections for treatment of voice tremor. The difficulty with local treatment, however, is that multiple muscles are involved in voice tremor (both intrinsic and extrinsic laryngeal musculature), so the benefit of simple thyroarytenoid–lateral cricoarytenoid muscle complex injection is not nearly comparable to benefit of botulinum toxin A seen in SD treatment. Medically refractory cases are treated with thalamotomy or deep brain stimulation (DBS); bilateral thalamotomy is associated with significant vocal side effects such as hypophonia and significant data for DBS in treatment of voice tremor is pending.

7.6.3

Parkinson’s disease (PD) affects nearly 1 million persons in the United States, and in severe forms, leads to considerable disability. The disease is caused by neurodegeneration within the nigrostriatal tracts of the basal ganglia, a neural center for motor control, which leads to decreased dopamine release. The hallmark clinical findings are bradykinesia, tremor, postural instability, and muscle rigidity. Phonatory effects include hypophonia, breathy dysphonia, and vocal tremor. The voice takes a monotonic quality. Many patients experience dysphagia and dysarthria. One study reported that 87% of PD patients demonstrated vocal fold bowing. The treatment of the voice component of PD involves a specialized voice therapy program, Lee Silverman Voice Treatment (LSVT), with or without vocal fold augmentation to improve glottic configuration and closure. Typically, LSVT is sufficient alone and vocal fold augmentation is not required. Treatment of PD is pharmacologic using dopamine agonists and medically refractory cases may undergo DBS or pallidotomy. No data are available currently regarding the effect of DBS on the voice in PD.

7.6.4 7.6.2

Essential Tremor

Essential tremor is the most common movement disorder, affecting 0.4–5.6% of those over age 40. However, the disease also appears to have a bimodal age distribution, with 4.6–5.3% of cases occurring in the first two decades of life. There appears to be a familial association in 17–100% of individuals transmitted in an autosomal-dominant inheritance pattern with variable penetrance. Three areas of the body may be involved to varying degrees: head, hands, and vocal tract. Essential tremor

Parkinson’s Disease

Muscle Tension Dysphonia

Muscletension dysphonia (MTD) is a term used to describe voice disorders that are related to excessive and poorly regulated laryngeal muscle activity during speech. Many synonyms are used in clinical practice and these include hyperfunctional dysphonia, muscle misuse, and tension-fatigue syndrome to name a few. The “muscletension” descriptor has been applied to muscle contraction patterns seen on flexible laryngoscopy of the endolarynx; these are classified from types I–IV, with type I being very mild constriction with an excessive posterior glottic chink, to type IV, a concentric closure pattern of the supraglot-

45

46

7

Nonsurgical Treatment of Voice Disorders

tis. Some of these patterns are seen in other disorders as well such as adductor SD or even in normal voices and these are not pathognomonic. MTD can present as a primary problem often associated with post-URI onset, inappropriate pitch use, reflux, or significant voice demands. It can also present in a secondary form as excessive compensation for glottal insufficiency. Circumlaryngeal massage has been used in conjunction with voice therapy to assist in reducing laryngeal height, as these patients frequently hold their larynges in an abnormally elevated position secondary to increased muscular tension. In the most severe or refractory patients, topical anesthetization of the endolarynx has assisted in decreasing laryngeal tension because of altered sensation and proprioception. Functional dysphonia or aphonia is a separate term that should be used for psychogenic dysphonia or conversion disorder. Those with conversion disorder have experienced significant psychological trauma from an event that causes the aphonia; as such, these patients require intense psychiatric treatment in addition to voice therapy. “Malingering” or “factitious dysphonia” would be included under this term.

7.6.5

 

Occasionally, psychiatric treatment may also be required. Some have attempted use of heliox (80% helium, 20% oxygen) to decrease work of breathing, but results have been mixed.

7.6.6

Postviral Vagal Neuropathy

Postviral vagal neuropathy (PVVN) is marked by chronic cough, with or without laryngospasm or PVFMD. The cough is thought to be a result of altered laryngeal sensitivity such as in post viral neuralgias of other cranial nerves. The trigger may be an irritant or even palpation of the larynx. Laryngeal electromyography (EMG) is used to confirm subtle neuropathic findings of paresis. These patients are frequently treated for allergies, LPR, and PVFMD and may be refractory to treatment. When faced with this situation, treatment with the anticonvulsive agent gabapentin should be considered, which decreases neural sensitivity. Treatment success ranges from 37.5 to 80%, depending on level of motor involvement of the neuropathy. A starting dose of 100 mg three times a day is recommended, increasing to 300 mg three times a day for symptom control.

Paradoxical Vocal Fold Motion Disorder

Paradoxical vocal fold motion disorder (PVFMD) is a disorder marked by desynchronized or paradoxical adduction of the vocal folds during inspiration and/or expiration. As a result, the patient exhibits inspiratory stridor and/or experiences a sensation of airway restriction. This is often confused with the wheezing of asthma that, in contrast, occurs in the expiratory phase. Symptoms also include choking, aphonia or dysphonia, and chronic cough. Many terms have been used in the past to describe this condition, including vocal cord dysfunction, factitious asthma, psychogenic asthma, irritable larynx syndrome, and episodic paroxysmal laryngospasm. The differential diagnosis is bilateral vocal cord paralysis, hereditary abductor paralysis, posterior glottic stenosis, or cricoarytenoid joint fixation. PVFMD has many causes and has been classified into five organic and two nonorganic categories, based on etiology. These include brainstem compression, severe cortical or upper motor neuron injury, nuclear or lower motor neuron injury, movement disorder, gastroesophageal reflux, factitious or malingering PVFMD, and conversion disorder PVFMD. When associated with a conversion disorder, it is seen in primarily high-achieving, perfectionistic adolescents who are usually athletes, as well as in young female professionals. Patients complain of exercise-induced episodes of airway restriction, irritant-exposure triggers, or symptoms after a meal. Flow-volume loops have been used to assist in diagnosis; however, both false positives and false negatives are generated, and there is no consistent pattern. The gold standard in diagnosis is demonstration of PVFMD during flexible laryngoscopy, which may be seen at rest of after administration of a trigger (exercise, perfumes, etc). Treatment consists of elimination or avoidance of triggers, including reflux and allergy treatment, and respiratory retraining therapy administered by the speech pathologist. Any coexisting asthma/reactive airway disease must also be aggressively treated.

7.7

Allergy and Voice Disorders

Allergic diseases can manifest in the larynx in several ways. The classic description is that of laryngeal angioedema, an acute life-threatening process initiated by exposure to a specific allergen. This process is associated with immunoglobulin IgE-mediated anaphylaxis, but it is also seen in a non-IgE-mediated anaphylactoid response. Treatment of this disorder involves immediate airway control and injection of epinephrine with use of steroids and H2 blockers after the initial episode. Food allergy may lead to milder swelling of the vocal tract with dysphonia and may actually stimulate or worsen LPR. Avoidance of the triggering allergen and antihistamines are the recommended treatment. Many patients also suffer from chronic postnasal drip secondary to allergic rhinitis. These patients tend to frequently clear their throats, which leads to maladaptive laryngeal muscle usage and can lead to the development of vocal fold lesions. Exposure and allergy to aerosolized irritants can also lead to muscle-tension dysphonia. Mold and volatile organic compounds (VOC) are the usual suspects. VOCs include alcohols, aldehydes, and ketones. Again, avoidance and/or removal of the source of the irritant are the mainstay of treatment. Immunotherapy is an important consideration for treatment of allergy in the professional voice user, as it avoids drying effects of antihistamines in the endolarynx.

7.8

Medications and Their Effects on Voice

Both allergy and post-URI patients can experience dysphonia related to persistent postnasal drip. Patients also experience

 

cough due to direct irritation from mucus or because of altered sensitivity of the endolarynx. Severe coughing can result in phonotrauma, leading to vocal fold hemorrhage and vocal fold lesion formation. As a result, many over the counter preparations are used for their antitussive and mucolytic properties. Guaifenesin is the most widely used mucolytic and works best when the patient is well hydrated. Codeine and dextromethorphan are added to many cold medicine preparations. Tramadol, which is a weak opiate, may have enhanced antitussive properties, without the significant opioid side effects associated with codeine. Antihistamines again should be used with caution in the professional voice user with allergy, as the drying effects on the vocal folds can be detrimental. Leukotriene inhibitors, such as montelukast, and nasal corticosteroids can be used in allergic patients, with less drying. Despite widespread clinical use of oral corticosteroids for acute dysphonia in the professional voice user, there is minimal scientific literature concerning this subject. The corticosteroid mechanism of action is to prevent capillary dilation and decrease capillary permeability, which consequently decreases edema. Typically, oral steroids are used in short bursts, with a tapering dosage to avoid adrenocortical insufficiency and minimize long-term side effects. Intramuscular use is also reported for the acute situation. A few studies have shown improvement in objective acoustic measures with use of steroids. However, if used for a more extended period, corticosteroids can lead to fluid imbalance, systemic muscle weakness and atrophy, gastrointestinal and neurologic problems, glaucoma, and electrolyte and metabolic disorders, and can lead to fungal infection. Corticosteroids have been linked to peptic ulcer development; therefore, any patient on long-term oral corticosteroids should be placed on at least an H2 blocker, preferably a PPI. Many medications have virilizing properties and should be used with great caution in the professional voice user, or any patient for that matter. These medications, such as Danazol, have been used for treatment of fibrocystic breast disease and endometriosis. Testosterone injections have been administered to women complaining of loss of libido or energy and have been reported in female athletes for enhanced performance. Nonphonatory side effects include acne, hirsutism, weight gain, and hairline recession. Voice effects including lowering of fundamental frequency, vocal instability with pitch breaks, loss of high frequency vocal range, and generalized dysphonia. For Danazol, the incidence may be as high as 10% in patients on the medication. Histologically, water retention in the muscle and fiber hypertrophy are seen. Although some reports have stated that effects are temporary and cease with discontinuation of the medication, there is potential for permanent voice change as can be seen in histological studies. This can be particularly damaging to the voice professional, so great caution must be used when considering prescribing these medications. During the premenstrual period of the menstrual cycle, many women exhibit pitch lowering secondary to presumed venous dilatation and edema of the vocal folds. Low-dose oral monophasic contraceptives have been shown to reduce this pitch variability and exhibit less androgenic side effects. One group of medications that should not be overlooked is herbal remedies. Many have anticoagulant properties and can predispose a person to vocal fold hemorrhage. These include dong quai (which actually contains coumadin), willow bark,

Chapter 7

primrose, garlic in high doses, vitamin E in high doses, gingko biloba, ginger, feverfew, and red root. Some may have crossreactivity to ragweed: goldenseal, chamomile after long-term use, echinacea, St. John’s wort, yarrow, dong quai. Some herbal medications also may have hormonal effects, e. g., dong quai may increase effects of ovarian and testicular hormones. Yam has progesterone-like properties, and licorice root also has progesteronic in addition to estrogenic effects and can change vocal pitch. Primrose is a natural estrogen promoter, and melatonin acts as a contraceptive in high doses.

7.9

Vocal Hygiene

A discussion of medical treatment of voice disorders would not be complete without discussing the importance of vocal hygiene. Elements of vocal hygiene include understanding that medical problems affect the voice, understanding effects of smoking, alcohol, drugs, hydration and nutrition, vocal stress and vocal exercise, and general vocal hygiene. Vocal hygiene involves knowledge, avoidance, or reduction of irritants such as gastric juices or tobacco smoke, dehydration and control of postnasal drip of any cause. The patient should be made keenly aware of the danger of “singing sick,” as vocal injuries are more likely to occur in the sick singer than in a healthy one. The sick singer should take adequate vocal rest, fluids, and medical care as needed. Vocal fold hemorrhage and vocal fold lesions are the most significant concerns, and changing bad habits early in younger performers is critical to long-term vocal health.

7.10

Role of the Speech–Language Pathologist in Voice Therapy

The speech–language pathologist is instrumental in teaching the voice disorder patient about laryngeal anatomy and vocal biomechanics, which are central to the voice therapy process for many disorders. The speech–language pathologist with special training in voice disorders is an essential member of the diagnostic and therapeutic team required for high-quality voice care. The speech–language pathologist specializes in assessing and treating behavioral issues of the speaking and singing voice. Many patients with dysphonia struggle from a variety of poor behaviors and/or speaking techniques or inappropriate use of the voice and these problems are all easily treated with the intervention of the speech–language pathologist, using the overall global term of voice therapy. A detailed description of voice therapy treatment methods for a variety of dysphonias is outside the focus of this book, but it is essential component of the treatment of a wide variety of voice disorders is a nonsurgical approach to voice rehabilitation with voice therapy. Thus, the speech–language pathologist plays a crucial role in all phases of modern voice care (diagnostic, therapeutic, and rehabilitative).

47

48

Nonsurgical Treatment of Voice Disorders

Key Points

7

■ Up to 50% of voice disorder patients may have coexisting LPR. ■ Twice-a-day therapy with a proton pump inhibitor results in the highest symptom resolution. ■ Muscletension patterns I–IV seen in MTD are not pathognomonic for this disorder and can be seen in other voice disorders such as spasmodic dysphonia, and even some normal voices. ■ PVFMD is treated best with multimodality treatment that includes respiratory retraining (voice therapy) and proton pump inhibitors, as LPR is a common trigger for PVFMD episodes.

Selected Bibliography 1

2

3 4

5

6

7

8

9 10

11

12 13

Park W, Hicks DM, Khandwala F et al (2005) Laryngopharyngeal reflux: prospective cohort study evaluating optimal dose of proton-pump inhibitor therapy and pretherapy predictors of response. Laryngoscope 115:1230–1238 Belafsky PC, Postma GN, Koufman JA (2001) Laryngopharyngeal reflux symptoms improve before changes in physical findings. Laryngoscope 111:979–981 Vaezi MF (2003) Gastroesophageal reflux disease and the larynx. J Clin Gastroenterol 36:198–203 de Lima Pontes PA, De Biase NG, Gadelha ME (1999) Clinical evolution of laryngeal granulomas: treatment and prognosis. Laryngoscope 109(Pt. 1):289–294 Walner DL, Stern Y, Gerber ME, Rudolph C, Baldwin CY, Cotton RT (1998) Gastroesophageal reflux in patients with subglottic stenosis. Arch Otolaryngol Head Neck Surg 124:551–555 Jaspersen D, Kulig M, Labenz J et al (2003) Prevalence of extraoesphageal manifestations in gastro-oesophageal reflux disease: an analysis based on the Pro-GERD study. Aliment Pharmacol Ther 17:1515–1520 Mehanna HM, Kuo T, Chaplin J, Taylor G, Morton RP (2004) Fungal laryngitis in immunocompetent patients. J Laryngol Otol 118:379–381 Roland NJ, Bhalla RK, Earis J (2004) The local side effects of inhaled corticosteroids: current understanding and review of the literature. Chest 126:213–219 Sulica L (2005) Laryngeal thrush. Ann Otol Rhinol Laryngol 114:369–375 Mirza N, Schwartz SK, Antin-Ozerkis DA (2004) Laryngeal findings in users of combination corticosteroid and bronchodilator therapy. Laryngoscope 114:1566–1569 DelGaudio JM (2002) Steroid inhaler laryngitis: dysphonia caused by inhaled fluticasone therapy. Arch Otolaryngol Head Neck Surg 128:677–681 Woo P, Mendelsohn J, Humphrey D (1995) Rheumatoid nodules of the larynx. Ear Nose Throat J 113:147–150 Nanke Y, Kotake S, Yonemoto K, Hara M, Hasegawa M, Kamatani N (2001) Cricoarytenoid arthritis with rheumatoid arthritis and systemic lupus erythematosus. J Rheumatol 28:624–626

  14 Devaney K, Ferlito A, Devaney SL, Hunter BC, Rinaldo A (1998) Clinicopathological consultation: Wegener’s granulomatosis of the head and neck. Ann Otol Rhinol Laryngol 107:439–445 15 Herridge MS, Pearson FG, Downey GP (1996) Subglottic stenosis complicating Wegener’s granulomatosis: surgical repair as a viable treatment option. J Thorac Cardiovasc Surg 111:961–966 16 Stappaerts I, Van Laer C, Deschepper K, Van de Heyning P, Vermeire P (2000) Endoscopic management of severe subglottic stenosis in Wegener’s granulomatosis. Clin Rheumatol 19:315–317 17 Bartels H, Dikkers FG, Lokhorst HM, Van der Wal JE, Hazenberg BPC (2004) Laryngeal amyloidosis: localized versus systemic disease and update on diagnosis and therapy. Ann Otol Rhinol Laryngol 113:741–748 18 Akst LM, Thompson LDR (2003) Larynx amyloidosis. Ear Nose Throat J 82(11):844–845 19 Sulica L (2004) Contemporary management of spasmodic dysphonia. Curr Opin Otolaryngol Head Neck Surg 12:543–548 20 Warrick P, Dromey C, Irish JC, Durkin L, Pakiam A, Lang A (2000) Botulinum toxin for essential tremor of the voice with multiple anatomical sites of tremor: a crossover design study of unilateral versus bilateral injection. Laryngoscope 110:1366–1374. 21 Sullivan KL, Hauser RA, Zesiewicz TA (2003) Essential tremor: epidemiology, diagnosis, and treatment. Neurologist 10:250–258 22 Zesiewicz TA, Elble R, Louis ED et al (2005) Practice parameter: therapies for essential tremor. Neurology 53:2008–2020 23 Blumin JH, Picolinksy DE, Atkins JP (2004) Laryngeal findings in advanced Parkinson’s disease. Ann Otol Rhinol Laryngol 113:253–258 24 Roy N (2003) Functional dysphonia. Curr Opin Otolaryngol Head Neck Surg 11:144–148 25 Altman KW, Simpson CB, Amina MR, Abaza M, Balkissoon R, Casiano RR (2002) Cough and paradoxical vocal fold motion. Otolaryngol Head Neck Surg 127:501–511 26 Maschka D, Bauman NM, McCray PB et al (1997) A classification scheme for paradoxical vocal cord motion. Laryngoscope 107:1429–1435 27 Morrison M, Rammage L, Emami AJ (1999) The irritable larynx syndrome. J Voice 13:447–455 28 Lee B, Woo P (2005) Chronic cough as a sign of laryngeal sensory neuropathy: diagnosis and treatment. Ann Otol Rhinol Laryngol 114:253–257 29 Amin MR, Koufman JA (2001) Vagal neuropathy after upper respiratory infection: a viral etiology? Am J Otolaryngol 22:251–256 30 Chadwick SJ (2003) Allergy and the contemporary laryngologist. Otolaryngol Clin N Am 36:957–988 31 Watts CR, Early SE (2002) Corticosteroids: effects on voice. Curr Opin Otolaryngol Head Neck Surg 10:168–172 32 Baker J (1999) A report on alterations to the speaking and singing voices of four women following hormonal therapy with virilizing agents. J Voice 13:496–507 33 Amir O, Biron-Shental T, Muchnik C, Kishon-Rabin L (2003) Do oral contraceptives improve vocal quality? Limited trail on lowdose formulations. Obstet Gynecol 101:773–777 34 Columbia University at New York Presbyterian Hospital, College of Physicians and Surgeons, Voice and Swallowing Center (2005) Herbal medications. http://www.voiceandswallowing.com/Voicetreat_herb.htm 35 Murry T, Rosen CA (2000) Vocal education for the professional voice user and singer. Otolaryngol Clin N Am 33:967–981

Chapter 8

Timing, Planning, and Decision Making in Phonosurgery

8.1

Fundamental and Related Chapters

Please see Chaps. 4, 5, and 7 for further information.

8.2

Key Components to Successful Care of Patients with Voice Disorders

This chapter addresses specific issues related to phonomicrosurgery for benign lesions of the vocal fold, phonosurgery for disorders of glottal incompetence, surgeries for airway enlargement, and tumor excision of the larynx. For many of the situations in voice care, the surgical procedures are elective, and thus the surgeon and patient have the ability to participate in maximum nonsurgical treatment modalities for the rehabilitation of the patient’s voice problem, psychological preparation for surgery, and an appropriate and thorough informed consent process.

8.3

Surgical Indications and Contraindications

8.3.1

Timing of Phonomicrosurgery

The majority of patients require a significant amount of time to recover after phonomicrosurgery. Thus, it is important that the surgeon and patient discuss the need for an adequate amount of time for voice recovery after these procedures. Often a short period of complete voice rest immediately after phonomicrosurgery is indicated. This can range from 2 to 14 days and typically averages 7 days. The time of voice limitation before allowing the phonomicrosurgery patient to use full speaking voice activities ranges from 7 to 30 days. Similarly, the vocal recovery time before full singing is allowed is individualized to the patient situation, but typically ranges from 30 to 90 days. Thus, the patient must cancel pending voice demands when scheduling phonomicrosurgery or delay the surgery date until there is a more appropriate time after the surgery to accommodate reduced voice demands. This is especially important for vocal performers, given that they have many demands on them from management and staff. Financial demands also pressure the vocalist to perform sooner than is medically appropriate. Similarly, schoolteachers have such significant vocal demands that any decision to proceed with phonomicrosurgery during the school year should be taken with great caution, or plans

8

should be made not to return for the remaining semester. For example, phonomicrosurgery to remove any type of benign lesion of the lamina propria from a schoolteacher during winter break—with expectations of resuming when school resumes at the start of the new year—is a plan fraught with danger and should be avoided. Phonomicrosurgery on teachers should only be done at the start of summer (June) or the teacher will need to be off work for half the school year.

8.3.2 Preoperative Considerations for Phonomicrosurgery Any conditions that will create temporary vocal fold edema prior to phonomicrosurgery should be avoided or treated prior to proceeding. Thus, heavy vocal demands such as singing, screaming, yelling, or lecturing should be avoided approximately 1–2 weeks before phonomicrosurgery. Similarly, comorbid medical conditions such laryngopharyngeal reflux disease and sinonasal allergic disease, and upper respiratory infection should be treated and may be reason to reschedule the surgery. In some instances, a short dose of oral steroids can be used to alleviate the temporary vocal fold edema associated with these conditions prior to phonomicrosurgery. The reason for avoiding temporary vocal fold edema immediately prior to phonomicrosurgery is to minimize the removal of vocal fold tissue (epithelium and/or lamina propria) that appears permanently pathological but, in fact, may represent temporary edema. If this occurs, excessive excision may result. Furthermore, most likely epithelium/lamina propria wound healing is compromised in the face of an acute inflammatory condition resulting in suboptimal postoperative voice rehabilitation. The psychological impact of phonosurgery on patients should be greatly appreciated. This is an area that is frequently overlooked by surgeons, especially by doctors who do not appreciate the unique relationship that professional voice users and heavy voice users have with respect to their psyche and their voice. It is important to realize that these individuals (to a large degree) identify themselves by their voice, and thus the consideration and realization of the need for surgery induces a significant amount of anxiety and concern. This must be identified by the voice care team preoperatively, and discussed and dealt with in a positive, successful fashion. This will ensure maximum postoperative voice quality, patient compliance, and minimal negative outcomes and activities during this stressful time. Preoperative voice therapy can often play a major role in addressing these issues. Furthermore, it is essential that the patient not feel pressured or rushed to decide on proceeding with

50

Timing of Phonosurgery

phonomicrosurgery. The amount of time it takes any patient to decide to proceed with phonosurgery is highly variable, and the decision-making process must be individualized. Patience should be exercised by the voice care team waiting for the patient to become comfortable with the decision to have phonosurgery. This will significantly improve the patient’s coping ability during this stressful process.

8.4

8

Decision Making in Phonosurgery

In most situations, phonosurgery is an elective procedure, and thus, the patient and surgeon are afforded an amount of time for nonsurgical treatment of the voice condition, and then are able to make a joint decision to proceed with surgery. On the other hand, surgery should not be delayed if the following are present: ■ Dysphagia associated with aspiration ■ Impending airway embarrassment ■ Risk for malignancy The majority of voice-related procedures in the category of phonomicrosurgery, laryngeal framework surgery, and vocal fold injection for benign lesions of the vocal fold/glottal incompetence are in fact non–life threatening. Thus, the decision making and preparation prior to surgery should be undertaken on a reasonable timetable that should be predominantly patient driven. Generally for most elective phonosurgeries, the patient should be offered and undergo nonsurgical rehabilitative measures prior to proceeding with surgery. Of course, this dictum must be utilized within reason, given that there are instances when the patient’s medical condition (large exophytic vocal fold polyp or lateralized vocal fold paralysis) dictate that nonsurgical treatment methods do not have a reasonable chance for significant improvement. Thus, it is unreasonable and poor use of resources to force all patients to undergo multiple nonsurgical rehabilitative measures (voice therapy, singing therapy, allergy therapy, medical therapy) if they have no reasonable expectation to make a significant improvement in the patient’s voice limitations and/or symptoms. If there is any possibility of the nonsurgical treatment options making a substantive difference, then it is worthwhile having the patient undergo these treatments. However, close observation of the patient needs to be maintained to assess the patient’s response after a short time period. Specifically, this is the case with respect to voice therapy. Often patients with benign vocal fold lesions or with conditions of glottal incompetence will be treated with one or two sessions of voice therapy and then reassessed for progress and potential for significant improvement. With a compliant patient and a skilled speech–language pathologist, the decision to proceed with phonomicrosurgery can be confidently made pending the outcome and progress after one or two sessions of voice therapy. Often after the initiation of voice therapy, the patient begins to notice substantive improvement, and thus all surgery should be delayed until voice therapy and possibly singing voice therapy is completed. A formal reevaluation

 

of their functional abilities and limitations should follow (see below.) The decision to proceed with elective phonosurgery should be a joint decision between the patient and the surgeon. The optimal role of the patient should be as the primary decision maker and the surgeon should serve as the educator in this process. After all nonsurgical rehabilitation methods have been employed, a formal reevaluation by the voice care team should be performed to decide if elective phonosurgery is indicated. An important component to this decision-making process is to encourage the patient to resume his/her voice activities after nonsurgical rehabilitation has been completed. When the patient resumes vocal activity, they should be asked to answer the simple (but essential) question: “Can you do what you need to with your voice?” or “Do you still have significant functional limitations (e. g., reduced range, reduced clarity, vocal fatigue)?” This assessment of functional ability is crucial in prompting the patient to decide if he/she should proceed with phonosurgery. It is essential that the surgeon not pressure or rush the patient’s decision. The surgeon’s most important role is to educate the patient on his/her specific voice condition and on the risks and benefits of the surgical procedure (see Sect. 8.5, “Informed Consent Regarding Phonosurgery,” below), as well as to discuss reasonable expectations of elective phonosurgery. With this information, the patient should be well equipped to be the primary decision maker for elective phonosurgery. It is essential for patients undergoing phonomicrosurgery to have had a recent voice evaluation. Specifically, a laryngo­ video­stroboscopy should be performed in the period shortly before surgery (1–3 weeks). This allows the surgeon to review and see the most recent status of the vocal fold pathology, and this can often factor into important intraoperative decision making. It is recommended that the surgeon review the recent stroboscopy examination either the day of the surgery or preferably immediately prior to (or during) the patient’s phonomicrosurgical procedure. Intraoperative decision making can be quite challenging for the phonosurgeon, and there are various guidelines for the types of laryngeal surgery being undertaken. For patients with cancer, intraoperative decision making is dictated by the location and nature of the cancer. However, if the surgeon is not comfortable with margins on frozen sections, then it is often wise to obtain conservative margins and delay the surgical procedure until permanent pathology is available. Then, if there is a positive margin, a return to the operating room can be undertaken. This approach avoids excessive resection of nonmalignant tissue. For patients undergoing phonomicrosurgery for benign lesions of the lamina propria, the intraoperative decision making process should be approached in a very conservative fashion. Difficult decisions regarding how much to resection of epithelium and/or lamina propria should be done on the conservative side; accepting the possibility a small number of patients may require repeat phonomicrosurgery for persistent or recurrent disease. These repeat phonomicrosurgery procedures are a small price to pay for minimizing the risk of overaggressive resection of epithelium and/or lamina propria, resulting in severe (and potentially irreversible) postoperative dysphonia from vocal fold scar.

 

Chapter 8

Intraoperative decision making regarding laryngeal framework procedures should follow this guideline: The best chance for a good outcome is with the first surgical procedure. Thus, all attempts, regardless of the chosen method, should work to achieve the best possible voice quality from the first surgical procedure. The reversibility and adjustability of revision laryngeal framework procedures may be limited. Intraoperative decision making for airway cases, especially for glottic enlargement procedures (transverse cordotomy, medial arytenoidectomy, total arytenoidectomy) should be done in a conservative fashion. All patients should be counseled that the greater the laryngeal airway that is created, the greater is the risk for decreased vocal function. Thus, a conservative (and, if needed, staged approach) to surgery for the enlargement of laryngeal airway should be the guiding principle for intraoperative decision making in this area.

8.5

Informed Consent Regarding Phonosurgery

The most important aspect of informed consent is education of the patient regarding the salient details of the surgical procedure, providing reasonable expectations, and discussing risks and benefits of the procedure. Documentation of the most important aspects of this process is also strongly advised. With phonomicrosurgery procedures for benign vocal fold lesions, the informed consent process should involve the patient’s individual pathology, specifically identified from stroboscopy and/ or from prior operative findings. The factors that play an important role in defining reasonable expectations of successful phonomicrosurgery include the patient’s vocal abilities and/or voice training and his/her postoperative vocal demands and expectations. A combination of all these factors should be synthesized and presented to the patient so he/she is offered the appropriate level of expectation. In general, appropriately performed phonomicrosurgery for benign lesions of the lamina propria in a compliant patient should have a success rate of > 95%. Success is defined as an improvement in voice quality and function. It is important for the surgeon to make the distinction between voice improvement and restoration to the patient’s premorbid vocal capabilities. The success rate to achieve the latter goal is going to be lower and will be directly related to the pathology of the vocal folds, ability/training of the patient, and vocal demands. It is important to inform the patient that there is a risk of postoperative scarring and permanent postoperative dysphonia that could even worsen his/her condition compared to preoperative status. This risk is quite small (1–2%), and similarly, there is a risk that significant improvement in vocal function will not be obtained despite the surgeon’s and the patient’s best efforts (1–2% incidence of “no improvement”). Appropriate informed consent for phonosurgeries involving patients with glottal incompetence should involve the specific expectations, voice improvements, and persistent limitations after surgery. Typically, these types of surgical procedures have a very high degree of success with respect to increasing volume, clarity, and endurance with normal speaking-voice use and normal speaking demands. There are often limitations af-

ter this type of surgery that persist involving loud speech and/ or singing. These limitations exist because of the persistent underlying pathologic condition such as vocal fold paralysis, vocal fold scar, and vocal fold paresis. Informed consent for surgical removal of laryngeal cancer should include reduction of vocal and swallowing function as well as the risk for additional surgery depending on permanent pathology results after surgery. Informed consent for airway procedures must involve discussion that as the surgical procedure obtains an increased airway for the patient, the greater the likelihood of diminution of the patient’s vocal function. The goal of the surgery is to obtain an adequate airway while at the same time minimizing the negative impact on the voice. Due to this voice–airway equation and the need for conservative removal of glottic narrowing, the patient should be informed of the likelihood of the need for repeat surgery. Patients with airway problems preoperatively that do not have a tracheotomy should also be consented for a possible tracheotomy depending on a variety of intraoperative situations.

Key Points ■ Most phonosurgical procedures are elective, and thus, the decision to proceed with surgery should be patient driven. The surgeon serves as educator, so that realistic goals of postoperative voice quality and function are clearly understood. ■ The key principle of decision making with respect to phonomicrosurgery is the use of nonsurgical rehabilitative treatment options (when appropriate) prior to proceeding with surgery. ■ With respect to microsurgery for benign lesions of the lamina propria, the most important question that must be answered before deciding for or against proceeding with phonomicrosurgery is: “Can the patient do what they need to do with his/ her voice after undergoing maximum of nonsurgical rehabilitation?” ■ Informed consent process for phonomicrosurgery should be individualized due to the specific pathologic condition present and the surgical approach recommended.

Selected Bibliography 1

2

Bouchayer M, Cornut G (1992) Microsurgical treatment of benign vocal fold lesions: indications, technique, results. Folia Phoniatr 44:155–184 Courey MS, Gardner GM, Stone RE, Ossoff RH (1995) Endoscopic vocal fold microflap: a three-year experience. Ann Otol Rhino Laryngol 104(Pt. 1):267–273

51

52

Timing of Phonosurgery 3

4 5

8

Dejonckere PH (2000) Committee on Phoniatrics of the European Laryngological Society. Assessing efficacy of voice treatments: a guideline. Rev Laryngol Otol Rhinol 121:307–310 Ford CN (1999) Advances and refinements in phonosurgery. Laryngoscope 109:1891–1900 Ford CN (2004) G. Paul Moore lecture: lessons in phonosurgery. J Voice 18:534–544

  6

7 8

Netterville JL, Stone RE, Luken ES, Civantos FJ (1993) Silastic medialization and arytenoid adduction: the Vanderbilt experience. A review of 116 phonosurgical procedures. Ann Otol Rhino Laryngol 102:413–424 Sataloff RT (2005) Professional voice: the science and art of clinical care, 3rd edn. Plural, San Diego Zeitels SM, Hillman RE, Desloge R, Mauri M, Doyle PB (2002) Phonomicrosurgery in singers and performing artists: treatment outcomes, management theories, and future directions. Ann Otol Rhino Laryngol 190(Suppl.):21–40

Chapter 9

Anesthesia and Airway Management for Laryngeal Surgery

9.1

9

Fundamental and Related Chapters

Please see Chaps. 13, 27, 28, 29, 39, 40, 45, 46, and 47 for further information.

9.2

Equipment

Airway management requires the following: 1. Ventilating laryngoscope a) Ossoff-Pilling b) Pilling subglottiscope 2. Jet ventilator device (preferably high frequency) 3. Jet ventilation conduit a) Hunsaker Mon-Jet jet ventilation tube (MedtronicXomed, Jacksonville, Fla.), or b) Jet Venturi needle 4. Laser-safe ETT a) MLT 5.0/5.5 or smaller 5. Tracheostomy tube/surgical tray 6. Rigid bronchoscopes 7. 4% lidocaine (LTA)

9.3

Surgical Indications and Contraindications

Sharing the airway with our anesthesia colleagues is one of the most important (and often neglected) aspects of successful laryngeal surgery. Lack of collaboration and preoperative planning with the anesthesiology team can turn an otherwisesimple microlaryngoscopy case into a chaotic, life-threatening airway crisis. The following general principles should always be observed: 1. A preoperative management plan for securing the patient’s airway must be discussed with the anesthesiologist prior to proceeding with surgery. An ideal plan (plan A), as well as one or two alternate strategies (plans B and C) should be established so that the airway management is automatic and algorithmic, as opposed to chaotic/reactive. Prior to bringing the patient into the operating room, both the surgeon and anesthesiologist should have the proper equipment in the room, open, and “ready to go” if alternative plans become necessary. 2. The patient should be placed in the “sniffing positioning,” with the head extended (at the atlanto-occipital joint), and

Fig. 9.1  Standard 5.0 endotracheal tube below (ETT) and 5.0 MLT

above (note longer length of MLT)

the neck flexed (along the cervicothoracic vertebrae) for optimal laryngoscopic exposure (see Chap. 10, “Principles of Phonomicrosurgery”). 3. Microlaryngoscopic surgery generally employs one of the following methods for maintaining the airway: a) Oral intubation using a small diameter endotracheal tube of adequate length: 5.0 or 5.5 MLT (microlaryngoscopy tube) (Fig. 9.1). MLT (microlaryngoscopy) endotracheal tube is a small-diameter ETT with an extended length. Most “regular” ETT (size 5.0 and smaller) are not long enough to adequately span the distance between the oral commissure and the subglottic/tracheal airway. b) Jet Venturi ventilation using one of the following methods: i. Subglottic Mon-Jet/Hunsaker jet ventilation tube (Fig. 9.2) ii. Supraglottic jet Venturi needle (via port within laryngoscope or attached to laryngoscope) (Fig. 9.3) 4. In general, lesions located on the anterior two thirds of the larynx (membranous vocal folds) can be adequately exposed/treated with a 5.5 or smaller ETT. Lesions of the posterior third of the larynx (vocal processes and posterior commissure/arytenoids region) require one of the following approaches: a) Jet ventilation b) Apneic technique c) ETT placement anteriorly, resting on top of the laryngoscope

54

9

Airway Management for Larygeal Surgery

Fig. 9.2  Subglottic jet ventilation tube (Medtronic-Xomed)

Fig. 9.4  Laser protected ETT (Medtronic-Xomed)

 

Fig. 9.3  Jet Venturi needle and jet ventilation tubing/pressure gauge

precision of fine surgical maneuvers. In addition, jet ventilation (containing 100% oxygen) must be suspended during firing of the laser. 8. Subglottic jet ventilation is more efficient when used for glottic laser surgery; the vocal folds are not as affected by ventilatory forces. Jet ventilation can proceed even while the laser is being fired. Another important advantage of the Hunsaker subglottic jet ventilation tube is the built-in CO2-monitoring port. This allows the anesthesia team to monitor end-tidal CO2 to ensure adequate exhalation time during jet ventilation. The potential drawback of subglottic jet ventilation is the increased risk of air trapping from the “ball-valve” phenomenon. Often, subglottic jet ventilation is performed distal to the airway obstruction, and if egress (escape) of air is prevented by the obstructed region, then air trapping results. Complications of this include pneumothorax (possibly bilateral), pneumomediastinum, and emergent ventilatory compromise. Increased vigilance must be practiced when this ventilation technique is employed.

5. In all cases where a surgical laser is employed, an appro-

priate laser-protected tube must be in place (Fig. 9.4). The only exception to this rule is when jet ventilation or apneic technique is used (both are also safe for the laser). 6. In instances where the patient has an indwelling tracheostomy tube: a) 5.5–6.0 reinforced ETT placed through the stoma into the trachea, laser protected when appropriate b) Apneic technique may be employed if airway surgery is carried out distal to the tracheal stoma site, using reinsertion of stomal ETT intermittently to restore oxygenation between treatment cycles. 7. Jet ventilation is safest when used proximally (supraglottic, as opposed to subglottic) However, passive movement of the vocal folds due to ventilatory air movement limits the

9.4

Principles of Airway Management: Subglottic and Tracheal Stenosis

1. Subglottic/tracheal stenosis presents a unique anesthetic

challenge. Ideally, the airway is not instrumented by the anesthesiology team; endotracheal intubation can result in traumatic injury to the subglottic mucosa and may precipitate an emergency in a patient with a marginal (but otherwise stable) airway. 2. Subglottic/tracheal stenosis in a stable airway should generally proceed as follows: a) Mask induction is performed using inhalational agents (sevoflurane):

 

Chapter 9

i. Paralytics are not used (especially succinylcholine). ii. Induction should be gradual (no “rapid sequence”). iii. Muscle relaxation must be present (via sevoflurane

or propofol).

iv. The surgical bed is rotated to the surgeon. v. Suspension laryngoscopy/subglottoscopy is ob-

tained, with placement of the tip of the scope just proximal to the stenotic region. vi. Jet ventilation is employed through the laryngoscope or with a ventilating tube (Hunsaker Mon–Jet catheter). vii. If oxygenation cannot be maintained by jet ventilation, or if CO2 retention is excessive, then ventilation through a rigid bronchoscope (as employed during rigid dilation of the stenotic region) can be used intermittently. viii. After surgical treatment of the stenotic region, the patient’s airway is returned to the care of anesthesia, and the patient is mask ventilated until reversed, and breathing spontaneously without assistance. ix. Reintubation at the end of the case should be avoided due to the risk of unnecessary mucosal trauma and/ or reactive airway edema. 3. Subglottic/tracheal stenosis in an unstable, emergent airway case should observe the following general guidelines: a) The surgical approach to the treatment of emergent/ urgent SGS should be individualized for each patient. Tracheostomy is the most conservative and safe option (exceptions noted below), especially in a patient with a “difficult surgical airway” due to coexisting anatomic conditions (retrognathia, trismus, base-of-tongue hypertrophy, limited neck flexion). However, if expert anesthesia and intensive care monitoring are available, then endoscopic treatments are generally preferable, and tracheostomy can be avoided. b) The location and nature of the stenosis is critical in determining the method of securing and maintaining the airway during surgical treatment: c) “High” SGS (confined to infraglottis/cricoid) can be treated as described in no. 2 above (jet ventilation without endotracheal intubation); however, tracheostomy under local is also a reasonable choice. The tracheostomy should be placed at least 1 cm inferior to the stenotic region, and not through the stenotic segment. This will facilitate endoscopic treatment at a later date, as the tracheotomy tube will not interfere with healing of the stenotic site after subsequent laser/dilation procedures. d) Subglottic/cervical tracheal narrowing due to cartilaginous collapse. This condition cannot always be anticipated preoperatively, but once recognized should be treated in the following manner: i. Endoscopic laser treatment is avoided, as it is ineffective. ii. The airway is obtained by performing a tracheostomy under local (alternate method: rigid bronchoscopy to secure the airway, followed by tracheostomy placement)

Fig. 9.5  Illustration of ideal tracheostomy entry point for cartilagi-

nous collapse of the airway (indicated by arrow A) The length of tracheal resection is reduced (segment A), compared with the amount that would need to be resected (segment B1) if the tracheostomy were placed more distally (arrow B)

iii. The tracheotomy entry point should be through the

collapsed segment.

iv. This step minimizes the length of trachea that must

be excised when a tracheal resection/cricotracheal resection is performed at a later date (Fig. 9.5) (see Chap. 47, “Tracheal Stenosis: Tracheal Resection with Primary Anastomosis”) e) Intrathoracic tracheal stenosis. In these cases, tracheostomy is not a viable option, because it is unlikely to bypass (enter below) the stenotic segment. The airway should be exposed by the surgeon using an laryngoscope as described in no. 2 above. Oxygenation is achieved via jet ventilation, or by passing a ventilating bronchoscope past the stenotic region. Rigid dilation/laser treatment can then proceed as indicated. Another viable alternative is placement of indwelling stent at the stenotic site.

9.5

Special Circumstances: Difficult Exposure of the Larynx

1. In some patients, unfavorable anatomy and difficult laryn-

geal exposure may render all of the previously mentioned principles moot. If the larynx cannot be exposed through the oral route using rigid laryngoscopy/bronchoscopy, then

55

56

Airway Management for Larygeal Surgery

 

or smaller should be used

alternative means of securing the airway must be employed. The following conditions may predict a “difficult exposure” perorally (Fig. 9.6): a) Retrognathia b) Lingual hypertrophy/Poor palatal visualization c) Trismus/reduced interincisor opening d) Short, thick neck e) Limited neck extension 2. Alternative methods of obtaining an airway in a “difficult exposure” case: a) Tracheostomy under local b) Awake, flexible laryngoscopy with nasotracheal intubation c) Laryngoscopy and intubation using specialized “anterior” laryngoscope i. Ossoff–Pilling laryngoscope d) Laryngoscopy and intubation without visualization of vocal folds i. Sliding Jackson laryngoscope plus curved ETT with stylet e) Laryngeal mask anesthesia (LMA) 3. Specialized techniques: a) Intubation using Ossoff-Pilling laryngoscope In patients in whom difficulty with rigid transoral airway exposure is anticipated/encountered, the Ossoff–Pilling (OP) laryngoscope is extremely valuable. In close to 99% of surgical patients, the OP laryngoscope allows successful transoral exposure of the glottis. i. The patient is pre-oxygenated, and mask induction is utilized. Paralytics are avoided, and spontaneous ventilation (or assisted mask ventilation) is maintained. When the patient achieves the desired level of anesthesia, the surgical table is turned 90°, facing the surgeon. ii. The OP laryngoscope is passed perorally and advanced to the level of the vocal folds (or ideally, slightly distal, into the infraglottis). A suspension device (Lewy) can also be used to achieve additional

Fig. 9.8  Removal of connector from ETT to facilitate passage of the

Fig. 9.9  Laryngeal cup forceps are used to grasp the ETT

Fig. 9.6  Illustration of anatomic features in a patient with “difficult

airway exposure”

9

Fig. 9.7  Intubation through an Ossoff–Pilling laryngoscope. A 5.0 ETT

tube through the laryngoscope

 

Chapter 9

anterior rotation of the laryngoscope in particularly difficult cases, but is not often necessary. iii. A 5.0 MLT (or smaller) is placed directly through the laryngoscope to secure the airway. The balloon can be inflated, position confirmed, and ventilation/ oxygenation established until the patient is stabilized (Fig. 9.7). iv. The laryngoscope can then be removed over the tube (with a pseudo-Seldinger technique), leaving the ETT in place: i. The plastic connector is removed from the proximal end of the ETT (Fig. 9.8). ii. A medium–large laryngeal cup forceps is used to grasp the proximal ETT (Fig. 9.9). iii. The surgeon backs the OP scope out of the oral cavity while holding the ETT stationary to prevent extubation. iv. When the intraoral portion of the tube can be visualized, it is secured by an assistant (Fig. 9.10).

v. The cup forceps is released, and the OP scope is

pulled back until the entire ETT and trailing cuffinflation tubing are passed through its lumen (Fig. 9.11). Larger cuff-inflation ports (especially the liquid-filled variety used in laser-protected ETTs), may get caught within the narrow distal lumen of the OP scope. The cup forceps can be used to push this device through the scope, however. b) Sliding Jackson laryngoscope In patients in whom it is impossible to visualize the vocal folds with the above (OP laryngoscopic) technique, a Sliding Jackson (SJ) laryngoscope can be used for peroral intubation in select cases. While the SJ scope does not provide superior visualization of the glottis in difficult, “anterior” patients, it can be used as a “familiar” intubation laryngoscope (analogous to the Miller blade used by anesthesiologists). In cases where the glottis cannot be visualized with the OP laryngoscope, the SJ is used to displace the base of tongue and provide a pathway for placement of an ETT “blindly.” A stylet must be used, with an exaggerated curve at the distal end of the ETT. This curve allows the tip of the ETT to extend further anteriorly, beyond the exposure provided by the laryngoscope, and into the glottic inlet. The ETT is advanced into the oral cavity lateral to the laryngoscope (entering at the oral commissure) and is guided toward the midline of the airway (from right to left) (Fig. 9.12). It should

Fig. 9.10  As the laryngoscope is removed, the intraoral portion of the

ETT is manually secured

Fig. 9.11  The cup forceps are released as the entire laryngoscope is

removed

Fig. 9.12  Intubation using a Sliding Jackson laryngoscope. Note the

acute bend at the distal end of the tube

57

58

Airway Management for Larygeal Surgery

be emphasized that this type of “blind” intubation is not a preferred method of securing the airway. Instead, is a “court of last resort” for peroral intubation when all other options have failed. Also, it should be noted that substantial experience with intubation/difficult laryngeal exposure is required before attempting this technique.

9.6

9

Anesthesia for Laryngeal Framework Surgery

Monitored anesthesia care for patients undergoing framework surgery is often suboptimal due to a lack of communication between the surgeon and the anesthesiologist. To most anesthesiologists, “monitored anesthesia care” for a patient undergoing a local procedure involves sedation via a propofol (Diprivan) drip. Propofol is felt to be superior to midazolam (Versed), due to its ease of rapid titration, faster wake-up times, and better quality of sedation. However, propofol is poorly suited for framework surgery performed under local anesthesia for the following reasons: ■ There is tendency for an “all-or-none” phenomenon; the patients is either deeply sedated (often snoring), or completely awake/alert and uncomfortable. ■ Due to the rapid nature of “emergence” from the sedated state, the patient often becomes disinhibited/combative when “awakened” and asked to phonate. This is likely exacerbated by the presence of a noxious stimulus (indwelling flexible transnasal laryngoscope). Midazolam (Versed) is much better suited for sedation in framework surgery patients, and results in a more relaxed, aware, and cooperative patient. In terms of local anesthesia, 1% lidocaine with epinephrine is infiltrated into the subcutaneous and deep tissues from the hyoid to the upper cricoid cartilage on the side of the proposed surgery, as well as 1 cm past the midline. The anesthetic solution should be infiltrated down to the depth of the thyroid cartilage. In general, 15–20 ml of solution is required. Additional supplemental injections are usually required during the surgical dissection, as needed. One must be careful to avoid injection into the paraglottic space and/or thyroarytenoid muscle, which could result in an inadvertent “injection augmentation.” In most cases, successful medialization and layered closure of the skin can be achieved without the need for further anesthesia at the incisional site.

Key Points ■ A preoperative management plan for securing the patient’s airway must be discussed with the anesthesiologist prior to proceeding with surgery. All necessary equipment should be opened and readily available in the operating room before proceeding.

 

■ In general, lesions located on the anterior two thirds of the larynx (membranous vocal folds) can be adequately exposed/treated with a 5.5 or smaller ETT. Lesions of the posterior third of the larynx (vocal processes and posterior commissure/ arytenoid region) require jet ventilation, displacement of the ETT anteriorly, or apneic technique. ■ Mask induction with inhalational agents, followed by jet ventilation is the preferred method of airway management for endoscopic treatment of subglottic/tracheal stenosis. Endotracheal intubation should be avoided in these cases. ■ Jet ventilation is safest when used proximal to the stenotic region; ventilation distal to the stenosis carries an increased risk of air trapping and pneumothorax. ■ If tracheostomy is performed in a patient with subglottic/tracheal stenosis due to intraluminal scar formation, then the airway should be entered at least 1 cm inferior to the area of the stenosis. Tracheostomy entry through the area of narrowing is ideal (though not essential) if cartilaginous collapse is present, however. ■ The following conditions may predict a “difficult exposure” perorally: ■ Retrognathia ■ Lingual hypertrophy/poor palatal visualization ■ Trismus/reduced interincisor opening ■ Short, thick neck ■ Limited neck flexion ■ Alternative methods of obtaining an airway in a “difficult exposure” case include: ■ Tracheostomy under local ■ Awake, fiberoptic nasotracheal intubation ■ Laryngoscopy and intubation using a specialized “anterior” laryngoscope ■ Ossoff–Pilling laryngoscope ■ Laryngoscopy and intubation without visualization of vocal folds ■ Sliding Jackson laryngoscope plus curved ETT with stylet ■ LMA ■ Topical 4% lidocaine (laryngotracheal anesthesia, commonly referred to as “LTA”) should be applied to the laryngotracheal region prior to instrumentation of the larynx. In addition, at the end of the surgical case, another application may be repeated (if greater than 45–60 min after the initial lidocaine treatment). Lidocaine reduces the incidence of laryngospasm.

Selected Bibliography 1

Hunsaker DH (1994) Anesthesia for microlaryngeal surgery: the case for subglottic jet ventilation. Laryngoscope 104(Suppl.):1–30

  2

Chapter 9 Sofferman RA, Johnson DL, Spencer RF (1997) Lost airway during anesthesia induction: alternatives for management. Laryngoscope 107:1476–1481

3

Hochman II. Zeitels SM. Heaton JT (1999) Analysis of the forces and position required for direct laryngoscopic exposure of the anterior vocal folds. Ann Otol Rhinol Laryngol 108:715–724

59

Part B Phonomicrosurgery for Benign Laryngeal Pathology

I Fundamentals of Phonomicrosurgery

Chapter 10

Principles of Phonomicrosurgery

10.1

Fundamental and Related Chapters

Please see Chaps. 1, 4, 8, 11, 12, 15, 16, 17, 18, 22, and 23 for further information.

10.2

Introduction

Phonomicrosurgery encompasses a variety of operations that has the primary goal of improving voice quality. These are elective operations that involve precision microsurgical removal of benign vocal fold pathology—most often from the subepithelial space of the vocal fold. The surgical procedures and principals are based on vocal fold physiology, specifically Hirano’s coverbody theory of vocal fold vibration (see Chap. 1, “Anatomy and Physiology of the Larynx”). Given the importance of the interaction between the epithelium–superficial layer of the lamina propria (cover) and the underlying deep layer of the lamina propria and muscle (body), phonomicrosurgery was born and has evolved to advocate the minimal disruption to the normal microarchitecture of the vocal fold while removing dysphoniainducing pathology. The overarching goal is to limit dissection to the most superficial plane possible and maximize epithelial and lamina propria preservation. The latter tenet is important to facilitate primary wound healing versus secondary wound healing. This is theorized to allow maximal functional recovery (vocal fold mucosal vibration) after surgery.

10.3

Surgical Indications and Contraindications

Phonomicrosurgery is an elective surgery, and thus, pressure should not be placed on the patient to proceed with surgery. The risks and benefits of the surgery should be detailed to the patient and most importantly, a realistic and thorough evaluation of the patient’s functional voice limitations and abilities (speech and singing) should be reviewed. Often this review process should be done over several weeks and involve the patient, physician, family members, a speech–language pathologist and possibly a singing voice specialist. When all nonsurgical treatment modalities have been exhausted and significant vocal functional limitations exist, the setting is appropriate for proceeding with phonomicrosurgery (see Chap. 8, “Timing, Planning, and Decision Making in Phonosurgery”).

10

Important preoperative measures before phonomicrosurgery include: ■ Avoiding aspirin, nonsteroidal anti-inflammatory medications or other anticoagulation medications ■ Avoiding significant vocal abuse and misuse immediately before surgery ■ Avoiding operating during the premenstrual period of a woman’s menstrual cycle, due to the slight edema occurring at this time as well as some increased fragility of the microvasculature of the vocal fold Preoperative voice therapy (one to two sessions) is extremely important in preparation for phonomicrosurgery for a variety of reasons: ■ Psychological preparation for surgery ■ Education regarding postoperative voice rest and voice use ■ Modification and improvement of improper speaking techniques and habits ■ Laying the foundation for postoperative voice therapy, both psychologically as well as from a behavioral perspective Preoperative voice therapy stresses to the patient the importance of changing inappropriate vocal techniques and implementing healthy voice behaviors in the postoperative period. Prior to phonomicrosurgery, the patient must realize he/she will be on voice rest and reduced voice use for a variable period (from 3 to 30 days). This is to ensure that the patient has adjusted his/her voice use to be compliant with the surgeon’s voice rest and reduced voice use limitations. Preoperative consent for phonomicrosurgery should involve the risks of general anesthesia, temporal mandibular joint injury, dental injury, and injury to the lingual nerve. The latter has been shown to be temporary in nature and lasts on average 2 weeks, with a maximum duration of 1 month. A discussion regarding postoperative voice quality after phonomicrosurgery should be taken seriously and done by the surgeon. Discussion should involve the small but real risk of either no improvement of the voice quality (~1–2% incidence) or a reduction in vocal function or voice quality (~1–2% incidence). The surgeon should review the patient’s most recent stroboscopy (last exam should be within previous 15–20 days) prior to phonomicrosurgery. Preferably, this review is done the day of surgery or 1–2 days before the surgery. The optimal situation for this preoperative stroboscopy review is to have the stroboscopy examination available for review in the operat-

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Principles of Phonomicrosurgery

ing room immediately before as well as during the procedure. This allows the surgeon to correlate stroboscopic findings with surgical findings and make important decisions on location of pathology, location of placement of incisions, and the degree Table 10.1  Standard microlaryngeal instrumentation

High-quality operating microscope with 400-mm lens Large-bore laryngoscope (largest diameter possible) Examples include: • Universal modular glottalscope (Endocraft) • Sataloff laryngoscope (Medtronic ENT) • Lindholm (Karl Storz) • Operating laryngoscope for anterior commissure (model #8458.011, Richard Wolf ) Specialized laryngoscopes for unique situations • Ossoff–Pilling for difficult exposure (Pilling) • Posterior-commissure laryngoscope (Pilling)

10

Suspension system • Boston University suspension (Pilling or Endocraft) (Figs. 10.16, 10.20) • Fulcrum suspension: Lewy suspension and table-mounted Mayo stand (Pilling) (Fig. 10.17) Operating chair with arm supports (Fig. 10.22) Instrumentation (Karl-Storz, Medtronic ENT, Instrumentarium) • Specialized blunt microelevators (Fig. 10.1) • Microcup forceps (1–2 mm in diameter) (Fig. 10.2) • Up-angled, right and left micro-ovoid cup forceps (Fig. 10.3) • Microscissors (Fig. 10.4) • Curved (left and right) • Up angled • Curved alligator forceps (left and right) (Fig. 10.5) • Straight alligator forceps • Microlaryngeal suctions (3, 5, and 7 French) • Triangular (Bouchayer) forceps (left and right) (Fig. 10.6) • Microlaryngeal knife (sickle or spear) Miscellaneous equipment • Cotton surgical pledgets (0.5 × 2 cm) • 1:10,000 epinephrine • Velcro strap or cloth/silk tape • Mouth guard (maxillary, ± mandibular) • Acrylic—custom made by dentist • Molded “athletic” tooth protector • Plastic “anesthesiologist” tooth guard, reinforced with layers of cloth tape (Fig. 10.18) • Foam from operating room headrest or “doughnut” (edentulous patients only) (Fig. 10.9) Optical telescope • Diameter: 4–5 mm, length: 20 cm or more • 0, 30, and 70° Microdebrider—skimmer blade (Medtronic ENT) Subepithelial infusion needle (25 or 27 g) • Zeitels needle (Endocraft) • Orotracheal injector (Medtronic ENT) Small-diameter, extended-length endotracheal tube (5.0 or 5.5) designed for microlaryngoscopy (Mallinckrodt) Tracheal jet ventilation tube (Hunsaker jet ventilation tube; Medtronic ENT)

The listed equipment/vendors are those the authors have utilized. This is by no means a complete list of all the vendors who make these products: Endocraft (Providence, R.I.), Karl Storz (Culver City, Calif.), Instrumentarium (Montreal, Quebec, Canada), Mallinckodt (Hazelwood, Mo.), Medtronic ENT (Jacksonville, Fla.), Pilling (Research Triangle, N.C.), Richard Wolf (Vernon Hills, Ill.)

 

 

Chapter 10

of dissection and excision using the preoperative stroboscopy and the operative findings as guides.

10.4

Equipment for Phonomicrosurgery

Specialized laryngoscopes are required for phonomicrosurgery. The larger the laryngoscope, the better for phonomicrosurgery, given that this results in significantly improved exposure and access to the surgical site(s). Multiple large and specialized laryngoscopes exist and a wide variety of laryngoscopes are necessary to manage all different types of phonomicrosurgical lesions and procedures. Specialized laryngoscopes for individualized laryngoscopy needs are important, e. g., posterior commissure laryngoscope for difficult posterior glottic exposure, and the Ossoff-Pilling laryngoscope for microlaryngeal surgery on patients with restricted upper aerodigestive tract anatomy (Table 10.1). The core set of instruments utilized for phonomicrosurgery includes specialized blunt microelevators, cup forceps, scissors, curved alligators, and small suctions (3, 5, and 7 French). These elevators are often used to palpate submucosal pathology at the start of surgery. In addition, a specialized set of instruments has been developed for microflap retraction. These are called triangular forceps or Bouchayer forceps. Most of the instruments described below are available from several manufacturers of phonomicrosurgery equipment, including Medtronic ENT (Jacksonville, Fla.), Karl Storz (Culver City, Calif.) and Instrumentarium (Montreal, Quebec, Canada). Key microlaryngoscopy instruments utilized for phonomicrosurgery involve: ■ Specialized blunt microelevators (Fig. 10.1) ■ The microelevators should be blunt and have several different angles and sized to allow the surgeon to work in various angles in different positions within the vocal fold, specifically, dissecting the vocal fold lesion off the overlying microflap.

Fig. 10.1  Angled elevators for phonomicrosurgery

■ Microcup forceps (Fig. 10.2) ■ Several small special cup forceps have been developed over the last 5–10 years to facilitate several specific situations that are encountered in phonomicrosurgery. These forceps have a sharp cutting edge but a very limited cutting surface, only the most distal 180º of the forceps cut. The most useful micro cup forceps is angled-up and has a 1-mm diameter. ■ Micro-ovoid cup forceps (Fig. 10.3) ■ Ovoid-shaped microcup forceps are also essential for removing small pieces of pathologic mucosa and papilloma (see Chaps. 15, “Vocal Fold Polyp” and 21, “Recurrent Respiratory Papillomatosis of the Larynx”). This instrument comes in two sizes and is valuable for precision removal of small amounts of tissue.

Fig. 10.2  Microcup forceps (1 mm) cutting surface limited to distal

180°

Fig. 10.3  Micro-ovoid cup forceps

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Principles of Phonomicrosurgery

■ Microscissors (Fig. 10.4) ■ The most commonly used microscissors are right and left curved as well as “straight up,” or angled scissors. These scissors should be maintained at all times to appropriate surgical precision and sharpness, given that they are the primary cutting tool for phonomicrosurgery. ■ Curved alligators (Fig. 10.5) ■ Epinephrine (1:10,000) and cotton pledget (0.5 × 2 cm) ■ Microlaryngeal suctions (3, 5, and 7 French) ■ Triangular forceps or Bouchayer forceps (for microflap retraction) (Fig. 10.6) ■ These instruments are designed to retract the microflap to allow vocal fold visualization and dissection while minimizing trauma to the microflap. They are made in a variety of sizes and designs for different situations.

10

 

■ Sickle knife (or spear-shaped knife) ■ These knives tend to become dull very quickly, and thus it is recommended that this knife be replaced with every case or at least on a very frequent basis. A dull knife can result in tearing of the mucosa and can significantly limit the efficacy of phonomicrosurgery ■ Microdebrider ■ The microdebrider is a powered instrument that provides simultaneous suction and cutting activity used for rapid removal of exophytic lesions in the larynx such as recurrent respiratory papillomatosis (RRP) (see Chap. 21, “Recurrent Respiratory Papillomatosis of the Larynx”). There are two different types of cutting blades: ■ Conservative (i. e., “skimmer blade”) ■ Aggressive ■ The conservative blade is the most commonly used for laryngeal surgery. The advantages of the microdebrider are expedient removal of a significant amount of laryngeal pathology; less pain after surgery (compared with the CO2 laser); less expensive than the laser; and potentially even safer, given the risks of laser laryngeal surgery. The disadvantages of microdebrider for laryngeal surgery include the powered instrument shaft is relatively large, and sometimes visualization can be limited, and the risk that the powered instrument may be too strong and injure delicate subepithelial tissues of the vocal fold or other endolaryngeal structures.

Fig. 10.4  Microscissors, curved and angled up

Suspension of the laryngoscope is a fundamental aspect of phonomicrosurgery. Two basic designs for placing the laryngoscope into a fixed and stable position exist. These are categorized as a gallows suspension device, and a rotation, or fulcrum device. The gallows suspension laryngoscope is favorable, given that there is more appropriate upward vector of the laryngoscope, which can provide optimal exposure of the en-

Fig. 10.5  Curved alligators for phonomicrosurgery

Fig. 10.6  Triangular (Bouchayer) forceps

 

dolarynx with minimal risk of dental injury, especially to the maxillary teeth. This device is not the most common due to traditional and historical use of rotation-fulcrum devices (i. e., Lewy suspension). Long Hopkins rod telescopes with various visualization angulations are an essential component to phonomicrosurgery. Rarely is the surgery performed utilizing these telescopes, but these telescopes are used to provide the surgeon a “three-dimensional visualization” of the vocal folds and their related pathology. The 30 and 70° telescopes, which are approximately 4–5 mm in diameter and 30 cm long, should be utilized immediately prior to phonomicrosurgical incision and are often used during phonomicrosurgery as well as at the end of the surgery to ensure that all appropriate pathology has been removed. These angled telescopes are readily available in most operating rooms, given they are used regularly for cystoscopy. Telescopes used for sinus surgery are too short to be effectively used for laryngeal imaging. The microscope used for phonomicrosurgery should be of the highest quality and provide the surgeon with a stable visualization method of the endolarynx. There should be significant adjustment as well as control over many different articulated angles of the microscope. This microscope should be the same microscope that is used for precision otologic procedures such as stapes surgery and other middle ear operations. The microscope that is routinely used for the placement of pressure equalizing tubes is typically not appropriate for phonomicrosurgery. Furthermore, the microscope should have the capability of being compatible with the CO2 laser micromanipulator attachment. Typical length of the lens used on the surgical microscope for phonomicrosurgery is 400 mm. This allows adequate space between the proximal end of the laryngoscope and the microscope for hand instruments to be used for phonomicrosurgery. Another important feature of the surgical microscope is articulated eyepieces; this allows for optimal surgeon ergonomics, which is important for lengthy phonomicrosurgery cases as well as for the long-term health of the phonomicrosurgeon. Lasers have a limited role in phonomicrosurgery surgical procedures (see Chap. 13, “Principles of Laser Microlaryngoscopy”). The most commonly used laser is the CO2 laser, which can be used for cautery of vascular ectatic lesions. The CO2 laser with the micromanipulator has also been used for making vocal fold incisions or removing free-edge lesions. However, there are no distinct advantages of the use of this laser in this setting, and the risks of thermal injury and costs of the instrument outweigh any potential benefits. The majority of phonomicrosurgery can and should be done with “cold-steel” instrumentation. Recently, the pulsed-dye (PDL) and pulsed-KTP lasers have been advocated for phonomicrosurgery. However, benefits over cold-steel surgery have not yet been demonstrated, but they may be complementary when dealing with vascular lesions associated with other vocal fold lesions (cyst, polyp, etc.). The CO2 laser does offer an “instrument-free” approach to surgery of the vocal folds, and in a very small, crowded surgical space, this can be an advantage. However, for most phonomicrosurgical situations this is not a major problem, and thus the CO2 laser is rarely indicated for this reason alone.

Chapter 10

10.5

Phonomicrosurgery Procedures, Techniques, and Methods

10.5.1 Anesthesia A working relationship based on mutual respect, communication, and teamwork with your anesthesia colleague(s) is essential for successful phonomicrosurgery (see Chap. 9, “Anesthesia and Airway Management for Laryngeal Surgery”). Phonomicrosurgery involves general anesthesia, and complete muscle relaxation should be implemented after the induction of general one and continuously monitored throughout the surgery. Preoperatively, one should administer i.v. steroids and Robinol™ (unless contraindicated). Placement of the endotracheal tube is extremely important, given that a misplaced or traumatic placement of the endotracheal tube can cause injury to the vocal folds and may result in cancellation of surgery and/ or injury to the vocal folds. The placement of the endotracheal tube should be under complete controlled conditions, and no stylet should be used for the placement of the endotracheal tube. Furthermore, the otolaryngologist should be present during the intubation to monitor the situation and be available to assist with intubation when the situation is required. Similarly, controlled extubation at the end of phonomicrosurgery is another important aspect of the necessary teamwork between the anesthesia team and the phonomicrosurgeon. Extubation should be done in a controlled fashion, and all measures should be used to reduce the likelihood of the patient coughing after extubation. The ventilation options for phonomicrosurgery are endotracheal intubation, jet ventilation, or apneic methods. The large majority of phonomicrosurgery is best performed using endotracheal intubation with a small (5.0 or 5.5), specialized endotracheal tube. This provides a still operating field and complete control of the airway. Sometimes the endotracheal tube can be in the way for the surgical procedure and may need to be repositioned or removed in its entirety. Jet ventilation for phonomicrosurgery should be done only on an as-needed basis and is best done when the jet ventilation is delivered from a small jet ventilation catheter placed in the mid-tracheal region. (see Chap. 9, Fig. 9.1; Hunsaker tube, Medtronic ENT) Tracheal jet ventilation is preferred compared with supraglottic jet ventilation, given that the former provides the surgeon with less vibration and desiccation of the vocal fold tissues while phonomicrosurgery is being performed, and allows end-tidal CO2 monitoring. Appropriate and successful phonomicrosurgery can rarely be performed using an apneic technique for anesthesia, given that the time between ventilations is too short for most phonosurgical procedures. An exception to this may be for bronchoscopy (flexible or rigid) and diagnostic laryngoscopy prior to the placement of an endotracheal tube.

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10.5.2 Patient Position Patients undergoing phonomicrosurgery are placed in a supine position on the operating room table. The optimal head and neck position for exposure of the endolarynx with the laryngoscope is neck flexion on the body and the head extension on the neck. A shoulder roll typically places the patient in a suboptimal position for optimal laryngoscope placement (neck extension), and thus should not be used. The neck flexion can be achieved by using an articulated head of the operating table, and the head extension on the neck is done by the surgeon during laryngoscopy and secured with the suspension device (Fig. 10.7). Another method of obtaining neck flexion is to use a

10

Fig. 10.7  Optimal patient position for suspension laryngoscopy (note

neck flexion and head extension)

Fig. 10.8  Alternative method of positioning patient without the use of

an articulated head of bed (note neck flexion due to pillow underneath the head)

 

pillow under the head to flex the neck on the body (Fig. 10.8). Dental and alveolar ridge protection prior to insertion of the laryngoscope is important. For patients who are edentulous on the maxillary teeth, the best way to protect the mucosa and the underlying alveolar ridge from laryngoscope placement and suspension injury is to place a small, high-density foam pad between the laryngoscope and the alveolar ridge. This foam padding is present in most operating rooms in the form of a headrest or pillow material (Fig. 10.9).

10.5.3 Laryngoscope Placement Laryngoscope placement is crucial to the success of phonomicrosurgery and can be quite daunting to the novice phonomicrosurgeon. An adequate amount of time and patience should be allocated for this important step. Insuring a proper head and neck position during laryngoscopy placement is a key step, as described above. The overall goal is to place the largest diameter laryngoscope into the endolarynx. A frequent impediment to this goal is the folding inward of the epiglottis (Fig. 10.10). When this occurs, the potential space to place the distal aspect of the laryngoscope into the endolarynx is significantly reduced, and the epiglottis is traumatized (Fig. 10.11). With the use of a large-diameter laryngoscope, the positioning of the laryngoscope can be quite difficult. Instead of aborting the use of the large-diameter laryngoscope, patience and persistence should be judiciously applied. As the laryngoscope is placed into the oral cavity, the lips and tongue should be retracted with the nondominant hand. The laryngoscope is then slid along the ventral surface of the tongue and advanced down toward the base of the tongue and posterior pharyngeal wall. At this juncture, there are a variety of techniques to place the laryngoscope under the epiglottis without folding or traumatizing the epiglottis. First, if there is adequate space, then the laryngoscope can be passed under

Fig. 10.9  High-density foam for protecting the alveolar ridge in an

edentulous patient during suspension laryngoscopy

 

Chapter 10

Fig. 10.10  Laryngoscope advancement causing “folding” of epiglottis

Fig. 10.11  “Folded” epiglottis above laryngoscope limits space for the

direct vision underneath the epiglottis and advanced into the endolarynx. This direct approach may result in the folding of the epiglottis when attempted with a large-diameter laryngoscope (Fig. 10.11). At this stage, it best to use one of the other laryngoscope placement techniques instead of resorting to the use of a smaller laryngoscope. The second option for laryngoscope placement is to place the laryngoscope between the posterior pharyngeal wall and the endotracheal tube and continue to advance the laryngoscope along the posterior pharyngeal wall (underneath the endotracheal tube). Once the laryngoscope is at the approximate level of the endolarynx, it can be drawn anteriorly into the en-

dolaryngeal space, thus allowing the endotracheal tube to slip around the side of the laryngoscope and be positioned in the posterior glottis. The third method to place a large-diameter laryngoscope into the endolarynx without damage or malposition of the epiglottis is to place the nondominant-hand index finger into the oral cavity and oropharynx toward the endotracheal tube and pick the endotracheal tube up off the posterior pharyngeal wall. With the endotracheal tube secured underneath the index fingertip, the laryngoscope can then be advanced along the posterior pharyngeal wall and drawn up into the endolarynx (Fig. 10.12). Using this technique, the endotracheal

Fig. 10.12  Placement of laryngoscope into endolarynx below non-

Fig. 10.13  Anterior deflection of endotracheal tube with the nondom-

folded epiglottis while the endotracheal tube is positioned anteriorly with a finger from the nondominant hand (note initially the laryngoscope will be posterior to the endotracheal tube)

placement of a large-diameter laryngoscope

inant hand to allow placement of laryngoscope into endolarynx

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Principles of Phonomicrosurgery

 

Fig. 10.14  Laryngoscope positioned above the epiglottis, which is

Fig. 10.15  Cup forceps placed outside the laryngoscope to control the

tube may be initially positioned anterior to the laryngoscope. When the laryngoscope is successfully placed in the endolarynx but the endotracheal tube is anterior to the laryngoscope, the endotracheal tube can be drawn gently and carefully down into the more appropriate posterior glottic position, without too much difficulty, using upward pressure of the suspended laryngoscope or the nondominant hand’s index finger (Fig. 10.13). The fourth technique for the placement of a large-diameter laryngoscope in a patient with difficult epiglottis anatomy (i. e., large, floppy) starts with positioning the laryngoscope immediately above the tip of the epiglottis (Fig. 10.14). With this visualization, a large up-cup forceps is passed outside the laryngoscope, down toward the proximal tip of the laryngoscope and used to grab the tip of the epiglottis firmly. With firm control of the epiglottis, the cup forceps can be used to pull or direct the epiglottis in an anterior direction (Fig. 10.15). With the epiglottis being held anteriorly, the laryngoscope is then advanced into the endolarynx on top of the endotracheal tube. Once the laryngoscope is successfully placed in the endolarynx, the forceps are opened and the epiglottis is released. The fifth option for laryngoscope placement involves placement of temporary suture through the epiglottis. A large-diameter laryngoscope is positioned by hand or suspension above the epiglottis. Working through the microscope, a 4.0 silk suture is placed through the tip of the epiglottis, and the two ends of the suture are brought out through the laryngoscope. The laryngoscope is completely removed from the body and then replaced above the epiglottis, with the suture through the epiglottis being kept outside the laryngoscope. Tension can be applied to the epiglottis suture to control and stabilize the epiglottis as the laryngoscope is passed underneath it into position. Once good position of the laryngoscope is achieved, the

suture is removed from the epiglottis. (Alternatively, the suture can be removed at the end of the case.) The optimal position of the laryngoscope within the endolarynx is determined by the vocal fold pathology and pending surgical procedure. However, in general, the laryngoscope should be positioned immediately above (superior to) the vocal fold pathology, specifically resulting in retraction of the false vocal fold tissues. Care should be taken to avoid contacting the superior surface of the vocal fold given that this will significantly alter the anatomic orientation and nature of the vocal fold and often distort the vocal fold pathology.

resting directly on the endotracheal tube

position of the epiglottis, allowing placement of the laryngoscope into the endolarynx without “folding” of the epiglottis

10.5.4 Suspension Device The gallows suspension device (Fig. 10.16), if used, should be positioned to provide upward and slightly forward (caudal) suspension of the laryngoscope in the endolarynx. This special angulation of the laryngoscope will provide optimal laryngoscopic visualization and minimal adjacent tissue injury or damage. For a rotation or fulcrum laryngoscope device holder (such as a table-mounted Mayo stand; Fig. 10.17), it is of the utmost importance to remember to provide special care and attention to the maxillary teeth as the laryngoscope holder is put into place. This is especially important given that as the fulcrum holder is adjusted, each amount of upward rotation at the distal tip of the laryngoscope results in an equal amount of downward pressure at the proximal aspect of the laryngoscope on the maxillary alveolar ridge. A tooth protector can be fashioned by using a standard thin plastic tooth guard commonly found in anesthesiology carts, and reinforcing it with multiple layers of cloth tape (Fig. 10.18).

 

Fig. 10.16  Gallows-type suspension device

Chapter 10

Fig. 10.17  Fulcrum type suspension device (Lewy apparatus suspend-

ed from a table-mounted Mayo)

Fig. 10.18  Tooth protector fashioned from a plastic tooth guard and

layers of cloth tape

Fig. 10.19  Velcro strap applied to anterior neck region (near the cri-

coid) to optimize vocal fold visualization during suspension laryngoscopy

10.5.5 External Counter-Pressure A Velcro strap or silk tape can be applied to the external neck (in the area of the cricoid or trachea) in a downward and slightly cephalad vector to improve the endolaryngeal exposure on an as needed basis (Fig. 10.19). The surgeon should look down the laryngoscope while applying external counter-pressure to judge the location and amount of external counter-pressure required. A small amount of gauze or a foam pad can be positioned between the tape or strap and the neck skin to prevent any injury to the overlying skin of the larynx (Fig. 10.20). It is extremely important that the surgeon remember this type of external counter pressure, which is often essential to optimal exposure of the endolarynx, puts the patient at risk if the

patient were to move unexpectedly as the anesthesia wears off. If this occurs, the first duty of the surgeon is to release the external counter pressure and secondly take the patient out of suspension laryngoscopy.

10.5.6 Telescopic Evaluation of Vocal Fold Pathology Using the 0, 30, 70° (and as needed, 120°) telescope for visualization in a “three-dimensional” fashion of the endolarynx is of

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Principles of Phonomicrosurgery

Fig. 10.20  Patient positioned for phonomicrosurgery. Note neck flex-

10

ion, head extension, and angle of Velcro strap positioning the larynx into an optimal viewing path of the laryngoscope

Fig. 10.21  Visualization of vocal fold pathology during suspension

laryngoscopy with angled telescopes

great value. This is done after the laryngoscope is suspended. This allows for unique visualization of the vocal fold pathology, photodocumentation, and surgical planning (Fig. 10.21). Specifically, decisions are often made about the optimal location for an incision when evaluating the vocal fold pathology, specifically with the 30 and 70° angled telescopes. In addition, these telescopes provide great visualization of the ventricles, subglottis, anterior and posterior commissure.

10.5.7 Operating Microscope and Surgeon Ergonomics After suspension of the laryngoscope and telescopic examination, the surgical microscope is brought in to position, and

 

Fig. 10.22  Proper support of surgeon’s arms for phonomicrosurgery

attention should be drawn to the position of the laryngoscope in relation to the microscope and the surgeon. Optimal hand control of instrumentation during phonomicrosurgery occurs when the forearms can be supported with a stable device, such as an operating room chair with arm supports. The wrists are the best location for precise control, and thus some type of surgical support should be identified (an ophthalmologist’s or plastic surgeon’s operating room chair with arm supports, or a Mayo stand) that will allow the most steady and stable hand and wrist motions, but supporting the arms at the level of the forearms (Fig. 10.22). Patient positioning should allow the surgeon’s upper arms to be held in a vertical position, with elbows and hands as low as possible to the surgeon’s lap. An alternative to these custom surgical chairs is to use a Mayo stand with pillows/foam padding. The Mayo stand is placed between the surgeon and the head of bed (Fig. 10.23). Paying attention to the surgeon’s neck, head, and back position during the surgical procedure is important for his/her longstanding neck and back health. Often, to facilitate optimal phonomicrosurgery ergonomics, the operating room table should be placed in a reverse Trendelenburg position. This brings the laryngoscope lower—into the surgeon’s lap—and the eye pieces of the surgical microscope should be utilized to allow the surgeon to sit with his/her back completely straight and upright (Fig. 10.22). Binocular vision at high-power magnification must be achieved during all aspects of the procedure. This will require minor but important adjustments of the position of the microscope and laryngoscope to ensure that the viewing access of the microscope is perfectly coaxial with the longitudinal aspect of the laryngoscope, thus allowing binocular vision. This is a very important component to phonomicrosurgery, and it should not be overlooked. The novice phonomicrosurgeon will initially struggle with this task, but patience and practice will allow success. The majority of phonomicrosurgical procedures should be done using the microscope’s highest magnification setting.

 

Chapter 10

Fig. 10.23  Alternative method for support of the surgeon’s arms, us-

ing a padded Mayo stand

10.5.8 Microflap Approach to Submucosal Pathology The microflap approach to submucosal pathology is a key aspect to most phonomicrosurgery operations. The core principles of the microflap approach to submucosal pathology include: ■ Making an incision through the epithelium at the closest possible location to the submucosal pathology ■ Disrupting the minimum of surrounding tissue to the vocal fold pathology ■ Staying in as a superficial plane as possible ■ Preservation of overlying normal mucosa (epithelium plus superficial lamina propria) There are multiple descriptions of various forms of microflaps, specifically lateral microflap, medial microflap, and mini-microflap. Over the years, many of these microflap approaches have merged into a single, philosophical microflap approach to submucosal pathology, which is described below. The incision for the microflap should be directly overlying, or immediately lateral to the vocal fold pathology. This results in minimal disruption of normal adjacent vocal fold mucosa. After the vocal fold pathology is palpated and an incision is planned, an incision is then made with a sharp sickle knife. It is important to note that the tip of the sickle knife should be used to penetrate the epithelium, and then the tip of the sickle knife can be drawn slightly superiorly, tenting up the epithelium as the incision is made in an anterior or posterior direction (Fig. 10.24). This prevents the sickle knife accidentally causing any type of injury to the submucosal pathology or deep vocal fold tissues. After the incision has been made, the vocal fold pathology may be able to be palpated and directly visualized through the

Fig. 10.24  Microflap incision placed lateral to the lesion with epithe-

lium tented up by the sickle knife

incision and a small curved elevator can be used to begin the elevation of the microflap in the plane between the vocal fold pathology and the overlying epithelium (i. e. medial to the lesion). This plane is the single most difficult step of phonomicrosurgery, and it should be performed with great patience and caution. It is often easiest to initiate and develop this plane anteriorly and posteriorly to the vocal fold lesion. Often, various angulated or curved elevators will be required to perform this aspect of the procedure, given that at the very start of the development of the microflap, the surgeon is initially working on the upper lip of the free edge of the vocal fold medially. Then as the microflap is carefully elevated and dissected from the submucosal pathology, the surgeon is working in the exact opposite direction on the inferior lip of the vocal fold laterally, and thus, different curved elevators are often required to work in different directions, especially to ensure minimizing the risk of microflap penetration or injury. Once a plane is developed anterior and posterior to the lesion, then careful submucosal dissection with a small, fine blunt elevator (curved or angled) is performed to complete the elevation and creation of the microflap (Fig. 10.25). There may be instances where small, microcurved scissors need to be used to release fibrous bands off the overlying microflap in adherent areas of the submucosal pathology or in a similar manner when the submucosal pathology is adherent to the deeper aspects of the vocal fold in the area of the vocal ligament (see Chap. 17, “Vocal Cord Cyst and Fibrous Mass”) Hemostasis is extremely important, and if bleeding is causing an obstruction of visualization, then the surgery should be temporarily stopped and the application of epinephrine (1:10,000)-soaked, small cotton pledgets should be utilized to quickly and successfully provide surgical hemostasis without

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much difficulty. Suctioning blood and secretions from this area should be done with a 3-French suction, usually without covering the thumb port. Great care should be taken not to tear or fenestrate the microflap as it is tediously and carefully elevated off the submu-

cosal pathology. The majority of benign vocal fold submucosal pathology is located in the immediate subepithelial plane and is often, to a varying degree, adherent to the overlying epithelium. This is the case in approximately 80–90% of cases; however, there will be situations where the pathology is not adherent to the overlying microflap and instead located deeper within the vocal fold (in the area of the vocal fold ligament) (Fig. 10.26). This is true for ligamentous vocal fold cyst and fibrous mass (see Chap. 4, “Pathological Conditions of the Vocal Fold”). When these pathologies are encountered, the surgeon will notice that the microflap elevation is quite easy; however, the deeper aspect of the dissection, creating a plane between the vocal fold pathology and the vocal ligament is quite difficult. In this situation, great care should be taken to use either a blunt dissection technique or microscissors to release the adherent bands between the vocal fold ligament and the pathology, always erring on the side of the pathology (in a superficial fashion). After the superficial and deep planes around the submucosal pathology have been elevated, there may be some additional connections to the vocal fold pathology within the vocal fold anteriorly and posteriorly. These bands can be released with blunt dissection or microcurved scissors. This allows the submucosal pathology to be removed and sent for pathologic examination. The microflap is then redraped with either the triangular forceps or a curved elevator (Fig. 10.27). It is often helpful to place an epinephrine (1:10,000)-soaked Cottonoid over the operative site for 1–2 min to reduce edema before making further surgical decisions. After the microflap has been redraped, palpation of the vocal fold should be performed to determine if there is any residual submucosal pathology that can be palpated and removed.

Fig. 10.26  Elevated microflap reveals that the pathology (fibrous

Fig. 10.27  Redraped microflap after removal of vocal fold lesion. Note

10 Fig. 10.25  Elevation of microflap off vocal fold lesion beneath

mass) is on the vocal ligament and not in the subepithelial space

copatation of the mucosa at the incision site and smooth free edge of the vocal fold

 

Chapter 10

The free edge of the vocal fold should be straight after the pathology is removed; if not, further investigation into either the under surface of the microflap or the deeper aspect of the vocal fold should be performed. If there is any residual pathologic tissue such as fibrous material or scar, then this tissue should be removed in a conservative and reasonable fashion. This material can be removed with a microelevator or microcup forceps. Extreme care is required at this juncture of the surgery because overly-aggressive removal of this material can result in significant scar formation as well as a permanent deformity of the free edge of the vocal fold. At the completion of the vocal fold lesion(s) excision, the free edge of each vocal fold should be completely straight without exophytic mucosal tags and without a soft tissue defect at the free edge of the surgical site.

10.6

Postoperative Care and Complications

Almost all phonomicrosurgical procedures are followed by some period of voice rest. This period can range from as short as 2 days and extend to possibly 14 days, depending on the specific nature of the surgery, compliance of the patient, the surgeon’s philosophy, and experience. In addition to voice rest, the patient should be encouraged to stay well hydrated, continue treatment for laryngopharyngeal reflux disease with a proton pump inhibitor, and maintain GERD behavior modification. At the end of the prescribed strict voice rest period, stroboscopy should be performed to evaluate the recovery and healing process of the vocal fold. If there is adequate epithelial coverage, then the patient can be transitioned to “light voice use,” which is usually defined as speaking using a breathy, “airy” type of voice (not a whisper) for 5–10 min per hour. Light voice use is often used for an additional 7–10 days after the period of strict voice rest. There is rarely an indication for antibiotics associated with phonomicrosurgery or long-term steroid use. Some surgeons may use immediate intravenous, intramuscular, or intralesional steroids perioperatively to minimize postoperative edema. It is advisable to involve a speech–language pathologist to assist the patient in transitioning from strict voice rest to light voice use to ensure that the patient is using the optimal postoperative voice technique to facilitate healing and prevent injury in this important time. Complications from phonomicrosurgery include failure of the microflap to appropriately redrape and adhere to the vocal fold. When this occurs, epithelial ingrowth underneath the microflap occurs, and surgical excision of the microflap is mandated. This is a rare complication. Excessive edema and even necrosis can occur to a microflap; this typically occurs when the microflap is overly traumatized or injured during the surgical procedure. Often, when this occurs, the vocal fold will heal adequately on its own with appropriate time and care. Dental injuries after phonomicrosurgery should be repaired to the patient’s satisfaction in a prompt fashion to minimize negative feelings of the patient toward the surgeon. Lingual nerve injuries such as numbness of the tongue and/or a change in taste

sensation occur in approximately 10–20% of patients after phonomicrosurgery. These symptoms are usually transitory, and thus the patient should be informed that these postoperative changes resolve on their own within the first month after surgery. Additional complications related to phonomicrosurgery are discussed in Chaps. 11, “Perioperative Care for Phonomicrosurgery” and 12, “Management and Prevention of Complications Related to Phonomicrosurgery.”

Key Points ■ Phonomicrosurgery is elective, precise surgery aimed to improve vocal function based on principles of vocal fold physiology. ■ Phonomicrosurgery utilizes small, delicate surgical instrumentation and is performed with maximum control via high-powered microlaryngoscopy for optimal results. ■ Conservative removal of submucosal pathology with preservation of overlying normal epithelium and superficial lamina propria allows healing by primary intention and optimal voice quality after phonomicrosurgery. ■ Microflap approach to submucosal pathology of the vocal fold is an essential component of most phonomicrosurgical procedures and is a challenging surgical task that requires patience, appropriate instrumentation, surgical skill, and experience.

Selected Bibliography 1

2 3

4 5

6 7

8

Andrea M, Dias O (1995) Rigid and contact endoscopy in microlaryngeal surgery: technique and atlas of clinical cases. Lippincott Williams & Wilkins, Philadelphia Bastian RW (1996) Vocal fold microsurgery in singers. J Voice 10:389–404 Bouchayer M, Cornut G (1992) Microsurgical treatment of benign vocal fold lesions: indications, technique, results. Folia Phoniatr 44:155–184 Courey MS, Garrett CG, Ossoff RH (1997) Medial microflap for excision of benign vocal fold lesions. Laryngoscope 107:340–344 Courey MS, Stone RE, Gardner GM, Ossoff RH (1995) Endoscopic vocal fold microflap: a three year experience. Ann Otol Rhinol Laryngol 104:267–273 Ford CN (1999) Advances and refinements in phonosurgery. Laryngoscope 109:1891–1900 Hirano M (1977) Structure and vibratory behavior of the vocal fold. In: Sawashima M, Cooper F (eds) Dynamic aspects of speech production. University of Tokyo, pp 13–30 Rosen CA, Andrade Filho PA, Scheffel L, Buckmire RA (2005) Oropharyngeal complications of suspension laryngoscopy: a prospective study. Laryngoscope 115:1681–1684

75

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Principles of Phonomicrosurgery 9

Sataloff RT, Spiegel JR, Heuer RJ, Barody MM, Emerich KA, Hawkshaw MJ, Rosen DC (1995) Laryngeal mini-microflap: a new technique and reassessment of the microflap saga. J Voice 9:198–204 10 Shapshay SM, Healy GB (1990) New microlaryngeal instruments for phonatory surgery and pediatric applications. Ann Otol Rhinol Laryngol 98:821–823 11 Thekdi AA, Rosen CA (2003) Surgical treatment of benign vocal fold lesions. Curr Opin Otolaryngol Head Neck Surg 10:492–496

10

  12 Zeitels SM, Vaughan CW (1994) External counter-pressure and internal distension for optimal exposure of the anterior glottal commissure. Ann Otol Rhinol Laryngol 103:669–675 13 Zeitels SM, Hillman RE, Desloge R, Mauri M, Doyle PB (2002) Phonomicrosurgery in singers and performing artists: treatment outcomes, management theories, and future directions. Ann Otol Rhinol Laryngol 190(Suppl.):21–40

Chapter 11

11

Perioperative Care for Phonomicrosurgery

11.1

Fundamental and Related Chapters

Please see Chaps. 8, 10, and 12 for further information.

11.2

Timing of Phonomicrosurgery

Phonomicrosurgery involves the surgical manipulation of the delicate epithelial and sub-epithelial tissues of the vocal fold (Fig. 11.1). Thus a variety of steps should be implemented to minimize edema and bleeding at the surgery sites(s) to maximize the surgeon’s precision and the voice outcome post-operatively. There are a variety of important aspects with regard to the timing and scheduling of phonomicrosurgery. First and foremost, the patient and the physician must be comfortable with the decision to proceed with surgery, having had a detailed discussion regarding the nature of the surgical procedure, perioperative treatment plan, and should have established reasonable expectations for the timing of recovery and voice outcomes (see Chap. 8, “Timing, Planning, and Decision Making in Phonosurgery”). It is important for the patient to stop all

anticoagulation medication such as nonsteroidal anti-inflammatories, aspirin, Coumadin, and Plavix, and other medications that may affect coagulation (over-the-counter medications, herbal supplements etc.). These medications should be stopped 7–10 days prior to surgery. It is also wise to avoid scheduling phonomicrosurgery during a woman’s premenstrual period (approximately 5 days before the onset of menses). This is especially important for singers and for patients with very small vocal fold lesions. The reason for avoiding the premenstrual time period when engaging in phonomicrosurgery is to avoid vocal fold edema and vascular fragility thought to be associated with premenstruation affect the surgical decision making and the surgical outcome. Lastly, the patient and surgeon should have a clear understanding of the voice demands for the next 2–3 months after phonomicrosurgery. This is extremely important for singers, schoolteachers, and individuals involved in sales and business (see Chap. 8).

11.3

Surgical Indications and Contraindications

It is important for the patient prior to phonomicrosurgery to minimize his/her voice demands for approximately 7 days before the scheduled surgery (see Chap. 8, “Timing, Planning, and Decision Making in Phonosurgery”). Voice therapy prior to phonomicrosurgery is important for a variety of factors, including: ■ Pre- and postoperative voice use plans ■ Voice rest, and education regarding use of the silent cough ■ Laying a foundation for healthy voice use technique after surgery ■ Discussing alternative communication options during the complete-voice rest phase

Fig. 11.1  Microscopic dissection of the epithelial flap using a 30° flap

elevator

If the patient has not had any voice therapy prior to surgery, then one to two sessions of voice therapy is optimal. It is also advisable prior to phonomicrosurgery to begin the patient on medical therapy for LPR treatment prophylactically. Even if the patient does not have any active symptoms of LPR, given the risk of reflux and its possible negative effects on wound healing of the vocal folds, GERD behavior modification and proton pump inhibitor therapy is typically started prior to phonomicrosurgery and extended for 1–2 months after surgery.

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Perioperative Care for Phonomicrosurgery

11.4

Considerations for the Day of Phonomicrosurgery

Psychological reassurance of the patient on the day of surgery is extremely important. This involves seeing the patient outside the operating room before surgery, discussing any last-minute questions, and reviewing the surgical plans as well as the postoperative voice rest and recovery issues. Intravenous steroids should be used (10–20 mg Decadron) prior to the induction of general anesthesia for phonomicrosurgery. There is no indication for antibiotics or prolonged steroid use with most phonomicrosurgery cases.

11.5

11

Postoperative Voice Rest

After phonomicrosurgery, a period of total voice rest is indicated in most situations. The duration of this voice rest is controversial and should be based on the nature of the pathology treated during surgery, compliance of the patient, and the degree of dissection performed at the time of the surgical procedure. It should be emphasized to the patient and family members that total voice rest involves no sound production whatsoever. Total voice rest includes no: ■ ■ ■ ■ ■ ■

Speaking Singing Whispering Humming Clicking Throat clearing

Alternative methods of communication should have been reviewed preoperatively and should be reviewed immediately postoperatively. They include the following: ■ ■ ■ ■ ■ ■

E-mail Pen-and-paper notes A wipe-off board Bell Whistle Text messaging

Silent cough is a helpful way to deal with the mucous sensation that sometimes occurs after phonomicrosurgery, minimizing trauma to the recently operated vocal folds. Silent cough involves the patient taking a large inhalation and performing a rapid, forced exhalation, without any sound production during the exhalation. Immediately after the exhalation, the patient should tuck his/her chin and perform a hard swallow. This in combination with frequent sips of water should address any issues patients have associated with mucous sensation and mucous build up in the throat while avoiding the use of phonotraumatic throat clearing activity. The typical duration for voice rest after phonomicrosurgery procedures ranges from 2 to 10 days. After the period of complete voice rest, light voice is

 

usually used for approximately 7–10 days. Light voice use often allows the patient to use a soft, conversational, breathy voice (this is not whispering) for approximately 5–10 min per hour. Patients should be reminded that this voice use limitation is not cumulative and should not be violated for any reason.

11.6

Postoperative Voice Care

At the completion of strict voice rest, it is optimal for the patient to work with a speech–language pathologist for a short period as they reinitiate voice production. During this session, the speech–language pathologist emphasizes proper breath support, airflow, resonant voice production, and minimizes the risk of whispering or falsetto voice use. Often, there are also psychological aspects associated with the patient transitioning from total voice rest to voice use and thus, the speech– language pathologist can be helpful working with the patient on these issues. Stroboscopy is an important monitoring tool after phonomicrosurgery and should be used to guide and assist in the graduation of the patient from total voice rest to light voice use to full voice use. Voice therapy after phonomicrosurgery is extremely important aspect of vocal recovery for almost all patients undergoing phonomicrosurgery. The optimal time for initiation of voice therapy after phonomicrosurgery is approximately 7–14 days after surgery. Singing voice therapy is also an important adjunctive treatment to the vocal rehabilitation of singers and nonsingers alike. Appropriate timing for initiation of singing voice therapy after phonomicrosurgery is highly variable, but typically, can be initiated approximately 3–4 weeks after surgery.

11.7

Intralaryngeal Steroid Injection to Soften Postoperative Scar in the Vocal Fold

A variety of factors known and unknown can contribute to significant postoperative stiffness and scarring of the vocal fold after phonomicrosurgery. When significant vocal fold stiffness after phonomicrosurgery is identified, often superficial steroid injections to the vocal folds are helpful to reduce permanent scar tissue formation and enhance wound healing of the vocal folds, resulting in better pliability, vocal fold closure and voice quality. Most frequently, this treatment is done on a monthly basis for 3 months, starting approximately 2–4 weeks after phonomicrosurgery. The steroid injection can often be done in the office under local anesthesia (see Chap. 33, “Peroral Vocal Fold Augmentation in the Clinic Setting”), using Decadron 10 mg/ml. Kenalog should be avoided due to the risk of particle deposits within the vocal fold.

 

Chapter 11

Key Points

Selected Bibliography

■ The importance of involving the patient in the decision making for phonomicrosurgery cannot be overemphasized. ■ It is important that the patient understand the importance of clearing their future voice demands for the 2–3 months after phonomicrosurgery to maximize the chances of successful recovery after surgery. ■ A short period of strict postoperative voice rest is typically indicated and helpful, and then graduated voice use can be implemented under the care of the speech–language pathologist to maximize vocal recovery. ■ Use of the speech–language pathologist for the preoperative and postoperative care of patients undergoing phonomicrosurgery is an important aspect of successful phonomicrosurgery and the patient’s optimal vocal recovery.

1 2

3

4

Behrman A, Sulica L (2003) Voice rest after microlaryngoscopy: current opinion and practice. Laryngoscope 113:2182–2186 Cho SH, Kim HT, Lee IJ, Kim MS, Park HJ (2000) Influence of phonation on basement membrane zone recovery after phonomicrosurgery: a canine model. Ann Otol Rhinol Laryngol 109:658–666 Tateya I, Omori K, Hirano S, Kaneko K, Ito J (2004) Steroid injection to vocal nodules using fiberoptic laryngeal surgery under topical anesthesia. Euro Arch Otorhinolaryngol 261:489–4923 Mortensen M, Woo P (2006) Office steroid injections of the larynx. Laryngoscope 116:1735–1739

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Chapter 12

Management and Prevention of Complications Related to Phonomicrosurgery

12.1

Fundamental and Related Chapters

Please see Chaps. 8, 10, and 11 for further information.

12.2

Overview of Management and Prevention of Complications Related to Phonomicrosurgery

There are a host of complications related to phonomicrosurgery that range from mild to serious and involve multiple factors, some of which are known (i. e., poor postoperative compliance with voice rest) and others unknown (i. e., unknown wound-healing phenotype). The sections below discuss the nature of the complications, remedies for the complications, the natural clinical course, and prevention of these complications. Several overriding principles associated with the management and care of patients experiencing complications should be kept in mind as individual complications are discussed. Most importantly, the lines of communication between the patient and the voice care team are extremely important. Multiple studies have shown that patient satisfaction after medical care is related in large part to the patient’s perception of the health care provider’s interest in their care, which in turn is directly related to the provider’s ability to communicate with the patient. Thus, the most essential aspect of managing complications associated with phonomicrosurgery is to establish and maintain excellent lines of communication between the patient and the voice care team members.

12.3

Surgical Indications and Contraindications

A variety of minor to major complications associated with phonomicrosurgery can occur in the oropharyngeal region. These include: ■ ■ ■ ■ ■

Dental injuries Temporomandibular joint disorder aggravation Lingual anesthesia Dysgeusia Throat pain

12

All of these complications are associated with the positioning and placement of the laryngoscope. Most likely, these complications are related to the size of the laryngoscope and the duration of suspension of the laryngoscope. People have hypothesized that intermittently taking the laryngoscope off suspension to allow blood flow to the lingual area and remove pressure off the adjacent nerves may prevent or minimize these types of complications. However, this has not been proven scientifically. Given that much of the success of phonomicrosurgery is based on precision of surgery—which is directly related to the adequacy of the exposure of the vocal folds with a large bore laryngoscope—many of these complications are difficult to avoid completely. In fact, some laryngologists believe that these are not complications, but expected aspects of phonomicrosurgery, comparable to abdominal pain after an appendectomy. Optimal management strategy for these complications includes pre- and perioperative communication with the patient regarding the possibility of these problems occurring and their subsequent management. A great majority of the time, lingual anesthesia, dysgeusia, and throat pain will be temporary in nature. Thus, the patient needs to be reassured that the symptoms that he/she experiences after phonomicrosurgery resolve with time. Dental injuries should be cared for by a dentist in a prompt fashion to shorten and minimize the patient’s aggravation and frustration. Dental injuries can also be minimized by taking great care of the dentition during placement of the laryngoscope and use of tooth guards over the mandibular and maxillary teeth. It is extremely rare for suspension microlaryngoscopy to induce temporomandibular joint disease; however, it is common that suspension microlaryngoscopy will aggravate preexisting temporomandibular joint pathology. For this reason, if the patient has temporomandibular joint disease, prior to phonomicrosurgery, it is wise to advise that most likely, the phonomicrosurgery procedure will exacerbate his/ her disorder, and that they may require medical or oromaxillofacial intervention postoperative to assist their recovery from this condition.

12.4

Postoperative Dysphonia

There are varieties of aspects related to postoperative healing that can result in postoperative dysphonia after phonomicrosurgery. These include vocal fold scar, dependent edema of the vocal fold, granulation tissue at the operative site, failure of the

82

12

Prevention of Phonomicrosurgery Complications

microflap to adhere, and recurrence of the vocal fold pathology. Another related complication contributing to postoperative dysphonia is a patient with unreasonable expectations of voice quality and function after phonomicrosurgery. When this occurs, patients complain of a persistent postoperative dysphonia or even an exacerbation of their dysphonia after phonomicrosurgery, even though this may not in fact be the case. Unreasonable expectations after phonomicrosurgery stem from poor communication between the voice care team and the patient, especially regarding the typical postoperative clinical course in rehabilitation, plan, and the ultimate outcome of their phonomicrosurgical procedure, especially accounting for unsuspected vocal fold pathology found during phonomicrosurgery. The most important prevention method for minimizing the risk of patients developing unreasonable expectations associated with phonomicrosurgery is to establish an excellent line of communication between the patient and the voice care team members. This can be enhanced by using a special consent form for phonomicrosurgery, which details in plain language the risk of exacerbating their dysphonia or failure to improve their dysphonia due to a variety of factors. It is also important to maximize the lines of communication between the patient and the voice care team members by including family members, singing teachers and speech–language pathologists involved in the decision making process to proceed with phonomicrosurgery and to avoid pressuring the patient into consenting to phonomicrosurgery (see Chap. 10, “Principles of Phonomicrosurgery”). Prevention of vocal fold scar formation after phonomicrosurgery can be optimized by adhering to conservative tissue handling techniques during phonomicrosurgery, ensuring that the patient is compliant with regard to voice rest and light voice use after surgery, and finally, considering the use of postoperative, intra-vocal fold steroid injections to minimize permanent vocal fold scar after phonomicrosurgery (see Chap. 11, “Perioperative Care for Phonomicrosurgery”). Physical complications after phonomicrosurgery of dependent edema of the vocal fold, granulation tissue at the operative site, and failure of the microflap to adhere are typically related to uncontrolled LPR, poor compliance with postoperative voice rest, and a foreign-body implantation associated with the surgical procedure. Difficulties with dependent edema of microflap can be solved with time, minimizing vocal abuse and treating concurrent LPR. Reducing the risk of granulation tissue at the operative site can be accomplished by reducing postoperative vocal abuse, treating LPR perioperatively and ensuring that there is no char from the laser or extraneous foreign bodies (e. g., metal flakes from instrumentation) implanted at the operative site during phonomicrosurgery. Difficulties with the microflap adhering are rare, but when they occur, it is most likely from varieties of issues. These include poor compliance with voice rest, overly traumatic handling of the microflap, and fenestration of the microflap inferiorly, which results in nonadherent epithelial coverage at the operative site, leaving the microflap nonadherent to the underlying vocal fold. Great care of the soft tissues of the microflap is essential for preventing these complications. The last aspect of poor voice results associated with phonomicrosurgery involves the formation of recurrent vocal fold

 

pathology after phonomicrosurgery. This can be associated with uncontrolled LPR, voice abuse, and/or incomplete excision of the vocal fold pathology. Prevention of the latter can be done by carefully examining the vocal fold at the time of microflap excision to ensure that all aspects of the vocal fold pathology have been completely removed. This can also be achieved by a performing careful vocal fold palpation with the back of a curved instrument, and feeling for persistent vocal fold pathology within the microflap or deep to the microflap. In addition, it is important for the surgeon to perform careful visual inspection of the operative site for persistent pathology.

12.5

Medical Complications Associated with Phonomicrosurgery

Fortunately, significant medical complications after phonomicrosurgery are extremely rare. They include airway compromise, bleeding from the operative site, and infection. Overly aggressive vocal fold injection, especially in the case of poor vocal fold abduction (unilateral with a contralateral vocal fold paralysis or bilateral) can result in airway compromise. This is most commonly treated with systemic steroids and careful observation. Bleeding from the vocal folds after phonomicrosurgery is extremely rare and most notably occurs after removal of recurrent respiratory papillomatosis. In fact, when there is significant bleeding after phonomicrosurgery for recurrent respiratory papillomatosis, it usually indicates incomplete removal of the recurrent respiratory papillomatosis disease. Infection rarely occurs after phonomicrosurgery, and in fact, for this reason antibiotics are rarely indicated for this surgery.

Key Points ■ The lines of communication and relationship between the surgeon and the patient are absolutely essential for the management and prevention of complications related to phonomicrosurgery. The surgeon should be completely forthright and honest when discussing with the patient potential and real complications of phonomicrosurgery and their subsequent management. ■ It is imperative for the surgeon to establish reasonable expectations regarding voice quality and timeline of recovery with the patient to optimize vocal recovery and achieve patient satisfaction from a voice quality perspective. ■ Many significant complications associated with phonomicrosurgery can be prevented by strictly adhering to principles of conservative tissue handling and excision.

 

Chapter 12

Selected Bibliography 1

2

Anderson TD, Sataloff RT (2004) Complications of collagen injection of the vocal fold: report of several unusual cases and review of the literature. J Voice 18:392–397 Rosen CA, Andrade Filho PA, Scheffel L, Buckmire RA (2005) Oropharyngeal complications of suspension laryngoscopy: a prospective study. Laryngoscope 115:1681–1684

3 4

Rosen CA, Villagomez VJ (2001) A unique complication of microflap surgery of the vocal fold. Ear Nose Throat J 80:623–624 Woo P, Casper J, Colton R, Brewer D. Diagnosis and treatment of persistent dysphonia after laryngeal surgery: a retrospective analysis of 62 patients. Laryngoscope 104:1084–1091

83

Chapter 13

Principles of Laser Microlaryngoscopy

13.1

Fundamental and Related Chapters

Please see Chaps. 6, 10, 21, 22, 24–30 for further information.

13.2

Laser Physics

The modern challenge of using medical lasers is the surgeon’s ability to deliver the right amount of energy at the right wavelength to the right tissue while minimizing damage to collateral tissue. This process by which laser energy is restricted to a particular site is a result of the selective absorption of the chromophores at that site and was first described by Anderson et al. as “selective photothermolysis.” The following section will consider the major concerns confronting surgeons when using lasers in a clinical setting.

13.2.1 Wavelength Unlike the energy emitted from ambient light sources, laser light is monochromatic and usually of a single wavelength, with all photons collimating into a single, thin beam of homogeneous energy. The challenge of laser surgery is finding a wavelength in which energy is absorbed by target tissue and scattered or transmitted by surrounding structures. When laser light is delivered to the chromophores within the target, energy is absorbed within that tissue. Some common chromophores targeted by surgical lasers are hemoglobin, melanin, water-containing soft tissue, and covalent bonds found in major structural proteins. Depending on the chosen wavelength, either coagulation, vaporization, or a combination both will take place. Tissues heated to 80–100°C will suffer plasma denaturation, resulting in vessel closure and hemostasis. Temperatures above 100°C will cause vaporization through rapid volumetric expansion of intracellular water stores, a technique that is useful for separating or ablating tissues. A laser’s wavelength also correlates with the depth at which the energy is delivered. Therefore, greater depths of tissue disruption are achieved at longer wavelengths until reaching the wavelength specific for the absorption of water, near 2,000 nm.

13

13.2.2 Tissue Interaction While appropriate wavelength determination is critical for specific tissue targeting, the time in which the energy is delivered is also of consequence. Under prolonged exposure times, photothermal effects cause collateral coagulation necrosis, as heat transfers uniformly to surrounding tissues. However, if the pulse width is too short, the absorbing tissue may heat rapidly. Extreme temperature differences between target tissue and collateral structures have been shown to cause vaporization and shock wave damage, commonly referred to as a photomechanical effect. Consequently, nonspecific thermal damage occurs when the pulse width exceeds the thermal relaxation time for the tissue. Thus, the larger the specific target, the larger the thermal relaxation coefficient. Generally, subcellular organelles achieve photolysis within a nanosecond domain, cellular disruption occurs on a microsecond scale, and hemostasis is achieved within millisecond exposure times. In actual practice, all of these interactions occur concomitantly, but by selecting the proper wavelength, intensity, and pulse duration, the surgeon can maximize the desired effects.

13.2.3 Delivery Systems While recent advancements in the field have provided more options for delivery systems, laser type is still the major determinant. Traditionally, the CO2 laser has been of the most use for laryngologists. Traditionally, an articulating arm is required for the delivery of CO2 laser energy to the treatment site. This delivery system requires a hollow tube with several joints or articulations that allow some maneuverability. At each articulation, a set of mirrors are positioned to reflect the beam around the corner. Great care must be taken when using such a system, as jarring or vibrations may cause misalignment within the internal mirror system. Laryngologists have also benefited from the addition of several attachments used at the end of articulating arms. Micromanipulators are used to couple laser operation and microscopy. A greater amount of precision and beam control can be managed by hand-manipulated devices. The micromanipulators can control laser spot size. This is an essential variable from an ultimate tissue interaction perspective. Spot size, power, energy setting, and duration have a major role in the effect of the laser on the tissue. The smaller the spot size, the greater the energy delivered per unit area. Thus, when working with the typical very small spot sizes found with the CO2 laser micromanipulators, the power settings should be kept quite low.

86

Principles of Laser Microlaryngoscopy

Many of the other lasers used in the field are delivered via fiberoptic cables. With the advent of this technology, laryngologists are able to use endoscopes, such as the flexible laryngoscope with a working channel to gain access. As with the articulating arm, fiberoptics is used in a noncontact manner. Normally a 1- to 2-mm distance from target tissue is optimal, as spot size rapidly increases with distance from tissue, causing a great reduction in laser energy delivered and lack of precision.

13.2.4 Types of Laser

13

Although a myriad of lasers are employed in the treatment of head and neck pathology, there are only a few types in the field of laryngology. Traditionally the CO2 laser is the workhorse of laryngologic lasers. Its specific wavelength of 10,600 nm is absorbed by water found in soft tissues and is independent of tissue color. CO2 lasers emit continuous or pulsed waves, which can be focused into a thin beam and used to cut like a scalpel or defocused to vaporize, ablate, or shave tissue. The CO2 laser’s ability to deliver energy endoscopically, utilize no-touch technology, and provide a marked reduction in postoperative swelling, contributing to its widely accepted clinical use. Pulse dye lasers (PDL) emit radiation at a 585-nm wavelength, which corresponds with the oxyhemoglobin absorption band. This wavelength penetrates the mucosa well, minimizes absorption by melanin in the overlying mucosa, and offers excellent selective absorption by microvasculature. A lasing medium of rhodamine dye is excited by flash lamps and is delivered with a pulse width just under the thermal relaxation time of small vessels. While pulse dye lasers have been employed in many areas of laryngology, relative small pulse width and the cost of replacement dye medium have detracted from the benefits of such technology. YAG lasers use a yttrium–aluminum–garnet crystal rod that is manufactured with specific rare earth elements dispersed within the crystal rod. The difference in the chemical properties of each element gives the laser a specific wavelength and thus a different surgical application. All YAG lasers may be continuous, pulsed, or Q-switched. Q switching, much like a capacitor in a circuit, is the ability to pulse the laser, while at the same time increasing peak energy power, shortening pulse width, and improving the consistency of the lasers output throughout the pulse. Normally, continuous and pulsed modes are delivered via fiber optic cables, while articulating arms use Q switching. The holmium:YAG (Ho:YAG) laser uses an active medium of YAG crystal with holmium dispersion. Its beam falls near the infrared region of the electromagnetic spectrum at 2,100 nm. Its principle use is to ablate bone and cartilage, and has found specific laryngologic application in laser incisions and dilation for the treatment of subglottic stenosis. The neodymium-coupled YAG (Nd:YAG) laser is one of the most clinically diverse lasers in current use. A near infrared light is emitted at 1,064 or 1,320 nm. Nd:YAG lasers may be delivered fiber optically to coagulate tissue or through sapphire probes, allowing for low-powered delivery with minimal ther-

 

mal diffusion. Sapphire probes create a cutting and vaporization effect similar to that of CO2 lasers. The potassium–titanyl–phosphate (KTP) laser uses a 1,064nm YAG laser filtered through a KTP crystal that effectively halves its wavelength to 532 nm, producing a brilliant green light, well within the visible spectrum. The KTP laser is the newest addition to the laryngologist armament. Its 532-nm wavelength corresponds to a greater specific absorption for oxyhemoglobin. Recent studies have shown great promise in the surgical use of this solid-state laser, including shorter pulse width and less nonspecific tissue damage. The KTP laser also can deliver energy through a small diameter fiber optic, resulting in less mechanical damage to endoscopic channels. It is important to recognize that a laser is nothing more than a tool in the surgeon’s armamentarium, much like forceps, microscissors, or bipolar cautery. It is a common misconception that microspot CO2 lasers allow increased precision over cold techniques. In fact, microlaryngeal cold instrumentation are superior to microspot laser technology in terms of precision, while avoiding collateral heat damage that can be associated with laser use.

13.3

Surgical Indications and Contraindications

Ideal indications for CO2 laser are: ■ Glottic/posterior glottic stenosis ■ Subglottic/tracheal stenosis ■ Bilateral vocal fold paralysis (arytenoidectomy, transverse cordotomy, …) ■ Teflon granuloma of the larynx ■ Squamous cell carcinoma of the glottis (T1–select T2) Additional indications for CO2 laser include: ■ Papillomatosis (especially with extensive disease) ■ Vocal fold varix (select cases) ■ Saccular cyst of the larynx Relative contraindications for CO2 laser are: ■ Most benign lesions of the vocal folds: ■ Nodules ■ Vascular lesions ■ Cysts ■ Polypoid corditis Indications for Nd:YAG laser comprise: ■ Large hemangioma of the larynx ■ Glottic/subglottic stenosis (CO2 laser generally preferred) Indications for pulse dye laser/pulsed-KTP laser are: ■ Papillomatosis

 

■ ■ ■ ■

Chapter 13

Leukoplakia Granuloma Vascular lesions Polypoid corditis

Dilation equipment:

•

Ventilating bronchoscopes: 5, 6, 7, and 8 French (if no trach present)

• •

Laryngeal rigid dilators: 20–50 French (if trach present) Pneumatic balloon dilator

Jet ventilation machine

13.4

Equipment: Laser Microlaryngoscopy Setup

High-quality operating microscope with 400-mm lens Large-bore laryngoscope (largest diameter possible if operating on vocal folds/supraglottis) (see Chap. 10, Table 10.1) Suspension laryngoscope with suction channel and jet ventilation port if operating on subglottis/trachea

•

Ossoff–Pilling effective for subglottis/upper trachea (proximal)

•

Subglottiscope for upper/mid-trachea (distal)

Suspension system

• •

Gallows suspension Fulcrum suspension (e. g., Lewy apparatus and table-mounted Mayo)

Operating chair with arm supports

•

Alternative: Mayo stand with pillow/foam

Instrumentation (available from Karl-Storz (Culver City, CA), Medtronic ENT [Jacksonville, Fla.], Instrumentarium [Montreal, Quebec, Canada])

•

Injection device for hydrodissection (Orotracheal injection device, Medtronic ENT)

• • • • • •

Small (0.5 × 2 cm) cotton pledgets

Laser safety materials

• • • •

Moistened eye pads Moistened towels/surgical drapes Laser-safe endotracheal tube (if applicable) Eye protection for operating room personnel

13.5

CO 2 Laser Safety Guidelines

13.5.1 General Guidelines (Fig. 13.1) In the vast majority of laryngeal laser surgery, relatively lowpower settings are employed to minimize collateral heat damage. For the purposes of this chapter, all laser settings described are used in the context of a micromanipulator with a 250-μm spot size. Laser settings are generally set below 10 W, using an intermittent or superpulse mode. Continuous firing mode is rarely employed and can sharply increase the chances of immediate (laser fire) or late complications (glottic web/stenosis), due to the substantial power delivery in this mode. Intermittent delivery or pulsed delivery (e. g., superpulse) allows some thermal relaxation time in between laser delivery, thus minimizing collateral heat damage.

1:10,000 epinephrine Velcro strap or cloth/silk tape Microcup forceps (see Chap. 10, Fig. 10.2) Micro-ovoid cup forceps (see Chap. 10, Fig. 10.3) Microscissors

– Curved, left and right – Up angled • • • • •

Curved alligator forceps Straight alligator forceps Microlaryngeal suctions Triangular (Bouchayer) forceps Hopkins Telescopes

– Diameter 4–5mm, length 30cm or more – 0, 30, and 70° CO2 laser Micromanipulator with 250-μm spot size (coupling device between microscope and laser) Jet Venturi needle or Hunsaker Mon-Jet tube

Fig. 13.1  Intraoperative photograph illustrating the key laser safety

concepts, including wrapping the patient’s head and upper body with moistened towels, the use of a laser-safe endotracheal tube, low-O2 settings, and eye protection for operating room personnel

87

88

Principles of Laser Microlaryngoscopy

13.5.2 CO2 Laser Settings (For most applications in the larynx, the following range of laser settings can be employed): ■ 4–8 W, intermittent mode (0.1 s “on” and 0.5 s “off ”) ■ Best for precision work at the vocal fold level ■ Least collateral damage ■ 4–8 W, superpulse mode ■ Increased tissue ablation ■ Use sparingly near vocal folds to minimize collateral damage ■ 4–6 W, continuous ■ Maximum laser ablation: useful for cartilage ablation (arytenoidectomy)

 

13.6.2 Protecting Surrounding Tissue from Laser Damage Platform suction can be used, as indicated above, or a moistened Cottonoid can be placed over the area to be protected.

13.6.3 Maintenance of a Clean Surgical Field The CO2 laser causes the accumulation of carbonaceous debris (Fig. 13.3), or char at the surgical site. This desiccated debris is resistant to laser penetration due to the low water content. Therefore, it must be removed periodically by wiping the tis-

13.5.3 Safety Protocol

13

The key to laser safety in the operating room (OR) is consistent and methodical adherence to an established protocol. A simple yet effective protocol is to fully address three areas of safety prior to proceeding (Fig. 13.1). The surgeon must answer affirmatively to the following questions before firing the laser: 1. Is the patient’s body protected? a) Moistened eye pads b) Soaked surgical towels around the face and upper chest 2. Is the endotracheal tube/airway protected? a) Laser-protected tube must be used b) Saline filled ETT balloon c) Moist Cottonoid covering/protecting the balloon d) O2 concentration of 30–35% or less If jet ventilation is used, then suspend ventilation during firing of the laser. 3. Are the OR personnel protected? a) Eyeglasses or plastic goggles with side protectors for all personnel b) Laser warning signs on all OR doors

13.6

Fig. 13.2  Platform suction device

Surgical Principles

13.6.1 Smoke Evacuation Laser vaporization results in significant smoke accumulation at the operative site, and must be rapidly removed to maintain visualization. Suction tubing should be connected to a side channel of the laryngoscope to maintain continuous smoke evacuation. It should be noted, however, that supplemental smoke evacuation may be necessary. Platform suction (Fig. 13.2) is often employed, which provides not only smoke evacuations, but also protects the distal tissues from inadvertent laser damage. Fig. 13.3  Carbonaceous debris from laser ablated tissue, right vocal

fold. This must be removed for efficient treatment of tissue with the CO2 laser

 

Chapter 13

sues with a saline-soaked Cottonoid, or suction removal. Also, active bleeding at the surgical site usually prevents laser vaporation. Hemostasis must be achieved before proceeding (by either defocusing the laser beam, or applying epinephrinesoaked Cottonoids for 1–3 min to the area of bleeding).

13.7

Complications and Their Treatments

13.7.1 Laser Fire A laser fire is the most feared complication in laryngology, although it is quite rare today. This is likely due to better education and awareness of laser safety issues, as well as improved laser-safe endotracheal tube design. In the unlikely event of a laser fire with an indwelling endotracheal tube, the following steps should be followed: ■ ■ ■ ■ ■

Immediate removal of ETT Turn off anesthetic gas/oxygen delivery Mask patient with 100% O2 Intubate with small 4.0–5.0 ETT Evaluate trachea with rigid bronchoscopy with carbon debris removal ■ Flexible bronchoscopy to evaluate more distal tracheobronchial tree ■ Manage airway after extent of injury is established (options to be considered): ■ Extubate, observe in monitored setting ■ Remain intubated, treat with corticosteroids/antibiotics ■ Tracheostomy

13.7.2 Tracheal Perforation This can lead to tracking of air into the neck and down into the mediastinum. Further dissection can lead to pneumothorax. Either condition should be evaluated with a chest x-ray and consultation with cardiothoracic surgery/pulmonology specialists.

Key Points ■ The key components that determine a laser’s interaction with tissue are wavelength, intensity, spotsize and pulse duration. ■ The CO2 laser is the workhorse laser for laryngotracheal work, and the ideal indications include: ■ Glottic/posterior glottic stenosis ■ Subglottic/tracheal stenosis ■ Bilateral vocal fold paralysis (arytenoidectomy, transverse cordotomy) ■ Teflon granuloma of the larynx ■ Squamous cell carcinoma of the glottis (T1–select T2)

■ Papillomatosis (especially with extensive disease) ■ Vocal fold varix (select cases) ■ Saccular cyst of the larynx ■ The CO2 laser is generally not a good choice for the removal of benign lesions of the vocal fold, such as polyps, or cysts, or nodules, due to decreased precision, and unintended collateral heat damage, which can result in scarring and dysphonia. ■ CO2 laser settings generally employ low-wattage settings (4–8 W) in an intermittent or superpulse mode to minimize collateral damage to the tissues. The continuous-beam setting should be used sparingly, and is most appropriate for cartilage ablation. ■ A laser safety protocol should be employed in all cases where the CO2 laser is used. The key concepts are protection of the patient (moist towels), protection of the endotracheal tube (laser safe, with O2 concentration of 35% or less), and protection of operating room personnel (safety glasses).

Selected Bibliography 1

2 3

4

5 6

Anderson R, Parrish J (1983) Selective photothermolysis: precise microsurgery by selective absorption of pulsed radiation. Science 220:524–527 Absten GT, Joffe SN (1985) Lasers in medicine. Chapman and Hall, London Buckmire R et al (2006) Lasers in laryngology. In: Merati AL, Bielamowicz SA (eds) Textbook of laryngology. Plural, San Diego, pp 190–199 Ossoff RH (1989) Laser safety in otolaryngology—head and neck surgery: anesthetic and educational considerations for laryngeal surgery. Laryngoscope 99(Suppl.):1–26 Schramm VL, Mattox ED, Stool SE (1981) Acute management of laser-ignited intratracheal explosion. Laryngoscope 91:1417–1426 Zeitels S, Anderson R et al (2006) Office-based 532-nm pulsedKTP laser treatment of glottal papillomatosis and dysplasia. Ann Otol Rhinol Laryngol 115:679–685

89

Chapter 14

Principles of Vocal Fold Augmentation

14.1

Fundamental and Related Chapters

Please see Chaps. 5, 31, 33, and 34 for further information.

14.2

Vocal Fold Augmentation: Advantages, Disadvantages, and Clinical Utility

There are primarily two treatment modalities that are used for the surgical treatment of glottic insufficiency: 1. Vocal fold augmentation (see Chaps. 31, “Vocal Fold Augmentation via Direct Laryngoscopy”; 33, “Peroral Vocal Fold Augmentation in the Clinical Setting”; and 34, “Percutaneous Vocal Fold Augmentation in the Clinic Setting”) 2. Laryngeal framework surgery (medialization laryngoplasty [ML], arytenoid adduction [AA]) (see Chaps. 38, “Silastic Medialization Laryngoplasty for Unilateral Vocal Fold Paralysis”; 39, “GORE-TEX® Medialization Laryngoplasty”; 40, “Arytenoid Adduction”; and 41, “Cricothyroid Subluxation”) There is a lack of consensus among laryngologists regarding the role of these two surgical approaches in the treatment of glottal closure problems. The scarcity of comparative studies for these two treatments has resulted in a lack of evidence to clearly support one over the other. Furthermore, not all forms of glottic insufficiency are the same, thus while some patients may be well served with either approach (i. e., mild–moderate gap with mobile vocal folds), other patients are clearly better served with a specific approach (i. e., ML with AA for a lateralized, shortened immobile vocal fold). The choice of procedure is often a reflection of the surgeon’s own preference. However, in general, vocal fold augmentation is used in the following settings: 1. Temporary correction in cases of unilateral vocal fold paralysis/paresis, when the prognosis for recovery is uncertain Vocal fold augmentation results in immediate improvement of voice and/or swallowing, while allowing a period for recovery of vocal fold function. After a period of weeks to months, the injected substance is typically resorbed (see Table 14.1). Also, temporary vocal fold augmentation can be done in cases in which it is not clear that the glottal insufficiency is the main communication deficit and thus, the temporary augmentation is done on a “trial” basis. If the patient re-

14

sponds to the surgery, then permanent correction can be done. 2. Permanent correction of mild-to-moderate glottic in­suf­fi­ ciency a) Vocal fold atrophy (as seen in presbyphonia) b) Vocal fold paralysis c) Vocal fold paresis d) Adjunctive augmentation of the vocal fold(s) after prior laryngeal framework surgery (“touch up”) Patients with minor degrees of glottic insufficiency (<1mm glottic gap on phonation) are usually better suited for vocal fold augmentation rather than framework surgery. Conversely, severe degrees of glottic incompetence appear to be more difficult to correct with vocal fold augmentation. A glottic gap of 3 mm or greater (during phonation) is generally better suited for a laryngeal framework surgical approach. 3. Glottic insufficiency due to loss of soft tissue in the vocal fold Examples of this clinical situation include sulcus vocalis, and scarring of the vocal fold after partial laser cordect­ omy.

14.3

Surgical Indications and Contraindications

■ Vocal fold augmentation is not as effective at closing large (3 mm or greater) glottal gaps compared with framework techniques. This especially true in the case of a large posterior glottal gap in some patients with unilateral vocal fold paralysis (UVFP); these cases are best suited for ML and AA. ■ Vocal fold augmentation can be less precise than laryngeal framework surgery. Most vocal fold augmentation procedures require some degree over-injection to allow for reabsorption, rendering fine adjustments to vocal fold position somewhat difficult. However, a similar problem is encountered in ML when factoring in perioperative vocal fold edema during the implant placement. The overcorrection of injection issue is especially true with lipoinjection. The vocal outcome is rendered even more uncertain in those patients who require a general anesthetic for injection, and whose voice result cannot be immediately assessed.

92

Principles of Vocal Fold Augmentation

■ Vocal fold augmentation is a more minimally invasive approach compared to laryngeal framework surgery. Most laryngeal framework surgery requires a trip to the operating room, i.v. sedation, and the risk of reactive airway edema postoperatively. In addition, the patient is usually required to lie supine for an extended period of time during the surgical procedure. Due to these limitations, many patients with acute/subacute UVFP may not be good candidates for laryngeal framework surgery. Often, the patient with an iatrogenic UVFP is unwilling to return to the operating room for another surgery, yet may be perfectly willing to undergo a vocal fold augmentation in a clinic-based setting (see Chaps. 33, “Peroral Vocal Fold Augmentation in the Clinic Setting” and 34, “Percutaneous Vocal Fold Augmentation in the Clinic Setting”)

14.4

Characteristics of Vocal Fold Augmentation Materials

14.4.1 Overview

14

The ideal vocal fold injection material would be readily available, inexpensive, inert, easy to use, and completely biocompatible. The search for such a material has been ongoing for almost 100 years, and significant advances in vocal fold augmentation material availability and design have occurred in the last 10 years. The original injection material was paraffin, which resulted in a significant foreign body response and rejection. Similar responses have occurred with Silicone injections as well as most recently with Teflon™ vocal fold injections. An additional requirement of all future vocal fold injection materials will be a matching of the biomechanical properties of the material with the biomechanical properties of either the superficial aspect of the vocal fold (superficial layer of the lamina propria) or the deep aspect of the vocal fold (vocalis, thyroarytenoid and lateral cricoarytenoid muscle).

14.4.2 Categories of Vocal Fold Augmentation Materials In general, augmentation substances can be divided into temporary and long-lasting (sometimes permanent) materials. Temporary injection substances include: ■ Bovine gelatin (Gelfoam™, Surgifoam™) ■ Collagen-based products (Zyplast™, Cosmoplast™/Cosmoderm™, Cymetra™) ■ Carboxymethylcellulose (Radiesse Voice Gel™) ■ Hyaluronic acid gel (Restylane™, Hyalaform™) Long-lasting injection substances include: ■ Autologous fat

 

■ Calcium Hydroxylapatite (Radiesse™) ■ Teflon

14.4.3 Description of Vocal Fold Augmentation Materials Characteristics General characteristics of the current materials available for vocal fold augmentation are listed in Tables 14.1 and 14.2. 1. Bovine gelatin Gelfoam and Surgifoam come as a gelatin powder that is derived from a bovine source. A moderate amount of preparation is required prior to injection, as the powder must be mixed with saline to form a paste. This material is quite viscous and thus requires a large bore injection needle (18 or 19 g) and pressurized injection device (e. g., Bruning syringe). Gelfoam has been widely used in the larynx for over 25 years with good success. The disadvantage of these products is the short duration of activity (4–6 weeks) and the inability to inject the substance through a fine-gauge needle. 2. Collagen-based products Collagen-based products have been used for vocal fold augmentation for over 20 years. The product with the longest track record is the bovine-derived cross-linked form of collagen, Zyplast. Although no serious adverse reactions have been linked to bovine collagen use in the larynx, there is a potential for an allergic response in up to 2% of the population. For this reason, skin testing is recommended prior to the use of Zyplast, which can delay treatment for 2–4 weeks. Zyplast has been found to last as long as 4–6 month. Newer collagen-based products include Cymetra (micronized cadaveric dermal tissue) and Cosmoplast/Cosmoderm (laboratory-engineered human collagen). Neither product carries the risk of allergic response, although Cymetra has the potential for infectious transmission due to the use of cadaveric tissue as the source. Cymetra has been used extensively for vocal fold augmentation, and although it has been reported to last up to 9 months or more, the authors believe 2–3 months is more accurate. Cosmoplast/Cosmoderm are relatively new substances that have not been used in the larynx, but have potential advantages over the other collagen-based substances due to the low likelihood of allergic response or infectious risks. 3. Hyaluronic acid gels (Hyalan gels) (Restylane, Hyalaform— Allegan-Inamed, Irvine, CA) Hyaluronic acid is a naturally occurring glycosaminoglycan that is abundant in human tissue extracellular matrix. Injectable preparations of this substance are composed of crosslinked chains of hyaluronic acid that take on a viscous, water-insoluble form. These substances have been widely used as injectable fillers in rhytid treatment for over 10 years in Europe. Although these substances have been rarely used for vocal fold augmentation in the United States, clinical reports in the European literature support their safety and efficacy in the temporary treatment of glottal insufficiency. These substances are polysaccharide-based, and thus the

 

Chapter 14

chance of immunogenicity is eliminated. Rare instances of hypersensitivity (0.6%) are reported, and are related to low levels of protein impurities in the manufacture of the product. The hyalan gels include Hyalaform (manufactured from rooster combs), and Restylane (manufactured by bacterial fermentation). The duration of effect for these substances is comparable to the collagen-based products, generally 4–6 months, although some reports suggests slightly longer effect of up to 9 months (see Table 14.1). 4. Radiesse Voice Gel (carboxymethylcellulose) Radiesse Voice Gel (Bioform Medical, San Mateo, Calif.) is currently the only temporary injectable substance that is U.S. Food and Drug (FDA) approved for vocal fold augmentation. The principle material in this substance is carboxymethylcellulose, which is the carrier substance in Radiesse, a long-acting injectable. There is an extremely low risk of allergic response to this substance. Radiesse Voice Gel typically lasts 2–3 months, depending on the volume injected. The voice quality and vocal fold vibration after vocal fold augmentation are good.

93

5. Polytetrafluoroethylene (Teflon)

Teflon vocal fold injection has been performed for over 40 years and was initially touted as an excellent vocal fold augmentation material. However, long term follow up of Teflon vocal fold augmentations revealed a significant complication of a foreign-body granulomatous response occurring up to 5–10 years after injection. The foreign-body response is quite intense and often requires surgical removal of the Teflon, resulting in significant destruction of the surrounding vocal fold (see Chaps. 24, “Endoscopic Treatment of Teflon Granuloma” and 42, “Translaryngeal Removal of Teflon Granuloma”). This removal results in vocal fold tissue loss, leaving a severe deficit and morbidity at the vocal fold augmentation site(s). Because of this significant complication of Teflon vocal fold augmentation, this substance presently has very limited utility. 6. Autologous fat Autologous fat vocal fold augmentation (a.k.a. vocal fold lipoinjection) has been widely used for the last 10–15 years, with varying levels of reported success. Vocal fold lipoinjec-

Table 14.1  Temporary injectable substances

Material

Length of effect Advantages

Disadvantages

Needle gauge

Gelfoam

4–6 weeks

Long track record

Short duration

18

Radiesse Voice Gel

2–3 months

FDA approved No allergy testing

Not as long lasting as collagen/hyaluronic acid gels (?)

27

Bovine collagen (Zyplast)

3–4 months

20-year track record

Allergy test required 2- to 4-week delay

27

Human-derived collagen (Cosmoplast/Cosmoderm)

3–4 months

No allergy testing

New product/limited experience

27

Micronized AlloDerm (Cymetra)

2–3 months

No allergy testing

More preparation time Unpredictable duration

18–23 recommended

Hyaluronic acid gels (Restylane, Hylaform)

4–6 months (?)

No allergy testing

Limited experience

27

Table 14.2  Long-term/permanent injectable substances

Material

Length of effect

Advantages

Disadvantages

Needle gauge

Ca Hydroxylapatite (Radiesse)

2–5 + years (?)

FDA-approved Long lasting

New product No long-term track record

25

Teflon

Permanent

Long lasting

Irreversible May cause vocal fold stiffness Risk of granuloma

18 or 19

Autologous fat

Several years– permanent (?)

Patient’s own tissue used “Forgiving” (defect over-correction rarely occurs)

Time, morbidity from fat harvest Performed in OR Unpredictable duration

18 or 19

94

14

Principles of Vocal Fold Augmentation

tion obviously has the advantages of using a material that is autologous and usually readily available. Sustained results in the correction of glottic insufficiency (>1 year) have been demonstrated in patients treated with lipoinjection for glottic insufficiency. In addition, radiographic presence of fat up to 2 years after lipoinjection has been demonstrated in a number of patients. However, the variable survival in the immediate postoperative period (2 months) is disconcerting to many surgeons, resulting in a lack of consensus regarding whether autologous fat is a good long-term or “permanent” correction option for glottic insufficiency. The success of lipoinjection appears to be operator dependent and the reasons for this have not been clearly identified; however, it is likely due to improper harvesting and preparation of the material as well as incorrect injection techniques. 7. Calcium hydroxylapatite (Radiesse) Calcium hydroxylapatite (CaHA) microspheres represent a new vocal fold injection material that has been extensively tested in laboratory animals and used clinically as an augmentation material in other parts of the body (nonlaryngeal). The clinical efficacy and long-term results are still pending in the larynx, although long-term augmentation has been demonstrated in other organ systems. This material is composed of microspheres of CaHA (25–45 μm in diameter) suspended in a temporary gel carrier (water, glycerin, carboxymethylcellulose), which allows for easy injection through a needle as small as 25 g. Efficacy up to 12 months has been demonstrated in a multi-institutional clinical trial at the time. Currently, it is the only FDA-approved potentially long-lasting glottic injectable. In contrast to Teflon, Radiesse is a naturally occurring substance in the human body; therefore, the risk of chronic granulomatous formation is theoretically small. Long-term animal studies and a short-term human study have demonstrated excellent host acceptance of the CaHA material in the larynx.

14.5

 

3. Vocal fold augmentation is generally directed at the poste-

rior and mid-membranous vocal fold in the treatment of glottic insufficiency. Ideal injection locations are identified at a point where a transverse line from the tip of the vocal process laterally intersects the superior arcuate line. A second injection site is sometimes needed at the mid-membranous vocal fold along the superior arcuate line. (Fig. 14.1).

Fig. 14.1  Illustration showing the correct injection site(s) for vocal

fold augmentation

General Principles of Vocal Fold Augmentation

1. Local anesthesia is generally preferred in most cases, so that

the patient’s voice can be monitored during the procedure. A notable exception to the rule is vocal fold lipoinjection, which is performed under general anesthesia to facilitate fat harvesting and preparation. 2. Injection techniques include: a) Peroral i. Curved injection device in the clinic setting (Chap. 33, “Peroral Vocal Fold Augmentation in the Clinic Setting”) ii. Straight injection device via direct laryngoscopy in the operating room (Chap. 31, “Vocal Fold Augmentation via Direct Laryngoscopy”) b) Percutaneous (Chap. 34, “Percutaneous Vocal Fold Augmentation in the Clinic Setting”) i. Translaryngeal (through thyroid cartilage) ii. Cricothyroid membrane puncture iii. Thyrohyoid membrane puncture

Fig. 14.2  Coronal section of the larynx, illustrating the correct depth

of needle placement for injection, slightly inferior to the free edge of the vocal fold

 

Fig. 14.3  The appropriate amount of overcorrection used for most injectables (15–30%, or an additional 0.1–0.2 ml of material), as depicted in this right vocal fold augmentation

The depth of injection is generally 3–5 mm, slightly inferior or at the level of the inferior lip of the free edge of the vocal fold (Fig. 14.2). 4. Injection into the superficial layer of the lamina propria (Reinke’s space) should be avoided, as this will result in loss of mucosal pliability and poor vocal quality 5. Overinjection in recommended, to compensate for resorption of the water-based component present in commercially manufactured injectables. In general, a 15–30% overcorrection is recommended (exception noted below), which translates to an additional 0.1–0.2 ml of substance for unilateral procedures. The overcorrection usually results in a slightly rounded, convex contour to the injected vocal fold (Fig. 14.3). The exception to this rule is autologous fat injection. Aggressive overcorrection (100%) is recommended in these cases to account for the substantial resorption of fat that generally occurs within the first 6–8 weeks after lipoinjection (Fig. 14.4).

Key Points ■ Vocal fold augmentation is a commonly used surgical treatment for glottic insufficiency. ■ Key differences between vocal fold augmentation and laryngeal framework surgery: ■ Vocal fold augmentation is less effective at closing large (3 mm or greater) glottal gaps, especially in the posterior membranous region of the vocal folds ■ Vocal fold augmentation may be less precise than framework surgery ■ Vocal fold augmentation is however, a more minimally invasive approach, and can be carried out in a clinic-based setting.

Chapter 14

Fig. 14.4  The appropriate amount of overcorrection used for vocal

fold lipoinjection, as demonstrated in this left vocal fold

■ Vocal fold augmentation is appropriate in a variety of clinical settings, but is commonly used in the following situations: ■ Temporary correction for unilateral vocal fold paralysis ■ Trial correction for glottal insufficiency (as a diagnostic measure) ■ Permanent correction of vocal fold atrophy (as seen in presbyphonia), vocal fold paresis (unilateral and bilateral), unilateral vocal fold paralysis ■ Adjunctive vocal fold augmentation after laryngeal framework surgery (“touch up”) ■ Glottic insufficiency due to vocal fold scarring/ soft tissue loss ■ A variety of injectable substances are available for vocal fold augmentation, and can be categorized into temporary (2–6 months) and long-acting/permanent (2 years or more). ■ Temporary injection substances include: ■ Bovine gelatin (Gelfoam, Surgifoam) ■ Collagen-based products (Zyplast, Cosmoplast/Cosmoderm, Cymetra) ■ Carboxymethylcellulose (Radiesse Voice Gel) ■ Hyaluronic acid gel (Restylane, Hyalaform) ■ Long-lasting injection substances include: ■ Autologous fat ■ Calcium hydroxylapatite (Radiesse) ■ Teflon ■ Local anesthesia is generally preferred with vocal fold augmentation (peroral or percutaneous approach), so that the patient’s voice can be used as a constant source of feedback during the procedure (Chaps. 33 and 34). ■ Augmentation is directed at the posterior and midmembranous vocal fold, along the lateral vocal fold (superior arcuate line), and at a depth of 3–5 mm.

95

96

Principles of Vocal Fold Augmentation

■ Injection into the superficial lamina propria (Reinke’s space) is to be avoided. ■ Overinjection (15–30%) is recommended to compensate for resorption of the water-based component present in most injectable substances. The exception to this rule is autologous lipoinjection, which requires substantial overcorrection.

Selected Bibliography 1 2 3

14

Brandenburg JH (1992) Vocal cord augmentation with auto­gen­ ous fat. Laryngoscope 102:495–500 Ford CN, Martin DW, Warner TF (1984) Injectable collagen in laryngeal rehabilitation. Laryngoscope 94:513–518 Ford CN, Bless DM (1986) Clinical experience with injectable collagen for vocal fold augmentation. Laryngoscope 96:863–869

  4

Hertegar S, Hallen L, Laurent C et al (2004) Cross-linked hyaluronan versus collagen for injection treatment of glottal insufficiency: 2-year follow-up. Acta Otolaryngol 124:1208–1214 5 Remacle M, Marbaix E, Bertrand B, Hamoir M, van den Eeckhaut J (1990) Correction of glottic insufficiency by collagen injection. Ann Otol Rhinol Laryngol 99:438–444 6 Rosen CA (2000) Phonosurgical vocal fold augmentation: procedures and materials. Otol Clinics North Am 33:1087–1096 7 Rosen C, Gartner-Schmidt J, Casiano R et al (2007) Vocal fold augmentation with calcium hydroxylapatite (CaHA). Otolaryngol Head Neck Surg 136:198–204 8 Schramm VL, May M, Lavorato AS (1978) Gelfoam paste injection for vocal cord paralysis: temporary rehabilitation of glottic incompetence. Laryngoscope 88:1268–1273 9 Simpson CB, Amin MR (2004) Office-based procedures for the voice. Ear Nose Throat J 83(Suppl.):6–9 10 Watterson T, McFarlane SC, Menicucci AL (1990) Vibratory characteristics of Teflon-injected and noninjected paralyzed vocal folds. J Speech Hear Disord 55:61–66

Part B Phonomicrosurgery for Benign Laryngeal Pathology

II Phonomicrosurgical Voice Procedures

Chapter 15

15

Vocal Fold Polyp

15.1

Fundamental and Related Chapters

Please see Chaps. 4, 8, 10, 11, and 12 for further information.

15.2

Disease Characteristics and Differential Diagnosis

A vocal fold polyp can have a variety of different features and presentation characteristics, and typical features involve an exophytic lesion with quite-thin mucosa (Fig. 15.1). The lesion is typically unilateral but can be bilateral. Often, there will be a hemorrhagic nature to the polyp, giving it a maroon or bloodcolored appearance. If the vocal fold polyp is not hemorrhagic, then it will be clear and may even have a translucent nature to it. The stroboscopic features of a vocal fold polyp include minimal dampening of the overall mucosal wave and an hourglass closure pattern. Physically, at the time of surgery, a disorganized gelatinous material is found within the subepithelial space in patients with a vocal fold polyp. The vocal fold polyp can be associated with

increased vascularity around the lesion, often noted as a varix feeding the lesion (see Chap. 22, “Vocal Fold Varix”). Typically, a vocal fold polyp is associated with misuse or heavy use of the voice, such as in a variety of phonotraumatic behaviors. These behaviors can result in a vocal fold polyp in a gradual/progressive fashion or in a sudden fashion often associated with an acute vocal fold hemorrhage. Differential diagnosis associated with vocal fold polyp includes: ■ ■ ■ ■ ■ ■

Reinke’s edema Vocal fold cyst Pseudocyst Vocal fold fibrous mass Localized edema of the vocal fold (temporary) Vocal nodules

15.3

Surgical Indications and Contraindications

Indications for surgery for vocal fold polyp include: ■ A combination of dysphonia and lack of significant response to nonsurgical treatment methods (voice therapy, medical management) ■ A vocal fold polyp that is associated with a significant vocal fold varix that is at risk for vocal fold hemorrhage Contraindications for surgery comprise: ■ Patients medically unable to tolerate general anesthesia ■ Inability to obtain proper visualization of vocal folds during microlaryngoscopy ■ A patient without vocal functional limitations

15.4

Surgical Equipment

1. Standard phonomicrosurgical equipment (see Chap. 10,

Table 10.1)

2. Bipolar or laser equipment for the treatment of associated

Fig. 15.1  Vocal fold polyp

vocal fold varix as needed (see Chaps. 13, “Principles of Laser Microlaryngoscopy” and 22, “Surgical Management of Vocal Fold Vascular Lesions”)

100

Vocal Fold Polyp

 

Vocal fold polyp is best surgically removed via a phonomicrosurgical approach (see Chap. 10, “Principles of Phonomicrosurgery”). There are two main methodological approaches to the surgical removal of a vocal fold polyp. First, using a microflap approach and second, a truncation approach. The decision

on which approach to select is based on the amount of healthy mucosa associated with the polyp. 1. Microflap approach for vocal fold polyp removal a) Exposure of lesion, preferably the entire membranous vocal fold i. Application of topical epinephrine (1:10,000) to the vocal fold lesion via a Cottonoid ii. Subepithelial infusion for vocal fold polyp is contra-

Fig. 15.2  Cordotomy at junction of polyp and vocal fold

Fig. 15.3  Microflap elevation

Fig. 15.4  Removal of polyp contents

Fig. 15.5  Dissection of polypoid material medially, preserving infra-

15.5

Surgical Procedures

15

glottic mucosa

 

Chapter 15

indicated, given that this could blur the demarcation of the junction between the vocal fold polyp and the normal vocal fold tissue. iii. Epithelial cordotomy is planned and made through the epithelium at the junction of the lateral aspect of the vocal fold polyp and the normal vocal fold mucosa, along the superior surface of the vocal fold (Fig. 15.2). iv. The microflap elevation is performed medial to the incision to expose the subepithelial pathologic contents of the vocal fold polyp (Fig. 15.3). v. Vocal fold polyp material is removed via either microsuction or direct removal of the abnormal material with small microcup forceps (1 mm) (Fig. 15.4). Alternatively, the lesion can be dissected medially with a 30° flap elevator, preserving additional inferior microflap mucosa (Fig. 15.5). vi. Redrape the microflap back over the vocal fold and evaluate the nature and status of the microflap mucosa (Fig. 15.6). vii. Trim abnormal mucosa that appears to have adherent polyp material, or is extremely thin and atrophic, or is excessive and will not serve as normal mucosa during the postoperative healing (Fig. 15.7). viii. Redrape the remaining microflap mucosa. Once the flap is redraped, use a blunt instrument (curved elevator) to palpate the operative site to ensure there is no remaining pathology under the flap (Fig. 15.8). ix. Treat the associated vascular lesion if needed (see Chap. 22, “Surgical Management of Vocal Fold Vascular Lesions”). x. 4% Lidocaine is sprayed onto the larynx (commonly referred to as a LTA [laryngotracheal anesthesia])

Fig. 15.6  Redrape and evaluate viability of microflap mucosa

2. Truncation of the vocal fold polyp a) Application of topical epinephrine to the vocal fold le-

sion

b) Subepithelial infusion for vocal fold polyp is contraindi-

cated, given that this could blur the demarcation of the junction between the vocal fold polyp and the normal vocal fold tissue. c) Grasp the vocal fold polyp with small triangular forceps in a medial direction (Fig. 15.9). The nature and approach to grasping the vocal fold polyp is extremely important and is a key determinant of the success of the procedure. The vocal fold lesion should be grasped in a location and manner that is perpendicular to the longitudinal axis of the vocal fold. With the nondissecting hand, careful control and gentle application of tension should be applied to the vocal fold polyp. d) Microscissors that are either slightly curved (away from the vocal fold) or straight up-cutting scissors are then used to incise the vocal fold polyp at the junction of the polyp and the vocal fold (Fig. 15.9). e) After removal of the majority or the entire vocal fold polyp, careful examination and palpation should be performed to see if there is any residual abnormal mucosa at the vocal fold polyp site that should be removed. To help with this assessment, an epinephrine-soaked Cottonoid can be placed on the operative site for several minutes. If there is residual abnormal mucosa, then a 1-mm microcup forceps can be used to remove this tissue. An alternative removal technique involves grasping of the “dogeared” mucosa with a microcup forceps or small triangle forceps and excising the material with a microcurved scissors (Fig. 15.10).

Fig. 15.7  Trim abnormal microflap mucosa

101

102

Vocal Fold Polyp

Fig. 15.8  Redrape microflap and palpate with curved probe

 

Fig. 15.9  Traction applied to polyp and truncation of polyp. Dashed

line indicates proposed line of excision

15

Fig. 15.10  Microscissors removal of residual mucosa

Fig. 15.11  Removal of residual mucosa with outside curve of curved

microscissors.

 

Chapter 15

15.6

Postoperative Care/Complications

Voice rest is typically used after surgical excision of a vocal fold polyp. This voice rest period can range from 2 to 7 days. It is wise to treat patients for perioperative laryngopharyngeal reflux, consisting of proton pump inhibitor and behavior modification. Complication of surgical excision of vocal fold polyp can be: ■ Excessive vocal fold scar formation ■ Granulation tissue at the operative site ■ Vocal fold hemorrhage in the region of the surgery

Key Points

Fig. 15.12  Straight edge of left vocal fold immediately after excision

of vocal fold polyp

f) If there are some residual tags or dog-eared mucosa, then

this tissue should be removed. If this tissue is too small to be grasped, then it can be removed by opening the blades of the microcurved scissors (curved away from the surgical vocal fold), sliding the scissors down over the tissue in a way that the blades straddle the tissue to be removed. With gentle, lateral pressure at the same time that the blades are closed, this tissue will be successfully removed (Fig. 15.11). g) After removal of the vocal fold pathology, careful examination visually as well as on palpation (using the outside curve of curved elevator or curved alligators) should be performed on the operative site(s). There may be some additional fibrous or gelatinous material that should be carefully removed to prevent a rapid recurrence of the vocal fold pathology. This material can be removed with a microelevator or microcup forceps. Extreme care is required at this juncture of the surgery, because overly aggressive removal of this material can result in significant scar formation as well as a permanent deformity of the free edge of the vocal fold. At the completion of the surgery, the free edge of each vocal fold should be completely straight, without exophytic mucosal tags and without a divot or concavity of the free edge at the surgical site (Fig. 15.12). h) Application of 4% plain lidocaine onto the endolarynx

■ Precision microsurgical removal of a vocal fold polyp is paramount. ■ Great care should be taken to avoid a “cookiebite” defect into the substance or main component of the vocal fold after surgical removal of a vocal fold polyp. ■ Most of the mucosa of the vocal fold polyp is usually not suitable for preservation due to its thin, atrophic nature. ■ However, some residual surrounding mucosa of the vocal fold polyp can be preserved and redraped to allow optimal vocal fold healing after surgery.

Selected Bibliography 1 2

3

Courey MS, Garrett CG, Ossoff RH (1997) Medial microflap for excision of benign vocal fold lesions. Laryngoscopy 107:340–344 Hochman II, Zeitels SM (2000) Phonomicrosurgical management of vocal fold polyps: the sub-epithelial microflap resection technique. J Voice 14:112–118 Johns MM (2003) Update on the etiology, diagnosis, and treatment of vocal fold nodules, polyps and cysts. Curr Opin Otolaryngol Head Neck Surg 11:456–461

103

Chapter 16

16

Vocal Fold Nodules

16.1

Fundamental and Related Chapters

Please see Chaps. 3, 4, 8, 10, 11, and 12 for further information.

16.2

Disease Characteristics and Differential Diagnosis

Vocal fold nodules are characterized as bilateral vocal fold lesions that are fairly symmetric (Fig. 16.1). On stroboscopy, the mucosal wave is normal or near normal. The stroboscopic closure pattern is an hourglass configuration. Typically, these patients have a history of vocal abuse or misuse (phonotrauma). These tend to occur in children and adult females (18–40 years of age). The differential diagnosis of vocal fold nodules includes: ■ Vocal fold polyp (bilateral or with a contralateral reactive lesion) ■ Fibrous mass (bilateral or with a contralateral reactive lesion) ■ Cyst (bilateral or with a contralateral reactive lesion) ■ Pseudocyst (bilateral or with a contralateral reactive lesion)

when present. Surgery for vocal fold nodules without a thorough and properly implemented nonsurgical therapy course is not appropriate. A relative contraindication to surgery for vocal fold nodules is a patient that has not been compliant with voice therapy nor changed the habitual phonotraumatic behavior that most likely led the formation of the lesions.

16.4

Surgical Equipment

1. Phonomicrosurgery instruments (see Chap. 10, Table 10.1) 2. CO2 laser optional (see Chaps. 10, “Principles of Phono-

microsurgery” and 13, “Principles of Laser Microlaryngo­ scopy”)

Cold-steel excision is the preferred method for vocal fold nodules removal; however, in rare instances, and with great experience and the optimal laser technical abilities, the CO2 laser can be used to remove vocal fold nodules as well.

Vocal fold nodules are typically treated with nonsurgical methods including voice therapy, voice rest, and treatment of comorbid medical conditions. It is extremely rare that true vocal fold nodules do not respond favorably to these nonsurgical modalities. Most often, when bilateral vocal fold lesions are still present after the nonsurgical treatment modalities, these lesions are in fact not vocal fold nodules, but other benign vocal fold lesions (see above list).

16.3

Surgical Indications and Contraindications

Surgery for vocal fold nodules is reserved for persistent and significant dysphonia (with functional limitations) after all nonsurgical treatment options are exhausted. Nonsurgical treatment options include high-quality voice therapy with good compliance by the patient—also, treatment of comorbid medical conditions such as reflux disease and allergic disease

Fig. 16.1  Vocal nodules

106

Vocal Fold Nodules

suspension laryngoscopy (see Chap. 10, “Principles of Phonomicrosurgery”). 2. The vocal fold lesions should be palpated gently under highpower magnification. During this, the vocal fold lesions should be assessed for their degree of submucosal pathology and examinined for associated pathologic lesions such as vascular lesions, evidence of scar, sulcus vocalis, and other vocal fold pathologies. Special attention should be given to the anterior commissure to evaluate if there is a presence of an anterior commissure microweb. Past reports have noted an increased incidence of anterior commissure microwebs with recalcitrant vocal fold nodules that require surgical excision. If a microweb is present, then asymmetric release of the microweb can be done with scissors or a sickle knife. Mitomycin C can be applied to the operative site. 3. The surgical removal of vocal fold nodules starts with a very careful grasping of one of the lesions with a small triangular or curved alligator instrument. The approach to the grasping of the lesion should be as close to perpendicular to the longitudinal axis of the vocal fold as possible and as superficially as possible. After the lesion is grasped, the lesion is drawn to the midline gently and very careful observation of the demarcation between vocal fold pathology and the normal vocal fold free edge should be identified. 4. Microscissors, either straight-up or curved (aimed in a direction away from the vocal fold) should be used for a submucosal excision of the vocal fold lesion (Fig. 16.2). As the excision is performed from posterior to anterior, care should be taken to ensure that the tips of the vocal fold

scissors do not extend deep into the vocal fold nor past the anterior border of the vocal fold lesion (Fig. 16.3). Without special attention to this area, excessive anterior vocal fold mucosa can be removed with the vocal fold lesion excision. It is best to watch carefully the path of the tips of the scissors to ensure that they are aimed purposely to finish the cut just anterior to the lesion and come through the free edge of the vocal fold anterior to the lesion. 5. If there are any residual mucosal irregularities at the excision site, then these should be removed in a careful, conservative fashion by either removal of the irregular abnormal mucosa with microcup forceps or by microsurgical scissors excision (Fig. 16.4). The former is best done with the microcup forceps being used to grab the intended mucosa for removal and allowing the sharp edge of the forceps to come through the mucosa without any forceful stripping of the mucosal tag. 6. After removal of the benign vocal fold lesions, careful examination visually as well as on palpation (using the outside curve of curved elevator or curved alligators) should be performed at the operative site(s). There may be some additional fibrous or gelatinous material at this location, which should be carefully removed to prevent a rapid recurrence of the vocal fold pathology. 7. This material can be removed with a microelevator or microcup forceps. Extreme care is required at this juncture of the surgery, because too-aggressive removal of this material can result in significant scar formation as well as a permanent deformity of the free edge of the vocal fold. 8. At the completion of the vocal fold lesion(s) excision the free edge of each vocal fold should be completely straight without exophytic mucosal tags and without a divot or concavity of the free edge of the surgical sites (see Chap. 15, Fig. 15.12).

Fig. 16.2  Submucosal excision of vocal fold lesion (start)

Fig. 16.3  Submucosal excision of vocal fold lesion (finish)

16.5

Surgical Procedure

1. Complete exposure of the membranous vocal folds with

16

 

 

Chapter 16

Key Points ■ Vocal fold nodules are bilateral, fairly symmetric, midmembranous vocal fold lesions that have normal stroboscopic or minimal impairment findings that result in an hourglass closure pattern. ■ Most patients with vocal fold nodules improve with nonsurgical treatment methods, however there may be some rare cases of recalcitrant vocal fold nodules that require surgical excision. ■ Surgical excision of vocal fold nodules should be extremely conservative, precise and performed in a subepithelial fashion. ■ The initial retraction or grasping of the vocal fold lesion is very important. This step in large part determines the success of the procedure.

Selected Bibliography Fig. 16.4  Removal abnormal mucosa from operative site

1

2

16.6

Postoperative Care and Complications

Voice rest is used for a variable length of time, depending not only on the size and nature of the lesion, but also on compliance issues of the patient. In general, compared with other phonomicrosurgical procedures, a shortened amount of voice rest can be used after vocal fold nodules removal if the patient will be compliant with light voice use instead of total voice rest. As an example, for an extremely compliant patient, voice rest may be needed only 1 or 2 days, proceeding to light voice use if the patient is continuing to be compliant, and the stroboscopy results are favorable. Complications from vocal fold nodules surgery are: ■ ■ ■ ■

Excessive scarring Submucosal hemorrhage Residual vocal fold pathology Excessive removal of vocal fold tissue, resulting in a “cookie bite” defect of the vocal fold

The latter complication can be prevented with very careful submucosal excision of the vocal fold lesion and utilizing great precision and control to prevent the surgical excision from entering into the deeper aspects of the lamina propria or vocal ligament.

3 4

5

6

7

8 9

Akif Kilic M, Okur E, Yildirim I, Guzelsoy S (2004) The prevalence of vocal fold nodules in school age children. Int J Pediatr Otorhinolaryngol 68:409–412 Benjamin B, Croxson G (1987) Vocal nodules in children. Ann Otol Rhinol Laryngol 96:530–533 Benninger MS, Jacobson B (1995) Vocal nodules, microwebs and surgery. J Voice 9:326–331 Courey MS, Shohet JA, Scott MA, Ossoff RH (1996) Immunohistochemical characterization of benign laryngeal lesions. Ann Otol Rhinol Laryngol 105:525–531 Ford CN, Bless DM, Campos G, Leddy M (1994) Anterior commissure microwebs associated with vocal nodules: detection, prevalence, and significance. Laryngoscope 104(Pt. 1):1369–1375 Holmberg EB, Doyle P, Perkell JS, Hammarberg B, Hillman RE (2003) Aerodynamic and acoustic voice measurements of patients with vocal nodules: variation in baseline and changes across voice therapy. J Voice 17:269–282 Holmberg EB, Hillman RE, Hammarberg B, Sodersten M, Doyle P (2001) Efficacy of a behaviorally based voice therapy protocol for vocal nodules. J Voice 15:395–412 Pontes P, Kyrillos L, Behlau M, De Biase N, Pontes A (2002) Vocal nodules and laryngeal morphology. J Voice 16:408–414 Shah RK, Woodnorth GH, Glynn A, Nuss RC (2005) Pediatric vocal nodules: correlation with perceptual voice analysis. Int J Pediatr Otolaryngol 69:903–909

107

Chapter 17

Vocal Fold Cyst and Vocal Fold Fibrous Mass

17.1

17

Fundamental and Related Chapters

Please see Chaps. 3, 4, 8, 10, 11, and 12 for further information.

17.2

Diagnostic Characteristics and Differential Diagnosis

A vocal fold cyst is a sac-like structure within the lamina propria of the vocal folds, typically yellow or white in color (Fig. 17.1). Vocal fold fibrous mass is an accumulation of fibrous material within the lamina propria of the vocal fold. It can be quite difficult to detect in some cases, and videostroboscopy is usually needed to make the diagnosis (see Chap. 3, “Videostroboscopy and Dynamic Voice Evaluation with Flexible Laryngoscopy”). Stroboscopy shows significantly reduced mucosal wave where the lesion is present. Both lesions are usually found in the midmembranous vocal fold and can be either in the subepithelial (SE) space or near the ligament (lig) of the vocal fold. Vocal fold cysts have a distinct and confined sac-like boundary, and in contrast, vocal fold fibrous masses are more diffuse and often have extensions anteriorly and/or posteriorly within the vocal fold. Differential diagnosis for vocal fold cyst or fibrous mass is: ■ ■ ■ ■

Vocal fold polyp Rheumatologic lesion of the vocal fold Vocal nodules Reactive lesion

17.3

Surgical Indications and Contraindications

Indications for surgery are symptomatic dysphonia and lack of resolution with maximum nonsurgical treatment (voice therapy). Contraindications for surgery comprise: ■ Patients medically unable to tolerate general anesthesia ■ Inability to obtain proper visualization of vocal folds during microlaryngoscopy ■ A patient without vocal functional limitations

Fig. 17.1  Vocal fold cyst (left)

17.4

Surgical Equipment

The surgical equipment required is a standard phonomicrosurgery instrument set (see Chap. 10, Table 10.1).

17.5

Surgical Procedure

The surgical approach to a vocal fold cyst or vocal fold fibrous mass uses a microflap (see Chap. 10, “Principles of Phonomicrosurgery”). There is little difference in the surgical technique for a cyst or fibrous mass. The technique described below applies to both lesions unless otherwise noted. 1. Microflap approach to a cyst or fibrous mass in the subepithelial location a) Intubation with 5.0 microlaryngeal endotracheal tube b) Expose larynx with laryngoscope i. Use the largest laryngoscope that will adequately expose the entire vocal fold (see Chap. 10, “Principles of Phonomicrosurgery”). c) Incision i. Make incision just lateral to, or directly over the lesion, in a posterior-to-anterior direction or anteriorto-posterior direction.

110

Vocal Fold Cyst and Vocal Fold Fibrous Mass

ii. Keep the incision superficial by maintaining a slight

pull on the knife superiorly (toward yourself), which “tents” up the mucosa, protecting the deeper layers (Fig. 17.2). iii. The incision should be slightly longer than the actual lesion to afford adequate space in which to work.

 

d) Separate the epithelial cover from the cyst/fibrous mass

(Fig. 17.3). i. Use the 30° flap elevator to develop a plane as superficially as possible between the overlying epithelium and the cyst/fibrous mass. ii. The instrument can usually be visualized through the thin, semitranslucent flap (0.2-mm thick) during this step. The tip of the elevator should be pointing medially. iii. Often there is adherence between the flap and cyst wall. It is best to start creating the dissection in undistorted tissue planes anterior and posterior to the lesion before dissecting directly over the lesion. iv. The dissection is continued to the inferior-most portion of the lesion. v. Use caution with the flap elevator inferiorly, as the tip of the instrument may perforate the delicate epithelial flap; gentle pressure laterally with the “back” of the flap elevator helps avoid perforation. vi. It is important to perform the medial aspect of the dissection first, when natural “counter-traction” is provided by adherence of the lesion wall to the vocal ligament. If the epithelial cover is separated as the last step, then this dissection becomes much more difficult. e) Separate the lesion from the vocal ligament. i. Dissect between the cyst/fibrous mass and the vocal ligament with a 30° flap elevator (Fig. 17.4). ii. The fibers of the vocal ligament run parallel to the long axis of the vocal fold and are white in color, with little vascularity. Great care should be taken to

Fig. 17.2  Mucosal cordotomy with sickle knife. Note how tip of knife

17

“tents up” mucosa to prevent possible injury to deep structures in the vocal fold

Fig. 17.3  Dissection between the epithelial cover and the cyst

Fig. 17.4  Dissection of plane deep to the vocal fold cyst, adjacent to

the vocal ligament

 

Chapter 17

avoid violation of the vocal ligament. Some scant gelatinous-appearing material (SLP) can often be seen, and should be preserved. iii. Avoidance of cyst wall rupture is tantamount to a successful surgery, as cyst dimensions may be difficult to define after rupture occurs. iv. If there is penetration of the cyst, then an attempt to prevent complete evacuation of the cyst should be done by grabbing the cyst at the penetration site with a small microalligator, and then dissection can be continued. If the cyst is ruptured completely, then careful and meticulous dissection and removal of all the cyst wall contents should be done. f) Removal of lesion i. Some sharp dissection with scissors may be necessary, if fibrous connections between the lesion and ligament cannot be bluntly dissected with the flap elevator. These fibrous connections are most commonly present anterior and posterior to the vocal fold cyst/fibrous mass and will need to be carefully lysed before the lesion can be removed (Fig. 17.5). ii. Often a fibrous mass will have fibrous extensions anteriorly and/or posteriorly. Depending on the thickness, these extensions can be left alone or removed. It is often best to cut these extensions at the location(s) of their attachment to the fibrous mass and then redrape the microflap to determine by palpation and visual inspection if any additional excision is required. Once all attachments of the lesion are freed, the lesion is removed and the flaps are replaced and allowed to coapt (Fig. 17.6). iii. Epithelial resection is normally not necessary.

Fig. 17.5  Release of fibrous attachments to the vocal fold cyst

g) Special considerations for vocal fold cyst/fibrous mass

near the vocal ligament i. After cordotomy and the start of the microflap elevation, the vocal fold cyst/fibrous mass will be clearly visible in the “deep” portion of the vocal fold near or on the vocal ligament. ii. When ligamentous pathology is present, the microflap is usually quite easily elevated, given that the lesion is deep to the area of dissection. iii. A triangular forceps can then be used to retract the microflap medially while a fine-angled elevator is used to dissect off the vocal fold cyst/fibrous mass from the vocal ligament (see Fig. 17.7). iv. Microscissors are sometimes required to complete the dissection of the lesion off the vocal ligament. v. The lesion is removed and the microflap redraped into its anatomic position. vi. The vocal fold should be palpated, feeling for persistent pathology causing irregularity of the vocal fold.

17.6

Postoperative Care and Complications

Postoperative care includes: ■ Complete voice rest for 1 week ■ Proton pump inhibitors (PPIs), pain medications as needed (tongue pain from suspension) ■ Follow-up in 1 week, begin graduated voice use under supervision of SLP (if possible)

Fig. 17.6  Redraping of microflap

111

112

Vocal Fold Cyst and Vocal Fold Fibrous Mass

 

Key Points ■ Diagnosis of vocal fold cyst and vocal fold fibrous mass may be difficult preoperatively; however, videostroboscopy greatly improves the chances of detection. Often exploratory cordotomy is required to differentiate between the diagnoses of a fibrous mass versus vocal fold cyst. ■ Delicate handling of the cyst is necessary to avoid rupture, which will complicate the removal. ■ Surgical dissection between the epithelial covering and cyst wall (medial dissection) should precede dissection between the lesion and vocal ligament (lateral dissection). ■ Postoperative recovery may be slower for vocal fold cyst and vocal fold fibrous mass lesions that are on or near the vocal ligament compared to lesions in the subepithelial space.

Fig. 17.7  Retraction of microflap demonstrating vocal fold fibrous

mass on vocal ligament

Complications can include (see Chap. 12, “Management and Prevention of Complications Related to Phonomicrosurgery”):

17

■ Chipped teeth (typically maxillary) ■ Anesthesia/hypoesthesia of tongue, loss of taste ■ Due to pressure neuropathy of lingual nerve from suspension laryngoscope ■ Resolves in 2–3 weeks typically, may persist for 3 months or more ■ Minimize by keeping suspension time to less than 2 hours ■ Prolonged postoperative dysphonia ■ Seen in cases where extensive scarring/adhesions are present, especially if cyst rupture has occurred prior to surgery. Occasionally, a sulcus vocalis deformity is seen, where the cyst extends into the vocal ligament, requiring dissection into the ligament and in some cases resection of vocal ligament fibers to remove the entire cyst wall. In these cases, prolonged hoarseness and slow recovery in voice quality can be expected. We recommend intensive voice therapy, oral corticosteroid taper, and reassurance. The use of steroids is especially indicated if erythema is present at the operative site. ■ Cyst recurrence ■ This is unusual except in the case of anterior commissure mucous retention cysts or type III sulcus vocalis. Recurrence is generally seen within 6–12 weeks after surgery. Revision phonomicrosurgical removal can be carried out after the third postoperative month, with meticulous detail paid to the removal of all cystic wall remnants; this may require limited vocal ligament fiber resection in some cases.

Selected Bibliography 1 2

3

4

5

6

7

8

Courey MS, Garrett CG, Ossoff RH (1997) Medial microflap for excision of benign vocal fold lesions. Laryngoscope 107:340–344 Courey MS, Shohet JA, Scott MA, Ossoff RH (1996) Immunohistochemical characterization of benign laryngeal lesions. Ann Otol Rhinol Laryngol 105:525–531 Dikkers FG, Nikkels PG (1995) Benign lesions of the vocal folds: histopathology and phonotrauma. Ann Otol Rhinol Laryngol 104(Pt. 1):698–703 Johns MM (2003) Update on etiology, diagnosis, and treatment of vocal fold nodules, polyps and cysts. Curr Opin Otolaryngol Head Neck Surg 11:456–461 Rosen CA, Lombard LE, Murry T (2000) Acoustic, aerodynamic and videostroboscopic features of bilateral vocal fold lesions. Ann Otol Rhinol Laryngology 109:823–828 Shohet JA, Courey MS, Ossoff RH (1996) Value of videostroboscopic parameters in differentiating true vocal fold cysts from polyps. Laryngoscope 106(Pt. 1):19–26 Thekdi AA, Rosen CA (2003) Surgical treatment of benign vocal fold lesions. Curr Opin Otolaryngol Head Neck Surg 10:492–496 Zeitels SM, Hillman RE, Desloge R, Mauri M, Doyle PB (2002) Phonomicrosurgery in singers and performing artists: treatment outcomes, management theories, and future directions. Ann Otol Rhinol Laryngol 190(Suppl.):21–40

Chapter 18

18

Polypoid Corditis

18.1

Fundamental and Related Chapters

Please see Chaps. 4, 7, 8, 10, 11, and 12 for further information.

18.2

wave is often amplified or increased due to the pliable nature of the gelatinous material in the SLP; however, with growth of the lesions, vibratory characteristics can be dampened and/or absent due to mass effect. One of the distinctive characteristics of polypoid corditis is the “saddle-bag” appearance the vocal folds take on, as the heavy, rounded vocal folds prolapse inferiorly with inspiration (Fig. 18.1).

Disease Characteristics

Polypoid corditis (commonly referred to as Reinke’s edema) is an alteration of the lamina propria that results in dysphonia, lowered pitch, and vocal instability (Fig. 18.1). The characteristic low-pitched, gravelly voice tends to be more easily identified in females because it is gender incongruous. It is a condition commonly associated with smoking—in fact, 97% of patients with polypoid corditis are smokers. In addition, LPR and phonotrauma are thought to be important contributing cofactors. In contrast to most other benign laryngeal lesions, polypoid corditis is a global, as opposed to focal, process of the vocal folds. The condition is almost exclusively bilateral, and involves expansion of Reinke’s space by an inflammatory gelatinous amorphous material that extends from anterior commissure to the vocal process. The disease can be quite subtle in the early stages, but over a period of years can grow to such proportions that the airway is compromised. Initially, the mucosal

Fig. 18.1  Polypoid corditis (bilateral)

18.3

Surgical Indications and Contraindications

Indications for surgical intervention include: 1. Symptomatic dysphonia (generally more noticeable in females) 2. Lack of response to anti-reflux management with PPIs, voice therapy, and smoking cessation Smoking cessation does not lead to resolution of the disease, but does halt its progression. 3. Airway obstruction due to advanced disease This may occur when a patient has a preexisting severe polypoid corditis and develops unilateral vocal fold immobility, or upper airway edema from an additional inflammatory process such as an upper respiratory infection. The inability to improve the airway via abduction can lead to airway compromise. 4. Concern of malignancy Some cases of polypoid corditis have overlying epithelial changes (e. g., leukoplakia) and can be worrisome for malignancy. In these cases, preservation of vibratory parameters does not guarantee benign disease because a microinvasive process can be camouflaged by the deep layer of gelatinous pliable material. In these cases, the diseased epithelial must be treated as displayed in Chap. 20, “Vocal Fold Leuko­ plakia.” Contraindication for surgical intervention include continued smoking, which will almost assuredly result in a recurrence of the disease postoperatively—though it may take months to years to recur. This is a relative contraindication, and must be exercised on a case-by-case basis. Obviously, suspicion of malignancy or airway concerns overrides this contraindication. Special consideration should be given (either preoperatively or intraoperatively) to whether to operate on both vocal folds or to stage the surgeries, one side at a time. A carefully planned incision (Fig. 18.2) can be used with bilateral surgery to avoid formation of an anterior glottic web. However, if this is not

114

Polypoid Corditis

possible, then a conservative approach is advocated, where unilateral surgeries are performed to avoid complications. Patients should be counseled preoperatively that the pitch of the voice will increase, they will likely have a short period of breathiness, and that voice therapy postoperatively will usually be required.

18.4

Surgical Equipment

Standard phonomicrosurgery instrument set (see Chap. 10, Table 10.1), high-powered suction (typically a liposuction device).

18.5

Surgical Procedure

1. Intubation with a 5 or 5.5 MLT Special care must be exercised to avoid vocal fold injury or damage, due to the limited space that is available for tube placement. 2. Expose larynx with suspension laryngoscope. 3. Incision (Fig. 18.3) a) Use a fresh sickle knife b) Incision at the superior/lateral aspect of the vocal fold, beginning at the vocal process and extending to within 3 mm of the anterior commissure

 

4. Raise the microflap between the epithelium and the polyp-

oid material (Fig. 18.4). Using a 30° flap elevator, the epithelium is separated from the underlying polypoid tissue, taking great care not to perforate the epithelial flap, which can be quite thin. As the dissection extends inferiorly, it is necessary to put lateral pressure on the flap elevator to get adequate visualization of the flap. In some cases, an extensive flap is required, extending well into the infraglottis, and from “stem-to-stern” of the entire membranous vocal fold. 5. Raise a plane between the vocal ligament and the overlying polypoid material (Fig. 18.5) Again, using a 30° flap elevator, the vocal ligament is identified at the superior/lateral aspect of the vocal fold, and a plane is developed between the vocal ligament and the diseased polypoid tissue. Once the material has been freed, it is ready for removal. It should be noted that some mild-tomoderate cases of polypoid corditis might not require much flap elevation (as described in this and step 4); in these cases, the material may aspirate more readily without the need for extensive flap elevation. 6. Removal of polypoid material Much of the polypoid tissue can be removed with suction; however, suction with a strong negative pressure is essential. Routine operating room suction units are frequently inadequate, and the liposuction units are generally employed. The larger suction tubing used in the units can be adapted to the smaller suction tubing using a “Christmas tree” adaptor. In general, a 5- or 7-French microsuction with closed thumb port is used (Fig. 18.6). Care is taken to retract the flap so it is not caught in the suction. One must allow a few seconds for the maximum pressure to be achieved after placing the suction into the polypoid material. Frequently, there are loculations of more fibrous material mixed in with

18

Fig. 18.2  Planned bilateral incisions in a typical case of polypoid

corditis. Note the lack of anterior extension on the left side, which is designed to minimize the chances of anterior glottic web formation postoperatively

Fig. 18.3  Sickle-knife incision running in an anterior-to-posterior di-

rection at the superior/lateral aspect of the vocal fold

 

Chapter 18

the gelatinous polypoid material, which cannot be removed by suction. This material must be manually extracted with a straight or up cups forceps (Fig. 18.7). One must resist the temptation to remove all the polypoid material, as some SLP must be left behind to regenerate Reinke’s space, and maintain vibratory properties. 7. Trimming of redundant mucosa There is usually a certain amount of redundant mucosa, which can be quite extensive in advanced cases of polypoid

corditis. This mucosa should be conservatively trimmed so that the epithelial edges coapt at the end of the case. (Fig. 18.8). It is best to redrape the flap prior to planning the trimming of mucosa. In cases of massive polypoid corditis, it is not infrequent to sacrifice this mucosa with a large excisional removal of polypoid material. In many cases, however, the epithelial removal will be the last portion of the case. It is best to try to trim the mucosa conservatively at first; more mucosa can always be removed later if needed.

Fig. 18.4  A 30° flap elevator is used to separate the polypoid disease

Fig. 18.5  Elevation is carried out between the vocal ligament and the

Fig. 18.6  Suction removal of polypoid disease

Fig. 18.7  Supplemental cup forceps removal of disease

from the epithelium

polypoid disease

115

116

Polypoid Corditis

Fig. 18.8  Trimming of redundant epithelium with up-cutting scissors

Long cuts across the mucosa are preferable to short cuts, and these tend to give a jagged contour to the cut edge. The incised edges of the flap should coapt closely, without a significant mucosal dehiscence (Fig. 18.9).

18

18.6

Postoperative Care and Complications

Postoperative care should include PPIs, pain medicine, and voice rest for 5–7 days. Smoking should be discontinued or significantly reduced in the postoperative period. Expected postoperative course: ■ The patient will experience a breathy voice postoperatively, primarily due to the preoperative high subglottal pressures that are used to drive the vibration of the polypoid material. In addition, the pitch of the voice will be significantly higher due to the loss of mass after the surgery. In general, recovery and stabilization of voice takes longer than with most other benign lesions, typically 6–8 weeks. ■ Complications are generally related to technical errors in the surgical procedure. The most serious complication is anterior glottic web, which can occur when raw surfaces are left at the anterior free edge of both vocal folds. The best way to avoid this complication is to make the incisions on the lateral aspect of the vocal fold, and not to extend the incisions to the anterior most aspect of both vocal folds.

 

Fig. 18.9  After epithelial removal with minimal mucosal dehiscence

■ Scarring of the vocal folds can also occur. A risk factor for unfavorable scarring is the removal of excessive amounts of the SLP/gelatinous material. The result is stiffness/loss of vibratory properties with rough, breathy dysphonia, vocal fatigue, and lack of projection.

Key Points ■ Polypoid corditis is a bilateral process characterized by expansion of Reinke’s space with gelatinous inflammatory material throughout the entire vocal fold, and is seen almost exclusively in smokers. ■ Surgical indications for polypoid corditis include symptomatic dysphonia despite medical management, airway encroachment/partial obstruction, or concern of malignancy. ■ Microflap surgery can be performed bilaterally, but incisions should not extend to the anterior vocal fold to avoid web formation. Alternatively, it is acceptable to operate unilaterally and stage the second procedure. ■ Removal of the polypoid material may require a high-vacuum suction device and/or manual extraction of loculated portions of the disease. ■ It is critical that some gelatinous material in the SLP should be left behind to reconstitute Reinke’s space and preserve vibratory characteristics.

 

Chapter 18

Selected Bibliography 1

2

Lumpkin SM, Bishop SG, Bennett S (1987) Comparison of surgical techniques in the treatment of laryngeal polypoid degeneration. Ann Otol Rhinol Laryngol 96:254–257 Lumpkin SM, Bennett S, Bishop SG (1990) Postsurgical followup study of patients with severe polypoid degeneration. Laryngoscope 100:399–402

3

4

Courey MS, Gardner GM, Stone RE, Ossoff RH (1995) Endoscopic vocal fold microflap: a three-year experience. Ann Otol Rhinol Laryngol 104:267–273 Zeitels SM, Bunting GW, Hillman RE et al (1997) Reinke’s edema: phonatory mechanisms and management strategies. Ann Otol Rhinol Laryngol 106:533–543

117

Chapter 19

19

Vocal Fold Granuloma

19.1

Fundamental and Related Chapters

Please see Chaps. 1, 4, 5, 10, 11, and 12 for further information.

19.2

Disease Characteristics and Differential Diagnosis

Vocal fold granuloma is inflammatory tissue arising from the perichondrium near the arytenoid cartilage (Fig. 19.1). The granuloma typically arises in the area where the vocal process adjoins the body of the arytenoid cartilage. Vocal fold granuloma can occur unilaterally or bilaterally. Granulation tissue can form on other locations of the vocal folds; however, these are different clinical entities and are not discussed in this chapter. Vocal fold granulomas are thought to occur from a perichondritis of the arytenoid cartilage. For perichondritis of the arytenoid cartilage to occur, it is thought that there needs to be a two-step process of (1) mucosal injury and (2) subsequent injury to the perichondrium of the arytenoid cartilage. Vocal fold granuloma is classically seen after endotracheal intubation. The intubation or endotracheal tube causes mucosal injury, and subsequent injury to the perichondrium can occur from persistence of the endotracheal tube or LPR. The most common causes of vocal fold granulomas are thought to

be laryngopharyngeal reflux, vocal misuse or hyperfunction, glottal incompetence with severe hyperfunction often associated with vocal fold paresis, vocal fold atrophy, vocal fold paralysis, vocal fold scar, and chronic cough. Patients with a vocal fold granuloma can experience globus sensation, dysphonia, and/or odynophonia. If the vocal fold granuloma is extremely large, then shortness of breath and dyspnea on exertion and other airway related symptoms can be present. The postintubation granulomas typically occur in females more than in males and are often associated with a comorbid condition of laryngopharyngeal reflux disease. Typically, these lesions can be treated expectantly as long as the LPR is controlled. This patient subgroup will do quite well and often not require surgical excision of the vocal fold granuloma. Differential diagnosis for vocal fold granuloma include: (It should be noted that all of the below diagnoses almost never present as isolated lesions at the vocal process/arytenoid): ■ ■ ■ ■ ■

Squamous cell carcinoma Carcinoma in situ Dysplasia Amyloidosis Tuberculosis of the larynx

19.3

Surgical Indications and Contraindications

Indications for vocal fold granuloma surgical removal include: ■ To rule out malignancy or infectious etiologies (e. g., tuberculosis, Klebsiella) ■ Airway obstruction ■ Symptoms of persistent disease despite nonsurgical treatment methods ■ Growth of lesion despite medical treatment Contraindication of vocal fold granuloma surgery comprise surgical removal without addressing the possible underlying etiologic conditions preoperatively (LPR, voice misuse and/or glottal insufficiency).

19.4

Fig. 19.1  Vocal fold granuloma

Surgical Equipment

The surgical equipment required is a standard phonomicrosurgery instrument set (see Chap. 10, Table 10.1), and a posteriorcommissure laryngoscope (as needed).

120

Vocal Fold Granuloma

19.5

Surgical Procedure

1. Philosophical overview for vocal fold granuloma removal The overall goal for surgical removal of vocal fold granuloma is to remove the vocal fold granuloma lesion in as an atraumatic fashion as possible. It is important recognize that after vocal fold granuloma removal, success of the operation (no recurrent granuloma disease) is dependent on the race between the underlying inflamed perichondrium and the surrounding normal mucosa. If the mucosa “wins” this race, then the patient will not have a recurrent granuloma; however, if the perichondrial inflammation continues, then a recurrent granuloma is highly likely. With this in mind, it is important that all aspects of the surgical removal of the vocal fold granuloma are aimed at: a) Maintaining as much normal mucosa surrounding the surgical site as possible b) Minimizing all possible irritation or trauma to the underlying arytenoid cartilage perichondrium 2. Exposure and preparation for vocal fold granuloma excision If the vocal fold granuloma is large or the anesthesiologist refuses to use a small endotracheal tube (5.0), then the surgeon should position the endotracheal tube anterior to the laryngoscope during laryngoscope suspension. This will allow an unfettered view of the posterior commissure, which is required for this surgery. The Pilling posterior-commissure laryngoscope facilitates the anterior displacement of the endotracheal tube because it has a slight notch to hold the endotracheal tube anterior during laryngoscope suspension. The other method to keep the endotracheal tube in an anterior position is to slightly alter the angle of the endotracheal tube as it goes through the larynx so it lays nonparallel to the longitudinal axis of the laryngoscope, with a

 

net result of keeping the endotracheal tube in an anterior location while the surgeon works in the posterior glottis (Fig. 19.2). The slight angulation of the laryngoscope also keeps the endotracheal tube anterior and provides optimal exposure of the arytenoid and posterior membranous vocal fold. The ideal exposure for vocal fold granuloma surgery is to have exposure and good visualization of the posterior aspect of the midmembranous vocal fold and the entire arytenoid and posterior glottic area on the side of the lesion. 3. After the laryngoscope is suspended and adequate exposure of the posterior glottis is achieved, examine the lesion at high-powered magnification, specifically gently retracting the lesion from its attachment from the arytenoid to view, and gain a sense of the size and location of the stalk. This can also be done by passing a small curved alligator between the vocal fold granuloma and the arytenoid cartilage; this will allow the surgeon to identify the exact location and nature of the vocal fold granuloma stalk. 4. For removal of the vocal fold granuloma, it is best to use a curved alligator (curved in the opposite direction of the side that the vocal fold granuloma is on) and gently grab the stalk that runs between the vocal fold granuloma and the arytenoid cartilage. Preferably, the alligator will grasp the stalk on its most medial aspect. The vocal fold granuloma stalk can then be gently retracted towards the midline, and a curved microscissors (curved in the same direction as the curved alligator) is then used to release or cut the stalk immediately lateral to the curved alligator, thus allowing the removal of the vocal fold granuloma (Fig. 19.3). 5. Application of epinephrine-soaked pledgets (1:10,000 dilution) will achieve hemostasis without any difficulty.

19

Fig. 19.2  Nonparallel placement of the laryngoscope and endotra-

cheal tube

Fig. 19.3  Retraction of vocal fold granuloma stalk with curved alliga-

tor and cutting of stalk

 

Chapter 19

6. Careful examination and palpation of the operative site will

reveal if there is any residual granulation tissue or inflammatory tissue. If this tissue is present, it is best to remove it very carefully and conservatively with l-mm cup forceps or the micro-ovoid cup forceps. Great care should be taken at this juncture to fully remove obvious exophytic tissue and not remove any surrounding normal mucosa or to reach deeply into the operative site. This will minimize the risk of traumatizing the underlying arytenoid perichondrium. 7. Adjunctive procedures to vocal fold granuloma surgery After the successful removal of the vocal fold granuloma, depending on the exact clinical situation, one should fully evaluate the size and nature of the vocal fold to consider if the patient requires vocal fold augmentation. If vocal fold augmentation is warranted, then vocal fold augmentation should be strongly encouraged and performed simultaneously to the vocal fold granuloma excision (see Chap. 31, “Vocal Fold Augmentation via Direct Laryngoscopy”). Another adjunctive treatment option especially for recurrent vocal fold granuloma surgery is to consider a vocal fold Botox injection to chemically “splint” or put the voice “at rest” after the vocal fold granuloma excision. Botox can be done during microlaryngoscopy by injecting into the TALCA muscle complex—direct the Botox needle lateral and slightly outward from the vocal process on the side of the vocal fold granuloma. However, ideally Botox injection should be done 3 days prior to the surgical excision of the granuloma (see Chap. 35, “Botulinum Toxin Injection”). Thus, the vocal fold is “at rest” at the time of the excision.

19.6

Postoperative Care and Complications

Postoperative care typically involves voice rest for a variable number of days (6–10 days). In addition, LPR treatment (despite the clinical history) should be implemented, including behavior modification and PPI therapy. Voice rest is indicated to maximize the chance of successful healing of the operative site and minimize a chance for recurrent vocal fold granuloma formation. Complications after vocal fold excision surgery include: ■ Recurrent lesion ■ Severe cartilaginous or membranous vocal fold defects from excessive or overly aggressive surgical excision of the vocal fold granuloma To address the problem associated with a recurrent vocal fold granuloma, it is important that all different etiologic possibilities are carefully and systematically reviewed prior to proceeding with a repeated surgical procedure. This includes speech–language pathology evaluation and voice therapy, LPR treatment, and assessment and treatment for glottal insufficiency.

Key Points ■ Vocal fold granuloma is a perichondritis of the arytenoid cartilage from various insults (voice misuse, endotracheal intubation, LPR, etc.). ■ Surgery should be performed if concern exists regarding a malignancy or infection, or all nonsurgical treatment options have been exhausted. ■ Underlying glottal insufficiency is a common cause of recurrent vocal fold granuloma, and patients should be carefully evaluated for the most common causes of glottal insufficiency and treated at the same time as vocal fold granuloma excision if appropriate. ■ Careful surgical excision of the vocal fold granuloma with minimal trauma to the underlying perichondrium and surrounding mucosa is essential to successful surgery for vocal fold granuloma.

Selected Bibliography 1

2

3 4

5

6

7 8

Benjamin B, Roche J (1993) Vocal granuloma, including sclerosis of the arytenoid cartilage: radiographic findings. Ann Otol Rhinol Laryngol 102:756–760 Devaney KO, Rinaldo A, Ferlito A (2005) Vocal process granuloma of the larynx: recognition, differential diagnosis and treatment. Oral Oncology 41:666–669 Hoffman HT, Overholt E, Karnell M, McCulloch TM (2001) Vocal process granuloma. Head Neck 23:1061–1074 Leonard R, Kendall K (2005) Effects of voice therapy on vocal process granuloma: a phonoscopic approach. Am J Otol 26:101–107 Ylitalo R, Hammarberg B (2000) Voice characteristics, effects of voice therapy, and long-term follow-up of contact granuloma patients. J Voice 14:557–566 Ylitalo R, Lindestad PA (2000) Laryngeal findings in patients with contact granuloma: a long-term follow up study. Acta Otolaryngol 120:655–659 Ylitalo R, Lindestad PA (1991) A retrospective study of contact granuloma. Laryngoscope 109:433–436 Ylitalo R, Ramel S (2002) Extraesophageal reflux in patients with contact granuloma: a prospective controlled study. Ann Otol Rhinol Laryngol 111(Pt. 1):441–446

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Chapter 20

20

Vocal Fold Leukoplakia and Hyperkeratosis

20.1

Fundamental and Related Chapters

Please see Chaps. 3, 4, 7, 8, and 10 for further information.

20.2

Diagnostic Characteristics and Differential Diagnosis

Vocal fold leukoplakia (Fig. 20.1) and keratosis are clinical disease processes of the vocal fold epithelium. The physical findings consist of a white plaque on the surface of the vocal fold. Histopathologically, leukoplakia can vary from the very benign (hyperkeratosis of the epithelium) to frankly malignant (microinvasive squamous cell carcinoma). The differential diagnosis of leukoplakia includes papillomatosis, fungal infections (especially candidiasis) and occasionally, tenacious mucous. Patients with vocal fold leukoplakia are typically smokers; however, other inflammatory conditions may contribute to the development of this epithelial change, such as LPR or possibly viral infection. The patient typically presents with a rough or coarse voice, but vocal fold leukoplakia may be found in an “asymptomatic” patient on routine flexible laryngoscopy. Videostroboscopy is essential in the evaluation of leukoplakia of the membranous vocal folds. Tenacious mucous can easily be distinguished from a leukoplakic plaque by observing the characteristic movement of the mucous during vibratory activity. More importantly, videostroboscopic characteristics

give valuable information regarding the potential for malignant invasion, as noninvasive pathology tends to preserve mucosal wave, whereas invasive disease leads to the loss of vibratory characteristics. Notable exceptions to this rule are the presence of coexisting polypoid corditis and microinvasive carcinoma of the vocal fold. In this example, the mucosal wave may be preserved due to extensive expansion of the SLP.

20.3

Surgical Indications and Contraindications

Indications include: ■ Leukoplakia of the vocal folds, where histopathology has not been established (especially in cases where mucosal wave is reduced or absent at the lesion site) ■ Change in the appearance or nature of preexisting leukoplakia A (relative) contraindication is a patient who is high-level vocal professional (i. e., singer) before attempting conservative management (antifungals, PPIs, etc.).

20.4

Surgical Equipment

The surgical equipment required is a standard phonomicrosurgery instrument set (see Chap. 10, Table 10.1).

20.5

Surgical Procedure

1. Intubate with 5.0 or 5.5 microlaryngeal endotracheal tube 2. Expose larynx with suspension laryngoscope. 3. Infiltrate into the submucosal space—superficial lamina pro-

Fig. 20.1  Leukoplakia of the vocal fold

pria or Reinke’s space—using a 27-g needle (Fig. 20.2). a) The mucosa will be distended, and generally, noninvasive leukoplakia will be noted to lift up from the underlying vocal ligament. Invasive areas of mucosa can sometimes be noted to remain adherent to the underlying vocal ligament, creating a depression, or “divot” (Fig. 20.3). b) The infiltration should be done slowly; generally, 0.1– 0.3 ml is all that is necessary. c) Ensure that the needle is primed, so that air is not infiltrated under the flap.

124

Vocal Fold Leukoplakia and Hyperkeratosis

 

Fig. 20.3  Invasion of epithelial lesion into the vocal ligament, creating Fig. 20.2  Submucosal infusion of 1:10,000 epinephrine in vocal fold

4. Incision (Fig. 20.4) a) Use a fresh sickle knife. b) Make the initial incision just lateral to the area of leuko-

20

plakia, in a posterior-to-anterior direction. i Note that if a diagnosis of malignancy has not been established, no “margins” are required. ii Keep the incision superficial by maintaining a slight pull on the knife superiorly (toward you), which “tents up” the mucosa, protecting the deeper layers. 5. Undermine the diseased epithelial layer from the underlying structures (Fig. 20.5). a) Use the 30° flap elevator to develop a plane in the subepithelial space, taking care to be as superficial as possible. b) Very early in the dissection, one must identify the vocal ligament. It is relatively easy to place the flap elevator into of the fibers of the vocal ligament, and begin the plane too deep. This is especially true in cases of re-excision for recurrent leukoplakia and inflammatory leukoplakic processes. c) Caution must be exercised when extending the dissection inferiorly, as the surgical plane does not continue in the same direction, but instead extends laterally. Because of this, it is easy to perforate the epithelial flap, if one is not careful. To avoid this tendency, one must push the back end of the flap elevator against the vocal ligament laterally, which improves exposure for inferior flap elevation (Fig. 20.6a, b) d) Ensure that the entire extent of the leukoplakia is undermined freely prior to proceeding. This is done by visualizing the flap elevator through the flap as the dissection proceeds.

a focal depression or “divot” within the otherwise distended SLP after submucosal infiltration

6. Make posterior, then anterior epithelial incisions (Fig. 20.7) a) Using an up-cutting scissors held sideways in one hand

and a flap elevator in the other, the leukoplakic flap is lifted up and the posterior boundary of epithelium is incised, followed by the anterior. 7. Complete the excision by making the inferior epithelial cut. a) It is often helpful to check that the microflap incision encompasses the entire diseased epithelium by periodically redraping the flap (Fig. 20.8) and rechecking the incisional line. b) The epithelial lesion is retracted with a microflap using a triangular forceps, while an up-cutting scissor is used to excise the lesion in a posterior to anterior direction. (Fig. 20.9) Special consideration should be given to: ■ Pinning and orienting the specimen for the pathologist can be very helpful in guiding future therapy. This can be accomplished by placing the epithelial specimen on a tongue blade, indicating the medial/lateral and anterior/ posterior orientation (Fig. 20.10). It is recommended that the surgeon review the histopathology personally with the pathologist, taking note of any anatomic regions that are severely dysplastic/and or invasive. Using this information, future endoscopic treatment can be directed to the specific region of the vocal fold that is involved. ■ Multiple patches of leukoplakia can be addressed in the same setting; however, one must be cautious to avoid bilateral anterior epithelial removal, which may result in anterior glottic web formation.

 

Chapter 20

Fig. 20.4  Sickle knife incision immediately lateral to leukoplakia

Fig. 20.5  Flap elevation (undermining) of leukoplakic lesion

Fig. 20.6  Coronal section of vocal fold depicting lateral pressure on

Fig. 20.7  Anterior flap incision is made after the posterior incision

the flap elevator to improve visualization of infraglottic flap

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126

Vocal Fold Leukoplakia and Hyperkeratosis

Fig. 20.8  Redraping of flap to ensure complete removal of pathology

 

Fig. 20.9  Final (inferior) flap incision

Complications can include: ■ Chipped teeth, hypoesthesia of tongue ■ Recurrence of leukoplakia Recurrence of leukoplakia is common in those patients that continue to smoke postoperatively; therefore, this should be part of pre operatively counseling. Patients may have other cofactors leading to the recurrence of leukoplakia, such as LPR, glottic incompetence, or HPV infection. These areas should be aggressively treated if they are suspected.

20

Key Points

Fig. 20.10  Typical orientation of excised leukoplakic specimen for pa-

thologist (A = Anterior, L = Lateral, P = Posterior, M = Medial)

20.6

Postoperative Care and Complications

Postoperative management includes: ■ Complete voice rest for 3–7 days ■ PPIs, pain medication ■ Follow-up 1–2 weeks to review pathology results

■ Videostroboscopy is an important component of the preoperative evaluation of vocal fold leukoplakia. ■ Loss of mucosal wave can be seen with invasive forms of leukoplakia, while noninvasive forms tend to have preservation of vibratory characteristics. ■ Subepithelial infusion is a very helpful adjunct in the surgical armamentarium, as it reduces intraoperative bleeding and lifts the diseased epithelium away from the vocal ligament, thus protecting it. ■ Complete excision of the area of leukoplakia should be checked by redraping the flap during the final excisional step. ■ Pinning and orienting the epithelial specimen can be very helpful in guiding any additional therapy.

 

Chapter 20

Selected Bibliography 1 2

Zeitels SM, Vaughan CW (1991) A submucosal true vocal fold infusion needle. Otol Head Neck Surg 105:478–479 Zeitels SM (1995) Premalignant epithelium and microinvasive cancer of the vocal fold: the evolution of phonomicrosurgical management. Laryngoscope 105:1–51

3

4.

Zeitels SM (1993) Microflap excisional biopsy for atypical and microinvasive cancer. Operat Tech Otolaryngol Head Neck Surg 4:218–222 Schweinfurth JM, Powitzky E, Ossoff RH (2001) Regression of laryngeal dysplasia after serial microflap exision. Ann Otol Rhinol Laryngeal Sep; 110(9):811–4

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Chapter 21

Surgical Treatment of Recurrent Respiratory Papillomatosis of the Larynx

21.1

Fundamental and Related Chapters

Please see Chaps. 4, 9, 10, 11, 12, and 13 for further information.

21.2

Disease Characteristics and Differential Diagnosis

Recurrent respiratory papilloma (RRP) is characterized by benign epithelial growths that are recurrent in nature after surgical removal. The lesions often have a distinct vascular “dot” in the center of individual papilloma growth (Fig. 21.1). RRP growths can be exophytic and/or superficial “spreading.” RRP can occur anywhere in the laryngotracheal area; however, the glottis is the most common site. It has been found that RRP tends to favor growth at the epithelial transition sites such as at the level of the glottis where the epithelium changes from stratified squamous epithelium to pseudostratified columnar epithelium. The etiologic agent of RRP is human papilloma virus (types 6–11 are the most common). Given the recurrent nature of RRP, careful and conservative surgery is crucial to

21

the surgical management of this disease. Often recurrent RRP patients have 50–100 surgeries in their lifetimes, and thus the surgeon must constantly remember that the primary goal for surgery is to remove the disease and minimize the sequela of surgery (vocal fold scar, web formation, etc.). With the recurrent nature of RRP disease and the need for multiple repeated surgeries, phonomicrosurgery principles, concepts, and techniques are ideal for the surgical therapy of RPP (see Chap. 10, “Principles of Phonomicrosurgery”). Differential diagnosis for RRP is: ■ ■ ■ ■

Squamous cell cancer Verrucous carcinoma Leukoplakia Granuloma

21.3

Surgical Indications and Contraindications

Indications include: ■ In pediatric cases of RPP, airway considerations are primal. For this reason, parent education on the importance of compliance with doctor’s visits and monitoring of symptoms and signs of airway difficulties are essential. Adult RRP surgery is usually indicated to rule out malignancy initially and to make a pathologic diagnosis. Subsequent to establishing the diagnosis of RRP, voice disturbance is the most common indication for surgical treatment of RRP. ■ A key management principle in RRP is to focus attention and efforts on preventing the need for a tracheotomy. Tracheotomy creates a new epithelial transition site in the trachea and may lead to new RRP growth at the tracheotomy site. The presence of new RRP at the tracheotomy site significantly increases the level of complexity of the surgical management of these patients. Contraindications include surgical excision without any voice, swallowing, or airway symptoms.

Fig. 21.1  Recurrent respiratory papilloma

130

Surgical Treatment of Papillomatosis

21.4

Surgical Equipment

1. Standard phonomicrosurgery instrument set (see Chap. 10,

Table 10.1) 2. Microdebrider (optional; described in Chap. 10) 3. CO2 or pulsed KTP laser (see Chap. 13, Sect. 13.4)

21.5

Surgical Procedure

1. Overview RRP is a recurrent disease process (99% of the time), and the most aggressive surgical excision does not equal better results, cure, or longer interval between surgical treatments. Thus, conservative removal and focus of improving functional improvement (airway, voice) not complete removal of the disease is important. This chapter describes the different surgical methods for RRP removal and then discusses surgical removal of RRP by different subsites within the larynx. When cidofovir injection is being combined with surgical excision, it can be done with any of the below described techniques (see “Cidofovir Laryngeal Injection for RPP,” below). 2. Microflap Removal of RRP (see Chaps. 10, “Principles of Phonomicrosurgery” and 20, “Vocal Fold Leukoplakia and Hyperkeratosis”) a) Place the largest laryngoscope over the RRP site (note that the surgeon may have to reposition the laryngoscope multiple times to work on several different locations within the larynx to address all RRP locations on an as needed basis).

 

b) Submucosal infusion of epinephrine throughout the in-

tended surgical area (see Chap. 10)

c) A sickle knife is then used to incise the epithelium im-

mediately lateral to the recurrent respiratory papilloma disease. Note that no margin is required in removing the recurrent respiratory papillomatosis, however, gross disease should not be left, and thus the incision should be immediately adjacent to the interface of RRP and normal mucosa. d) Subepithelial dissection (undermining of the RRP disease is then done with curved and angled elevators and sometimes with microcurved scissors). Great care should be exercised to stay very superficial (Fig. 21.2). Not staying as superficial as possible will result in unnecessary loss of vocal fold lamina propria and scar formation. e) Incision through the epithelium can then be made anteriorly and posteriorly to the RRP, once again, with no need for a mucosal margin. f) The RPP that is contained within the microflap can then be held with triangular forceps or a curved alligator, and then superficial dissection underneath the RRP can then be performed until the entire RRP has been incorporated within the microflap. g) Immediately redraping the microflap to assess the extent of the dissection and to determine if the entire papilloma area is included within the microflap is extremely helpful. Inferior incision underneath the area of the microflap containing the RRP can then be done with a sickle knife or microscissors. This releases the RRP completely and specimen can be sent for pathologic examination (Fig. 21.3). h) Hemostasis can be obtained with an epinephrine-soaked pledget.

21

Fig. 21.2  Microflap removal of RRP

Fig. 21.3  Release of microflap containing RRP

 

Chapter 21

i) Inspection (visual and by palpation) for RPP at the op-

erative site is important. This should be done with both high-power microlaryngoscopy as well as with angled telescopes (see Chap. 10). j) If more RRP is present, then further surgical removal can be done using another microflap approach or microforceps removal technique (see below). 3. Microforceps removal of RRP a) Inject epinephrine subepithelially throughout the intended RRP excision site. This allows for hydrodissection of the RRP from the deeper structures of the vocal fold as well as enhances hemostasis. b) Place epinephrine-soaked pledgets on the RRP site for several minutes. c) Gently and precisely grab a part of the RRP to be removed (depending on size of lesion) with 1–2 mm microforceps (cup/or ovoid). Make sure that the forceps are only holding on to the most superficial aspect of the RRP and not any deeper part of the mucosa or vocal fold. d) The RRP within the forceps can then be gently avulsed by pulling the tissue in either a cephalad or caudal direction. Superior or inferior direction of avulsion is the safest (Fig. 21.4). e) Avoid pulling the RRP anteriorly or posteriorly since this may result in “stripping” of normal adjacent mucosa inadvertently. f) These steps can be repeated until all the intended RRP has been carefully removed. It is most expedient to have two microforceps available of similar size and nature to perform this type of surgical removal. This allows the surgeon to hand the RRP-laden instrument to the surgical assistant and receive the second instrument to continue the RRP removal while the assistant removes the RRP

from the first instrument. This cycle can be continued until all the RRP is removed in a fairly rapid fashion. g) Epinephrine-soaked pledgets can be applied to the operative site to obtain hemostasis on an as needed basis. 4. Laser surgery for RRP a) Exposure of RRP with the largest possible laser laryngoscope b) Submucosal infusion of epinephrine to intended area of RRP excision. c) Implementation of all laser safety precautions (see Chap. 13, “Principles of Laser Microlaryngoscopy”) d) It is best to use a “defocused spot size” 0.5–0.75 mm, with a low power (2–4 W) on intermittent superpulse setting. e) The laser is used to vaporize the RRP; care should be taken to only ablate the RRP tissue and not the deeper aspect of the vocal fold. Power, spot size, and duration of exposure can be adjusted to prevent damage to deeper structures and transmission of thermal injury to surrounding regions. This surgery should be performed at high power magnification for maximum control and precision of the RRP removal. f) Carbonaceous material from the laser ablation site should be removed frequently with suction cannulas (5 or 7 French). g) Surrounding areas not intended for excision (i. e., contralateral, vocal fold, anterior commissure, false vocal fold, etc.) should be retracted or covered with saline-soaked pledgets to protect inadvertent injury or damage. h) Laser ablation should be done in a controlled fashion and great care is required to insure that repeated “doses of laser energy” are not delivered to the same exact location consecutively. This can be achieved by moving the

Fig. 21.4  Cup forceps removal of RRP

Fig. 21.5  Microdebrider removal of RRP. Note blunt probe adjacent to

disease, which is used to “pin” the vocal fold so that deeper structures are not drawn into the microdebrider

131

132

21

Surgical Treatment of Papillomatosis

laser beam in a smooth, controlled, and expedient fashion, thus preventing the same location from receiving repeated laser energy, which may result in deep tissue injury. 5. Microdebrider removal of RRP a) Placement of the largest laryngoscope to expose the area of RRP removal b) Submucosal injection of epinephrine c) Epinephrine-soaked pledgets placed on the area of the RRP intended for excision and then removed d) The smallest and most conservative microdebrider blade should be placed on the microdebrider handle, especially at the start of the case. This is especially true for the subglottis, glottis, and posterior glottis. e) The microdebrider starting setting should be 800–1200 and then can be adjusted accordingly. f) The safest method for RRP removal is to hold the microdebrider “blade or port” 1–2 mm over the RRP disease and allow the suction from the instrument to draw the RRP tissue away from the deeper aspects of the laryngeal tissue and be removed by the internal blades of the microdebrider. It is often helpful to “pin” the vocal fold in a stationary position with an adjacent blunt probe to prevent the deeper tissues (e. g., ligament) from being suctioned into the microdebrider chamber (Fig. 21.5). g) As the settings are adjusted and comfort level of the surgeon is increased, the microdebrider can be placed closer to the RRP tissue, always attempting to apply minimal pressure to the RRP tissue with the microdebrider hand piece. Controlled removal of the RRP can be done in a fairly expedient fashion due to the rapid RRP removal afforded by the microdebrider. h) Apply epinephrine-soaked pledget to the surgical site to obtain hemostasis after removal of the RRP. i) To “capture” the RRP tissue for pathologic examination, a suction trap can be placed “inline” with the microdebrider suction and at the end of the procedure sent for pathologic examination. 6. Recurrent respiratory papilloma sites: technical aspects and methods for surgical removal: telescopic RRP surgery Standard microlaryngoscopy visualization can be limited in several locations (ventricle, subglottis) Angled telescopes can be used for telescopic removal of the RRP utilizing a 30 or 70° telescope and angled cup forceps and/or a micro­ debrider. Angled telescopic examination of this area is absolutely essential at the end of each surgical procedure for RRP to ensure thorough removal of gross disease in this region. a) Supraglottis The anatomic components of the supraglottis include laryngeal ventricles, false vocal fold, anterior face of the arytenoid cartilage, supraglottic portion of the arytenoid cartilages and the laryngeal surface of the epiglottis. The laryngeal ventricles are clearly the most difficult anatomic area to visualize and operate on within the larynx. Thirty and 70° telescopes are important adjuncts for visualization of this area and sometimes may need to be used for surgical removal of a papilloma in this area (see above telescopic RRP surgery). Surgical removal of gross

 

Fig. 21.6  Removal of RRP at the anterior commissure. (Note that the

blue shaded region should be preserved to prevent anterior glottic webbing)

papilloma disease from all other areas in the supraglottis can be done in an expedient and safe fashion using a microdebrider (preferred technique). Cold-steel surgical excision of papilloma of supraglottic or CO2 laser area also all reasonable options for this region. Care should be taken to avoid demucosalization of the anterior aspect of the free edge of each false vocal fold to prevent supraglottic stenosis. b) Glottis The region of the glottis incorporates the superior surface of the vocal fold, the free edge of the vocal fold, and the infraglottic region. It also encompasses the anterior commissure. This area is of prime importance given the phonatory dependent nature of these tissues and because of the known predilection of RRP to occur in this zone. The preferred surgical removal of RRP in this region is a cold-steel approach (microflap, microforceps or microdebrider usually after submucosal infusion). It must be stressed and remembered that RRP is a superficial disease, and thus only epithelium needs to be removed. If RRP is extensively located on the superior surface of the vocal fold, then the complete visualization and subsequent removal can be further facilitated with submucosal infusion to medialize the disease for better visualization. Specifically in the anterior commissure, the importance of precise and conservative surgical removal of disease in a unilateral nature to prevent glottic web formation is paramount. Telescopic examination is of further value for complete assessment of the disease at the anterior com-

 

missure and in the infraglottic regions. When working at the anterior commissure, in addition to not violating the contralateral mucosal or RRP covered tissue, careful retraction of the vocal fold for full exposure of the anterior commissure is essential (see Fig. 21.6). This can be done with a contralateral hand instrument or a self-retaining retraction instrument. When surgically removing RRP from only one side of the anterior commissure, it is wise to make an initial “incision” or “cut” through the RRP at the anatomic midline. Then unilateral RRP removal can proceed with little chance of accidental bilateral RRP removal. c) Level of the subglottis RRP disease in the subglottis is of great concern due to the airway limitations and minimal dimensions of this region. Optimal surgical technique and removal of disease in this area involves either cold steel excision or microdebrider. If visualization is particularly difficult, a CO2 laser can have an advantage given that hand instruments can be used for retraction while the CO2 laser is used for excision or ablation of the RRP. It must be stressed that the CO2 laser must be used in a conservative fashion, including protection of surrounding laryngeal tissues and using the laser in a low-power and intermittent delivery mode. d) Posterior commissure The posterior commissure is the region of the larynx extending from the arytenoid region down into the subglottis. Careful examination of this region is mandatory during all operative procedures relating to RRP and typically will require anterior displacement of the endotracheal tube for complete and detailed examination of this region (if an endotracheal tube is being used). To facilitate further exposure in this region, often instrumentation is required to retract the arytenoid cartilages to examine fully this region. Telescopic examination (30 and 70° telescopes) is helpful to visualize this area and determine the nature and extent of the RRP disease. Surgical removal in this area should be in a conservative fashion given that excessive surgical removal by any technique can lead to significant posterior glottic stenosis. Microforceps or microdebrider are good methods for unilateral, staged excision of RRP to prevent posterior glottic stenosis. 7. Cidofovir laryngeal injection for RPP Cidofovir is an antiviral agent that has been used extensively recently as an adjunct treatment for RPP. This antiviral agent has been used as sole therapy without removal of disease and has been used at the same time as recurrent respiratory papillomatosis is surgically removed. Presently, the most common method of cidofovir use is laryngeal injection of cidofovir after conservative surgical removal of the RRP. The best RRP disease control occurs with repeated cidofovir injection at the same time that staged surgical excision is performed. Typically, patients receive intralesional cidofovir injection on a monthly basis for three or more total injections times. There is no standard dose of concentration of cidofovir for injection, however, 5 mg/ml is a reasonable dose used by many.

Chapter 21

The surgical technique associated with cidofovir injection involves a two key principles. First, it is important to remember that the etiologic viral agent of RRP, human papilloma virus, is known to be present throughout the mucosa of the entire upper airway. For this reason, it is prudent to inject cidofovir in normal appearing mucosa in a wide region around and inside the larynx. Secondly, cidofovir can be injected submucosally prior to a surgical excision as well as immediately after the surgical excision. This is strictly up to the surgeon’s preference and based on the total dose of cidofovir to be used and the specific nature and location of the RRP. Cidofovir injection can be done with a fine-gauge needle (25–27 g) and should be done in a superficial (subepithelial) fashion. Cidofovir injection is done in this location, given that past research has identified the human papilloma virus in the epithelium of the upper airway. Cidofovir intralaryngeal injection after surgical excision can be done in anatomic subunits to insure wide mucosal distribution of the antiviral agent. Cidofovir injection should be done in a caudal to cephalad direction. The typical sequence of intralaryngeal cidofovir injection will cover the following areas in this order: subglottis, posterior commissure (bilateral), free edge of vocal fold (bilateral), superior surface of vocal fold and ventricle (bilateral), false vocal fold (bilateral), and supraglottic larynx on an as-needed basis. When there is mucosa present in the area to be injected, the injection needle should be placed in the subepithelial plane. Often cidofovir can be infused submucosally in a large area of the laryngeal subunits described above with a single injection. Cidofovir injection into areas without mucosa, due to recent RRP removal, should be done in the most superficial plane possible. In these settings, multiple superficial injections are required since the tissue planes are absent or distorted, negating the ability to distribute cidofovir over a large area with a single injection.

21.6

Postoperative Care and Complications

Postoperative care includes: ■ Intravenous and oral steroids can be used as clinically indicated ■ LPR treatment if necessary (proton pump inhibitor and behavior modification) ■ Pain medicine on an as-needed basis ■ Limited or no voice rest as indicated Complications include: ■ Laser fire and thermal injury to larynx ■ Glottic web (anterior/posterior) ■ Excessive vocal fold scar formation or tissue destruction

133

134

Surgical Treatment of Papillomatosis

Key Points ■ RRP is a recurrent disease that requires precise and conservative surgical removal. ■ RRP surgical removal often requires different surgical methods (microflap, microforceps, laser, or microdebrider). ■ Angled telescopes especially (30 and 70°) are helpful in evaluating laryngeal RRP immediately prior to excision, during surgical excision, and at the completion of RRP removal.

 

Selected Bibliography 1

2

3

4

5

21

Kashima H, Mounts P, Leventhal B et al (1993) Sites of predilection in recurrent respiratory papillomatosis. Ann Otol Rhinol Laryngol 102:580–583 Lee AS, Rosen CA (2004) Efficacy of cidofovir injection for the treatment of recurrent respiratory papillomatosis. J Voice 18:551–556 Mounts P, Sha KV, Kashima H (1982) Virtual etiology of juvenile and adult onset squamous papilloma of the larynx. Proc Natl Acad Sci USA 79:5425–5429 Steinberg B, Topp W, Schneider P et al (1983) Laryngeal papilloma virus infection during clinical remission. N Engl J Med 308:1261–1264 Zeitels SM, Sataloff RT (1999) Phonomicrosurgical resection of glottal papillomatosis. J Voice 12:1323–1327

Chapter 22

Surgical Management of Vocal Fold Vascular Lesions

22.1

22

Fundamental and Related Chapters

Please see Chaps. 4, 8, 10, 11, 12, and 13 for further information.

22.2

Diagnostic Characteristics and Differential Diagnosis of Vocal Fold Varicosities

In healthy vocal folds, blood vessels run parallel to the vibratory margin and are somewhat tortuous. The parallel arrangement helps prevent obstruction of the microcirculatory system of the vocal fold mucosa during high-pressure shearing movement during phonation; the tortuosity helps the vessels maintain functional patency when the vocal fold length is altered during pitch changes. Although there are numerous arteriovenous anastomoses, there is little or no direct connection between the microvasculature of the superficial lamina propria of the vocal fold, and the thyroarytenoid muscle. This arrangement helps optimize the mucosal cover’s flexibility during shearing, permitting the shearing motions required for normal mucosal wave motion without vasculature accidents. Considering the delicacy of vocal fold blood vessels and the force to which they are subjected, it is not surprising that vascular pathologies occur. It is convenient to divide common vascular lesions into three categories. A varix is an enlarged vein, or a large, acutely tortuous vessel. Varices may be parallel to the vibratory margin (normal orientation) or more perpendicular to the edge of the vocal fold (Fig. 22.1). A papillary ectasia is a blood-filled venous enlargement that appears similar to a spheroid hemangioma. Papillary ectasias may occur in small clusters and appear similar to coalescent hemangiomas (Fig. 22.2). A spider telangiectasia is a delicate network of inappropriately oriented blood vessels (Fig 22.3). Diagnosis is generally based on visual inspection. Examination should include high-quality, magnified visualization of the vocal fold. Strobovideolaryngoscopy is helpful not only in defining the extent of a lesion and its mobility or fixation to underlying tissues, but also the presence of surrounding stiffness that may have resulted from previous traumatic hemorrhage. Most varicosities and ectasias occur on the superior surface of the vocal fold, particularly near the mid portion of the musculomembranous portion of the vocal fold, where shearing forces are greatest. However, these lesions may occur on the vibratory margin and below the vibratory margin, as well. Hence, it is helpful to view the vocal fold tangentially

Fig. 22.1  Vocal fold varix (see arrow)

Fig. 22.2  Vocal fold papillary ectasia

with a laryngeal telescope during office evaluation, and to observe the vocal folds using 0, 30, and 70° laryngeal telescopes intraoperatively in order to map the vasculature accurately. True hemangiomas of the vocal fold are rare, but have occurred. In addition, other structures that may be mistaken for varicosities or ectasias include:

136

Surgical Management of Vocal Fold Vascular Lesions

 

22.4

Surgical Equipment

1. Standard phonomicrosurgery set (Chap. 10, Table 10.1). 2. Sataloff vascular knife (Medtronic-ENT, Jacksonville, Fla.),

or custom-made vascular knife, fashioned by bending a 30mm laryngeal injection needle 3. CO2 laser with a microspot delivery system (Chap. 13) 4. Pulsed dye laser or pulsed-KTP laser (Chap. 13)

22.5

Fig. 22.3  Vocal fold spider telangiectasia

■ ■ ■ ■

Limited acute hemorrhage Posthemorrhagic vocal fold cyst Vocal fold fibrous mass Normal blood vessels that are dilated from causes such as inflammation, premenstrual hormonal influences, pregnancy, recent extensive voice use, and other factors ■ Hemorrhagic vocal fold polyp

22.3

Surgical Indications and Contraindications

Indications for surgery comprise:

22

■ Hemorrhage from the lesion, particularly recurrent hemorrhage ■ Dysphonia caused by a lesion on or near the vibratory margin, interfering with vibration or glottic closure ■ Dysphonia or fatigue caused by a vascular lesion that engorges (“pumps up”) during heavy voice use, altering the mass and vibratory characteristics of the vocal fold Relative contraindications include: ■ Vascular abnormalities that occur only premenstrually and are unassociated with hemorrhage ■ It is usually possible to control these with hormonal manipulation. ■ Lesions associated with Osler–Weber–Rendu syndrome. ■ Minimally symptomatic lesions that have not bled, in high sopranos (coloraturas), because of increased risks of adverse effects on performance from even minimal postoperative stiffness. ■ Asymptomatic lesions that pose no significant risk of hemorrhage

Surgical Procedure

There are three primary approaches to vascular lesions including operative resection, operative CO2 laser coagulation or vaporization and pulsed laser therapy. This chapter concentrates on intraoperative resection, but all three options are addressed at least briefly below. 1. Operative resection a) Intubation with a 5.0 laser-safe endotracheal tube Although the laser will not be required in most cases, it is appropriate in some patients; and it is prudent for it to be available, and for appropriate airway precautions to be in place (see Chap. 13, “Principles of Laser Microlaryngoscopy”). b) Expose the larynx with suspension laryngoscopy. Use the largest laryngoscope that exposes the entire vocal fold adequately (see Chap. 10, “Principles of Phonomicrosurgery”) Anterior laryngeal pressure (stabilized with silk tape) can be used to bring the anterior commissure into view, if necessary. However, this maneuver alters vocal fold tension, slackens, and distorts the blood vessels, and can make blood vessel resection more difficult. It is preferable to obtain anterior commissure exposure through optimal laryngoscope selection. c) Careful evaluation of the vocal fold should be done with the 30 and 70° telescope through the suspended laryngoscope. Care should be taken to identify abnormal vascular lesions at the anterior commissure, midmembranous vocal fold region and near the vocal process. These are the areas in which vascular lesions are most commonly seen. The angled telescopes are especially useful for identifying vascular lesions arising in the infraglottic portion of the vocal folds. d) Vocal fold palpation should be done under high-power magnification looking for associated vocal fold pathology (sulcus vocalis, scar, polyp, etc.). e) Incision A superficial epithelial incision should be made immediately adjacent to the blood vessel. This can be made with a laryngeal sickle knife, but use of the knife is rarely required. The tip of the vascular knife is a sharp point. If the vascular knife is oriented parallel to the blood vessel and placed adjacent to it, then slight downward pressure with the back surface of the vascular knife tip is usually sufficient to create a small incision (2–3mm) adjacent to the varicosity (or other vascular lesion) (Fig. 22.4).

 

Chapter 22

f) Elevate the vessel Turn the vascular knife 90° and insert it underneath the vessel, hugging the vessel as closely as possible. The undersurface of the vascular knife is blunt and should not damage underlying tissues. The crook of the vascular knife is a right angle, and the vessel should rest in the crook of the instrument. In performing this maneuver, the point of the instrument is brought up through the epithelium on the other side of the blood vessel, allowing epithelial isolation with little or no epithelial resection (Fig. 22.5). – With gentle downward pressure (toward the vocal fold), the vascular knife is advanced anteriorly and posteriorly under the vessel, isolating and elevating it. The principle is similar to that used when placing a right angle clamp under a jugular vein to isolate and resect it during radical neck dissection. – Although there are no deep, penetrating vessels in normal anatomy, such vessels occur occasionally during resection of varicosities and ectasias. If possible, it is best to allow them to bleed until resection of the vessel is completed, and then to control them using a Cottonoid with topical epinephrine (ideally), further resection if the bleeding vessel is superficial, or CO2 laser cautery (1 or 2 W, 0.1 s, 30–40 mJ, slightly defocused). – Separate the vessel. Once the vessel has been elevated beyond the limits of abnormality, it is resected and preserved for histopathologic analysis. – Either the anterior or the posterior limit can be divided first. Simply cutting the vessel with the scissors is usually sufficient and bleeding from the normal vessel stops spontaneously. However, dividing the vessel with a brief CO2 laser burst is equally acceptable.

Fig. 22.4  Incision immediately lateral to vascular lesion

– The specimen is grasped gently with a microlaryngeal

alligator forceps, and the second end of the vessel is resected in a similar manner (Fig. 22.6). The lesion is removed and sent for histopathologic analysis. g) There is usually no bleeding. If there is mild hemorrhage, it can be controlled with one of the methods described in step f), above. More severe hemorrhage can also be controlled with cautery or the laser. This is not desirable near the vibratory margin, but in the lateral half of the vocal fold, this technique can be used safely when necessary. CO2 lasers are not effective at controlling vessels larger than 0.6 mm in diameter. h) If topical anesthetic was not applied to the larynx at the beginning of the case, it should be applied at the end of the case. 2. Operative CO2 laser cautery/vaporization a) Intubation and exposure are performed as described in above b) Instrumentation includes a CO2 laser with a microspot, suction, forceps and Cottonoid (see Chaps. 10, “Principles of Phonomicrosurgery” and 13, “Principles of Laser Microlaryngoscopy”). c) All laser safety precautions should be implemented including wet Cottonoids or wet gauze strips over the cuff of the endotracheal tube (see Chap. 13). d) In general, this author prefers not to use the laser for lesions on the vibratory margin or on the medial half of the vocal fold. Thermal injury in this area can cause stiffness that impairs vibration and can lead to permanent scarring. If the laser is used in the medial half of the musculomembranous vocal fold, then great care should be taken to be certain that the laser beam is tangential to the vibratory margin. When possible, an alligator or heart-shaped forceps should be used to gently retract the

Fig. 22.5  Dissection underneath vascular lesion

137

138

Surgical Management of Vocal Fold Vascular Lesions

Fig. 22.6  Excision of isolated vascular lesion

22

vibratory margin vessel into the glottis, so that the laser contact point is as far as possible from the vocal ligament (Fig. 22.7). For lesions on the superior surface, an alligator and small Cottonoid can be used to gently retract the mucosal laterally, so that the laser impact on the vessel is occurs not over the medial portion of the vocalis muscle, but rather lateral to the midline of the superior surface vocal fold. Lesions that occur laterally on the vocal fold (beyond the halfway point) can be treated effectively either by resection or vaporization. Chilling the vocal fold with ice, and using submucosal infusion of saline/adrenaline 1:10,000 solution, also help limit thermal injury. e) There are two approaches to CO2 laser management of varicosities and ectasias. The classic approach is cautery using 1–2 W, 0.1 second exposure time, 30–40 mJ, slightly defocused. This creates superficial cauterization of the vessel and minimizes thermal transfer to underlying tissues. The disadvantage of this technique is a fairly substantial recurrence rate (the vessel is found present a few months after surgery). Other laser surgeons (including Abitbol) use a focused beam and divide the vessel completely at several points. This may increase the risk of deeper thermal injury and stiffness, but it decreases the likelihood of recurrence. 3. Pulsed dye laser/pulsed-KTP laser The pulse dye and pulsed KTP laser are relatively new instruments, currently being evaluated for safety and efficacy in the treatment of various vocal fold lesions. They have an affinity for vascular structures. Preliminary experience suggests that these lasers may be an excellent tool for management of varicosities and ecta-

 

Fig. 22.7  Vascular lesion along free edge of the vocal fold; the mu-

cosa/varix is manipulated laterally with the alligator forceps by lateral traction

sias. They are utilized in an outpatient setting through a flexible endoscope with a working channel or passed peroral during simultaneous flexible laryngoscopy. As additional research is completed and clinical experience is acquired, laryngologists should consider this technology as a possible adjunct to, or replacement for, the options detailed above.

22.6

Postoperative Care and Complications

(See also Chap. 11, “Perioperative Care for Phonomicrosurgery”) If the lesion is on the vibratory margin, then voice rest for up to approximately 1 week is recommended. If the surgery has been limited to the superior surface of the vocal fold, voice rest generally is limited to 2–3 days, to be followed by gentle voice use. In some cases, voice rest is not prescribed at all (particularly if the cut ends of the offending vessel are in the anterior and posterior thirds of the vocal folds, where the shearing forces are much less likely to disrupt a blood clot than they are in the middle third of the vocal fold). For patients placed on voice rest, a session with a speech– language pathologist is arranged to bring the patient off voice rest at the appropriate time. After voice rest has been completed, gentle voice use is employed for at least 3–6 weeks from the time of surgery, to permit firm healing of the blood vessels before they are subjected to the phonatory forces of loud phonation or singing.

 

Postoperative care includes anti-reflux medications that were started prior to surgery and are continued after surgery. Pain medications that do not alter coagulation are prescribed. Drugs that do affect clotting are discontinued prior to surgery (the patient is provided with a list), and not resumed until at least 1 week after surgery, unless there is compelling medical necessity to start medications sooner (such as Coumadin). Antibiotics and steroids are not used routinely. Complications can include: ■ ■ ■ ■

Dental injury Pain, anesthesia/hypoesthesia of the tongue Dysgeusia Recanalization or recurrence of the vessel (particularly after laser cauterization) ■ Vocal fold stiffness, scarring, and consequent dysphonia Postoperative pain and neurologic dysfunction usually resolves spontaneously. Most commonly, recovery occurs within 2–3 weeks, but recovery may take 3 months. All patients receive preoperative and postoperative voice therapy. Vocal fold scarring is extremely rare with excision of vascular lesions. It occurs more commonly after laser treatment of vascular lesions. Scarring may produce disruption of the mucosal wave and substantial dysphonia when it occurs near the vibratory margin. However, scarring that occurs laterally also may impair voice function and be troublesome, especially to high-performance voice users. Adhesion of the mucosa to underlying tissues along the superior surface prevents the normal excursion and reflexion of the mucosal wave. Care should be exercised to minimize operative trauma at any point along the vocal fold, using cold or laser techniques, especially in singers.

Key Points ■ Vocal fold vascular lesions may occur at any location on the vocal fold and are categorized as: ■ Varix ■ Papillary ectasia ■ Spider telangiectasia

Chapter 22

■ Only vascular lesions that have caused bleeding or other symptoms should be treated surgically in most cases. ■ Some vascular lesions respond to hormonal manipulation or are asymptomatic and do not require surgical intervention. ■ Resection of vascular lesions with minimal disturbance of surrounding tissues provides the best chance to avoid scarring and recurrence. ■ The CO2 laser can be used for varicosities, particularly those not in the medial half of the vocal fold, but it adds an additional risk of thermal injury. Precautions must be used to minimize these risks if CO2 laser treatment is utilized. ■ Office-based treatment using pulsed dye laser/ pulsed KTP laser treatment is possible and should be considered in appropriate clinical settings. ■ Postoperative dysphonia is not common, particularly after resection with cold instruments but may occur, and patients should be counseled accordingly.

Selected Bibliography 1

2

3

4 5

Hirano S, Yamashita M, Kitamura M, Takagita S (2006) Photocoagulation of microvascular and hemorrhagic lesions of the vocal fold with the KTP laser. Ann Otol Rhinol Laryngol 115:253–259 Hochman I, Sataloff RT, Hillman RE, Zeitels SM (1998) Ectasias and varices of the vocal folds: clearing the striking zone. Ann Otol Rhinol Laryngol 108:10–16 Hsiung MW, Kang BH, Su WF, Pai L, Wang HW (2003) Clearing microvascular lesions of the true vocal fold with the KTP/523 laser. Ann Otol Rhinol Laryngol 112:534–539 Postma GN, Courey MS, Ossoff RH (1998) Microvascular lesions of the true vocal fold. Ann Otol Rhinol Laryngol 107:472–476 Zeitels SM, Akst LM, Burns JA, Hillman RE, Broadhurst MS, Anderson RR (2006) Pulsed angiolytic laser treatment of ecstasies and varices in singers. Ann Otol Rhinol Laryngol 115:571–580

139

Chapter 23

23

Vocal Fold Scar and Sulcus Vocalis

23.1

Fundamental and Related Chapters

Please see Chaps. 4, 7, 8, 10, 32, and 48 for further information.

23.2

(Fig. 23.3). Frequently, this mucosal bridge causes diplophonia and severe dysphonia because of its separate vibratory characteristics from the main vocal fold.

Disease Characteristics and Differential Diagnosis

Vocal fold scar (Fig. 23.1) and sulcus vocalis (Fig. 23.2) are two similar pathologic processes that involve derangement and abnormalities of the lamina propria resulting in dysphonia, glottic insufficiency, and severe abnormality in the pliability of the vocal fold. The primary difference between vocal fold scar and sulcus vocalis is the type of alteration that occurs within the lamina propria. Sulcus vocalis is characterized by an absorption or loss of the lamina propria resulting in a deep, linear furrow along the free edge of the vocal fold. Vocal fold scar is characterized by a deposition of abnormal tissue within the lamina propria, typically thick, fibrous tissue. The symptoms of patients with vocal fold scar and sulcus vocalis include dysphonia, decreased volume, effortful phonation, diplophonia, increased pitch, and a breathy, severe, harsh voice quality. The etiology of sulcus vocalis is usually associated with an acquired condition due to excessive voice use or trauma to the vocal folds. There are also reports of a congenital deformation of the vocal fold resulting in sulcus vocalis; however, this is a much rarer condition. Vocal fold scar is an acquired condition from some type of traumatic activity of the vocal folds. This can occur from repeated vocal fold hemorrhage, external laryngeal trauma, intubation injury, and excessive laser or cold-steel phonomicrosurgery. The most common cause of vocal fold scar, and most likely sulcus vocalis, is phonotraumatic behavior characterized by misuse, overuse, or inappropriate use of the voice. This typically occurs over a prolonged period, resulting in either absorption of the lamina propria (sulcus vocalis) or deposition of abnormal tissue within the lamina propria (vocal fold scar). A variety of associated lesions can occur with sulcus vocalis and vocal fold scar, most notably, vocal fold cyst and fibrous mass. These two lesions can occur in a subepithelial or ligamentous area (see Chap. 4, “Pathological Conditions of the Vocal Fold”). Unique to sulcus vocalis is the formation of a mucosal bridge. A mucosal bridge is a thin band of mucosa that runs parallel to the vocal fold. It is connected anteriorly and posteriorly but not attached to the free edge of the vocal fold

Fig. 23.1  Sulcus vocalis

Fig. 23.2  Vocal fold scar

142

Vocal Fold Scar and Sulcus Vocalis

Fig. 23.3  Mucosal bridge associated with sulcus vocalis

Differential diagnosis of vocal fold scar and sulcus vocalis include: ■ ■ ■ ■

Fibrous mass Polyp Vocal fold cyst Rheumatologic lesions of the vocal folds

Vocal fold atrophy due to muscle loss and a thinned lamina propria can have a similar appearance on laryngeal exam to sulcus vocalis, given that in both entities the vocal fold will have a “bowed” appearance. The difference between vocal fold atrophy and sulcus vocalis is the lamina propria stiffness that occurs in sulcus vocalis but is not present in vocal fold atrophy.

 

Often the first surgical step is a diagnostic microlaryngoscopy. This is important for planning purposes and to determine the severity of the vocal fold pathology and the severity of the condition as well as to remove associated lesions such as fibrous mass, cysts, and/or mucosal bridge. One of the key aspects of the indications for surgery and the surgical approach for the treatment of patients with vocal fold scar/sulcus vocalis is to ascertain the degree of glottal insufficiency associated with the vocal fold scar and sulcus vocalis as well as the symptoms of vocal fatigue and decreased volume. For patients with a significant amount of glottal insufficiency and the primary symptoms of vocal fatigue and decreased volume, a vocal fold augmentation procedure or medialization procedure is often the appropriate first step for patients with vocal fold scar and sulcus vocalis (see Chaps. 31, “Vocal Fold Augmentation via Direct Laryngoscopy”; 33, “Peroral Vocal Fold Augmentation in the Clinic Setting”; 34, “Percutaneous Vocal Fold Augmentation in the Clinic Setting”; 38, “Silastic Medialization Laryngoplasty for Unilateral Vocal Fold Paralysis”; and 39, “GORE-TEX® Medialization Laryngoplasty”). After the patient’s glottal insufficiency has been addressed by vocal fold augmentation or medialization if needed, often a direct approach to the lamina propria deficit associated with vocal fold scar and sulcus vocalis is indicated. This can be achieved with the following different approaches: 1. Excision of associated lesion (Chaps. 10, “Principles of Phonomicrosurgery” and 17, “Vocal Fold Cyst and Vocal Fold Fibrous Mass”) 2. Excision of sulcus vocalis/vocal fold scar and mucosal reapproximation (see below) 3. Vocal fold fat graft reconstruction (see below) 4. Superficial vocal fold injection of collagen based materials (Chap. 32, “Superficial Vocal Fold Augmentation via Microlaryngoscopy”) 5. Gray minithyrotomy (Chap. 48, “Gray Minithyrotomy for Vocal Fold Scar/Sulcus Vocalis”) Contraindications comprise:

23.3

23

Surgical Indications and Contraindications

The medical and surgical approaches to patients with vocal fold scar and sulcus vocalis are very similar. As in the approach to most voice disorders, maximum nonsurgical approach should be utilized for the treatment of voice disorders for patients with sulcus vocalis and vocal fold scar. This typically includes treatment of medical conditions such as LPR and allergic disease, as well as optimizing speaking and singing techniques with voice therapy and singing voice therapy (see Chap. 7, “Nonsurgical Treatment of Voice Disorders”). After maximum nonsurgical therapeutic applications, a careful evaluation of the functional limitations associated with the patient’s voice disorder should be undertaken, especially by using a multidisciplinary approach with a medical and a speech–language pathology evaluation. Surgery is indicated if the significant functional limitations remain after nonsurgical treatment (see Chap. 8, “Timing, Planning, and Decision Making in Phonosurgery”).

■ Unreasonable expectations regarding voice quality improvement (i. e., complete resumption of normal voice) ■ Persistent phonotraumatic behavior ■ Untreated LPR ■ Active rheumatologic disease (rheumatoid arthritis, Wegener’s granulomatosis, etc.) ■ Anatomic factors resulting in poor laryngoscope visualization (relative) In summary, a comprehensive approach to patients with sulcus vocalis and vocal fold scar involves the following: 1. Detailed, multidisciplinary evaluation (may include diagnostic microlaryngoscopy) 2. Maximum nonsurgical rehabilitation 3. Proper assessment of functional voice limitations and establishment of reasonable goals with surgical therapy 4. Excision of associated lesions 5. Augmentation or medialization of the vocal folds if warranted

 

Chapter 23

6. Direct reconstruction of lamina propria using: a) Superficial vocal fold injection (Chap. 32, “Superficial

Vocal Fold Augmentation via Microlaryngoscopy”) b) Fat graft reconstruction via microlaryngoscopy (see below) c) Gray minithyrotomy (Chap. 48, “Gray Minithyrotomy for Vocal Fold Scar/Sulcus Vocalis”)

23.4

Surgical Equipment

Surgical equipment includes the following: ■ ■ ■ ■ ■

Standard phonomicrosurgery set (Table 10.1) Knot pusher Regular insulin (100-U bottle) Lactated ringers (l liter) 5.0, 6.0, and 7.0 absorbable suture with a variety of small microsurgical needles (often found in ophthalmology operating room supplies) ■ Microlaryngoscopy needle holder

23.5

Surgical Procedure

1. Excision with reapproximation via microlaryngoscopy

The goal of this procedure is to remove invaginated epithelial tissue associated with sulcus vocalis and reapproximate adjacent normal mucosa with sutures. This approach can also be used with vocal fold scar, using a microflap approach, excising abnormal vocal fold scar in the subepithelial plane and then reapproximating adjacent normal mucosa with microsutures. A concern regarding this approach should be the eventual “rounding” of the vocal fold morphology, especially along the free edge of the vocal fold. Thus, this approach is indicated when there is only small epithelial defects or when there has been no mucosal excision required as part of the approach. The advantage to this approach is that it will result in a straight, smooth vocal fold edge, which is often a preparatory step for later reconstruction using fat graft reconstruction or Gray’s minithyrotomy or superficial vocal fold injection with collagen based material. a) Complete exposure of vocal folds with a large laryngoscope (see Chap. 10) b) Endoscopic visualization with angled endoscopes and vocal fold palpation with high-powered microlaryngoscopy assessing the severity and nature of the vocal fold pathology c) Subepithelial infusion of 1:10,000 epinephrine in attempt to hydrodissect and clearly delineate the area of the sulcus vocalis/vocal fold scar d) Mucosal cordotomy at the junction of normal vocal fold epithelium and the sulcus vocalis deformity at both the upper and lower aspect of the deformity e) Submucosal excision of the sulcus vocalis

f) Subepithelial dissection of a superiorly based flap (back

elevation) and subepithelial elevation of an inferiorly based mucosal flap in preparation for reapproximation g) Suture reapproximation of cut edges of the mucosa resulting in approximation of the mucosal cut surfaces (see part 4., below) 2. Vocal fold slicing technique via microlaryngoscopy (as described by Paulo Pontes) The objective of the vocal fold slicing technique is to reduce the glottal gap and to increase vocal fold vibration in order to improve phonation in cases presenting with severe sulcus vocalis and vocal fold scar. Contraindications a) Lack of patient understanding of the procedure b) Lack of acceptance of aphonia for 4 months c) Limitations for receiving postoperative voice therapy Surgical procedure: methods and techniques The main principle of this technique is to “break” the tension caused by the ligamental alteration in order to obtain vibration and to reduce the glottal gap, which is achieved by the resultant displacement of a more flexible and bulky tissue from the free edge of the vocal fold. a) General anesthesia and orotracheal intubation b) Endolaryngeal exposure with suspension microlaryngoscopy c) Incision on the superior surface of the vocal fold (anterior–posterior), parallel to the free edge of the vocal fold The cordotomy should be made 3–4 mm lateral to the free edge of the vocal fold (Fig. 23.4).

Fig. 23.4  Sulcus vocalis with proposed incision lines (dashed) for the

slicing technique of Pontes

143

144

Vocal Fold Scar and Sulcus Vocalis

Fig. 23.5  Raising deep flap with flap elevator

23

Fig. 23.7  Asymmetric superior-inferior incisions through the vocal

fold microflap

 

Fig. 23.6  Slicing of deep flap

d) Deep dissection to create a mucosal flap The vocal ligament is included inside this flap and, if it remains thin, a portion of the muscle may be also included to preserve arterial supply (Fig. 23.5). e) The dissection should extend inferiorly to approximately 3 mm beneath the inferior border of the sulcus. f) Place small incisions, caudally oriented, in the superior margin of the flap to create three or four smaller flaps (inferiorly based) (Fig. 23.6). Gradually deepen the incisions to avoid retraction of the initial flap (Fig. 23.7). g) The central microflaps should be of different lengths and should pass over the ligament in the inferior lip. Different lengths are useful to maintain ligament fragments in different heights, which must be intraoperatively observed as soon as the microflaps retract themselves. h) The technique should be done bilaterally when there is bilateral disease not dependent on the sulcus asymmetry. i) Care is taken to preserve intact mucosa on both sides around the anterior commissure. j) Glue or sutures are not useful or needed. Postoperative care a) Prophylactic oral antibiotics b) Voice rest for 3 days c) Vocal exercise, speech therapy i. Vocal exercises should begin around the seventh postoperative day, initially with vibration exercises to make tissues flexible and to help remove fibrin, thus avoiding adherences.

 

Chapter 23

Fig. 23.8  Placement for incision and area of proposed elevation of

Fig. 23.9  Elevation of pocket in preparation for fat graft implantation

ii. Voice quality will remain poor for 3–4 months. When healing has completed (~4 months), the vocal fold surfaces appear more regular compared to the preoperative pattern. The vocal folds exhibit greater flexibility and vibration in spite of the reduction or absence of the mucosal wave. The glottic gap disappears or is dramatically reduced. Complications a) Thin adherences can occur and should be cut in 2–3 weeks. b) Granulomas can occur but can be left intact because spontaneous remission typically occurs, avoiding the creation of depressions. They should only be resected if too large and/or fibrotic. 3. Vocal fold fat graft reconstruction via microlaryngoscopy This procedure is aimed at developing a pocket in the pathologic lamina propria with or without excision of the associated vocal fold scar and laying small grafts of autologous fat into the pocket for “reconstruction” of the lamina propria and improved lamina propria function postoperatively. This entire procedure is done via microlaryngoscopy with simultaneous fat graft harvest. The fat graft harvest technique is discussed separately (see below). a) Place largest possible laryngoscope for allowing full visualization of the vocal fold. (Note: This procedure is difficult to perform via a small laryngoscope because of the complexity of the dissection and the need for placement of sutures within the vocal fold.) b) Angled visualization of the vocal fold pathology via telescopes (see Chap. 10, “Principles of Phonomicro­ surgery”)

c) Vocal fold palpation to assess vocal fold scar and sulcus

overlying microflap for vocal fold fat graft reconstruction

vocalis pathology and severity (during the palpation and angled visualization steps, potential surgical incisions on the vocal folds should be considered) d) An incision is then made with a microknife (sickle) through the mucosa immediately lateral to the area of the vocal fold scar/sulcus vocalis. The placement of the incision should be carefully done to allow enough mucosa medial and lateral to the incision for microsuture placement. It is wise to make this incision longer in the anterior–posterior dimension than typically required to have complete exposure of the area of vocal fold scar/sulcus vocalis (Fig. 23.8). e) Carefully elevate the mucosa off the ligament and underlying vocal fold scar. This should be done in a slow, careful fashion, making great effort to avoid fenestration of the overlying mucosa. This will significantly hamper the success or ability to perform fat graft reconstruction (Fig. 23.9). f) Remove any associated lesion or scar once the microflap elevation is performed. g) Verify that there is a wide pocket in the area of the vocal fold scar/sulcus vocalis, in both the anterior–posterior dimension as well as the superior–inferior dimension. h) Place suture through the cut mucosal edges both medial and lateral but not tying or throwing any knots with this suture now (Fig. 23.10). Each free end of the suture can be secured outside the laryngoscope with a small bulldog clamp (see below section on placement of sutures in vocal fold.) i) Directly implant fat grafts into the pocket. The pocket should be filled with the maximum amount of fat graft

145

146

Vocal Fold Scar and Sulcus Vocalis

Fig. 23.10  Pocket in area of vocal fold scar elevated and sutures placed

through mucosal edges

possible, allowing complete or close approximation of the mucosal edges at the incision location (fat harvest techniques as described below) (Fig. 23.11). j) Tie three knots of the previously thrown suture through the mucosal cut edges (see below) (Fig. 23.12). k) Palpate free edge of vocal fold to ensure the fat graft implants are stable in the pocket and do not easily come out of the mucosal incision with a moderate amount of pressure along the free edge of the vocal fold.

 

Fig. 23.11  Placement of fat grafts into pocket of previously elevated

vocal fold scar

4. Placement of sutures in the vocal fold

Placement of sutures in the vocal fold is intended to assist the reapproximation of mucosal flaps in the vocal fold. This is most commonly used for fat graft reconstruction but can also be used for a variety of microflaps associated with glottic web surgery. Placement of sutures should be carefully planned to allow adequate mucosal closure of the vocal fold without distortion of the shape of the vocal fold. If too “aggressive” placement of a suture on either side of the mucosal

23

Fig. 23.12  Postoperative result after fat graft reconstruction

Fig. 23.13  Placement of needle through mucosa during suturing of

the vocal fold mucosa

 

incision is done, a “pinching” of the vocal fold will occur at the suture site and this will be counter productive to the surgical procedure at hand. The direction of passing from right to left or left to right depends on which vocal fold is being sutured and the handedness of the surgeon. In general, it is difficult to backhand the suture via a microlaryngoscopy approach and thus, a right-handed surgeon will typically pass the suture through the cut edges of the mucosa right to left (vice versa for a lefthanded surgeon). The needle should be placed within 1–1.5 mm of each mucosal edge. a) Typically, the microsuture is placed through each mucosal edge in a separate pass of the needle and thus, the surgeon should plan not to pass the needle through both cut edges in one movement of the needle. This allows for more control of the placement of the needle through the mucosal edge, which is essential. Furthermore, the mucosal free edge does usually not need to be held with another instrument while the needle is placed, given that with the proper angle preparation of the microsurgical needle, it will pass quite easily through the mucosal flap. The needle is typically held and passed through the mucosal flap using a microlaryngoscopy needle holder. Another option is using a straight alligator, however, the microlaryngoscopy suture holder has somewhat broader jaws, which will hold the needle in a more stable fashion and allow better control of the needle as it passes through the mucosal flap. After the first part of the needle has penetrated and passed completely through the mucosal surface, the suture holder is released and either the suture holder or a curved alligator is used to complete the passing of the needle through the mucosal edge. As the needle is drawn through the mucosal edge, the curve of the needle should be continued in a careful and gentle fashion to avoid applying undue stress or trauma to the vocal fold, which may tear the mucosal flap (Fig. 23.13). b) After the needle is passed through each side of the free edge of the mucosa, both ends of the suture are brought out through the proximal portion of the laryngoscope. c) A moderate amount of tension should be placed on the suture during high-powered microlaryngoscopy visualization to ensure that the suture has been placed through the free edges of the mucosa in the appropriate fashion. If the surgeon is dissatisfied with the suture location, then the suture should be removed and the process repeated. d) Using the two ends of the suture outside the laryngoscope, a simple knot can be tied using a straight alligator and a free hand (Fig. 23.14a). e) After a single knot has been tied, one end of the suture is held with the surgeon’s nondominant hand outside the laryngoscope, and the other end can be loosely held by an assistant. f) The knot pusher is then placed around the knot outside of the laryngoscope and slowly used to pass the knot down the laryngoscope towards the vocal fold. As the knot pusher moves the knot down the laryngoscope, the assistant and the surgeon’s other hand can be used

Chapter 23

to maintain a “relaxed” tension on the suture arms, thus allowing the knot to be slipped down into position at the vocal fold (Fig. 23.14b). g) Once the knot is close to the vocal fold, the free ends of the suture are released by the surgeon and the assistant. h) The two strands of the suture coming off the knot near the knot are then grasped with a straight and/or curved alligator under visualization with high-powered microlaryngoscopy. i) The knot is then slowly tightened with the alligators, with great care taken to not overtighten the knot. If the knot is too tight, then the vocal fold morphology will be significantly distorted and will then result in a poor vocal outcome (Fig. 23.14c). j) The knot should be tightened enough to allow close approximation of the mucosal edges, but not strangulation of the associated tissue and deformation of the morphology of the vocal fold. An approximately 1-mm gap should be preserved between the mucosal surface of the vocal fold and the tied knot (Fig. 23.12). k) Scissors can be used to cut the ends of the suture, approximately 2–3 mm away from the knot, after two more additional knots have been thrown in the exact same fashion. Alternate method of suture placement/knot tying a) Both ends of the suture are grasped with mosquito hemostats, and an additional hemostat is placed between sutures distal, close to the opening of the laryngoscope (Fig. 23.15a). b) The left (white suture in Fig. 23.15a) suture is looped around the right suture a total of three times clockwise. The free end of the left (white) suture is advanced toward the initial (distal) crossing of the two strands of suture (Fig. 23.15b). c) The free ends of the left (white) suture are used to create a slipknot around the open loop adjacent to the distal stationary hemostat. Microlaryngeal alligator forceps are used to grasp the left (white) suture at its final “crossing”; this step prevents the knot from forming prematurely and subsequently breaking. The end of the suture is marked with a pen for easier identification under the microscope during knot tying (Fig. 23.15c). d) The loose knot assembly is advanced down the laryngoscope by pushing distally with microalligator forceps while pulling back on the other (black) suture. When the level of the vocal folds is reached, the knot assembly is released, taking care not to allow the loose knot assembly to untie (Fig. 23.15d). e) The microscope is then brought into the field and the free end of the left (white) suture is grasped with microalligator forceps and advanced distally, while providing counter-tension with the opposite (black) suture. A secure knot will form at the level of the vocal folds, as depicted (Fig. 23.15e). 5. Fat graft harvest and preparation A small amount of fat of various sizes is required for fat graft vocal fold reconstruction. The harvest locations can be the ear lobe, axilla, umbilicus, or prior scar location. The fat

147

148

Vocal Fold Scar and Sulcus Vocalis

 

23.14   a Tying of suture outside proximal end of the laryngoscope. b Knot pusher passing knot down the laryngoscope. c Final position and

23

tension applied to the knot with bimanual control of the two suture ends

is typically taken from subcutaneous area. The axilla is the author’s preferred site, making a small incision at the anterior axillary line, because this area is easily accessible during microlaryngoscopy and the incision is hidden in the axilla. a) Inject local anesthesia at the proposed harvest site. b) Prepare the skin with antiseptic. c) A small skin incision is used to expose the subcutaneous fat (approximately 5 mm).

d) Harvest fat with scissors, taking care not to include any as-

sociated dermis, hair follicles, or to use electric cautery

e) Cut fat into small pieces approximately 1 × 1 × 1 mm. f) Rinse the harvested fat with approximately 1 liter of sa-

line.

g) Soak the fat in regular insulin for 5 min (see Chap. 31,

“Vocal Fold Augmentation via Direct Laryngoscopy”)

 

Chapter 23

Fig. 23.15a–e  Initial configuration of alternate knot tying method. b Counterclockwise looping of suture. c Addition loop is passed proxi-

mally, while the end of the suture is marked. d The knot assembly is advanced down the laryngoscope. e Final tying of knot under the micro­ scope

149

150

Vocal Fold Scar and Sulcus Vocalis

23.6

Postoperative Care and Complications

To avoid possible complications postoperatively: ■ Strict voice rest for 6–7 days and subsequently graduated voice use ■ Perioperative antibiotic use is appropriate ■ There is no indication for prolonged use of perioperative steroids ■ Continue LPR treatment, which is optimally started perioperatively and continued postoperatively for a short period Complications associated with vocal fold fat graft reconstruction microlaryngoscopy include (see Chap. 12, “Management and Prevention of Complications Related to Phonomicrosurgery”): ■ Fat extrusion at the mucosal cut edge ■ Fat reabsorption ■ Further vocal fold scar at the operative site. This is a theoretical complication and has not been seen.

 

Selected Bibliography 1

2

3

4 5

6

7 8

Key Points 9

23

■ Surgery for vocal fold scar and sulcus vocalis can be very rewarding to the severely impaired voice patient. Reasonable expectations and willingness to have several surgeries are required in most cases. ■ Maximum nonsurgical therapy should be done prior to proceeding with surgery for vocal fold scar/sulcus vocalis. ■ Patients with vocal fold scar and sulcus vocalis with significant glottic insufficiency related symptoms (vocal fatigue, decrease volume, etc.) should strongly consider having vocal fold augmentation or medialization as the first step of treatment and potentially the only treatment needed. ■ Direct rehabilitation of the injured lamina propria can be done via superficial vocal fold injection, excision of the vocal fold scar/sulcus vocalis and reapproximation, fat graft vocal fold reconstruction or a Gray’s minithyrotomy.

Fleming DJ, McGuff S, Simpson CB (2001) Comparison of microflap healing outcomes with traditional and microsuturing techniques: initial results in a canine model. Ann Otol Rhinol Laryngol 110:707–12 Ford CN, Inagi K, Khidr A, Bless DM, Gilchrist KW (1996) Sulcus vocalis: a rational analytical approach to diagnosis and management. Ann Otol Rhinol Laryngol 105:189–200 Neuenschwander MC, Sataloff RT, Abaza MM, Hawkshaw MJ, Reiter D, Spiegel JR (2001) Management of vocal fold scar with autologous fat implantation: perceptual results. J Voice 15:295–304 Pinho SR, Pontes P (2002) Escala de avaliação perceptive da fonte glótica: RASAT. Vox Brasilis 8:11–13 Pontes P, Behlau M (1993) Treatment of sulcus vocalis: auditory perceptual and acoustical analysis of the slicing mucosa surgical technique. J Voice 7:365–376 Pontes PAL, Behlau M (1993) Treatment of sulcus vocalis: auditory perceptual and acoustical analysis of the slicing mucosa surgical technique. J Voice 7:365–376 Rosen CA (2000) Vocal fold scar: evaluation and treatment. Otolaryngol Clin N Am 33:1081–1086 Sataloff RT, Spiegel JR, Hawkshaw M, Rosen DC, Heuer RJ (1997) Autologous fat implantation for vocal fold scar: a preliminary report. J Voice 11:238–246 Woo P, Casper J, Griffin B, Colton R, Brewer D (1995) Endoscopic microsuture repair of vocal fold defects. J Voice 9:332–339

Chapter 24

24

Endoscopic Management of Teflon Granuloma

24.1

Fundamental and Related Chapters

Please see Chaps. 8, 10, 13, and 42 for further information.

24.2

Disease Characteristics and Differential Diagnosis

In every Teflon injection, an inflammatory response to the Teflon occurs. In most cases, the inflammatory response remains localized, and no significant clinical complications are noted. However, there is a risk of clinically evident expansile granuloma formation in these patients. Often this occurs years after the initial injection, after a prolonged period of good voice. Anecdotal evidence suggests that subsequent laryngeal trauma (i. e., intubation) may contribute to growth of the granuloma. Teflon granuloma is typically a submucosal smooth mass that presents as a bulge in the false vocal cord, ventricular mucosa and/or the true vocal fold (Fig. 24.1). The granuloma may grow inferiorly resulting in a subglottic bulge as well. Videostroboscopy is quite consistent in these patients, revealing a stiff, nonvibratory vocal fold mass. This is due to either mass effect (stretching of vocal fold mucosa with dampening of wave) or, more commonly, the infiltration of the granuloma into the lamina propria and/or mucosa. Glottic incompetence is commonly present, secondary to the mass lesion. Occasionally, the patient’s airway is compromised, especially if the granuloma is subglottic. It is helpful to obtain a CT scan of the neck with contrast to assess the location of the Teflon and the extent of granuloma formation. In this way, superficial Teflon granulomas can be distinguished from granulomas that are more extensive. Typical CT appearance is a brightly enhancing, fairly well-circumscribed mass in the paraglottic space.

24.3

Contraindications are: ■ Attempted complete removal of granuloma—this is not possible endoscopically with these lesions ■ Severe medical comorbidities that preclude surgery

24.4

Surgical Equipment

Equipment comprises standard laser microlaryngoscopy set (Chap. 13, “Principles of Laser Microlaryngoscopy”).

24.5

Surgical Procedure

The procedure is performed as follows: 1. Intubate patient with laser-protected tube. Protect patient, ETT, and OR personnel, (see Chap. 13., “Principles of Laser Microlaryngoscopy”). 2. Palpate involved vocal fold, and examine with angled telescopes to define the extent of the granuloma in a vertical plane.

Surgical Indications and Contraindications

Indications include: ■ Dysphonia due to expanding Teflon granuloma, especially if the granuloma appears to extend to the medial edge of the vocal fold ■ Airway compromise due to expanding granuloma ■ Desire for subtotal removal of granuloma

Fig. 24.1  Photo of Teflon granuloma on the left vocal fold. Note con-

vex bulge due to expansile granuloma

152

Endoscopic Management of Teflon Granuloma

 

Fig. 24.2  Planned incision for Teflon granuloma removal

Fig. 24.3  Laser ablation of Teflon mass

Fig. 24.4  Coronal diagram of Teflon granuloma

Fig. 24.5  Diagram depicting the area of proposed removal of the

3. The CO2 laser with the micromanipulator should be placed

5. The laser can be used to ablate the Teflon mass in the para-

24 on a setting between 4 and 8 W superpulse or intermittent with an on time of 0.1 s/off time of 0.5 s. 4. Outline the incision (using spaced laser marks) at the lateral aspect of the superior surface of the true vocal fold (Fig. 24.2). Dissection with the CO2 laser and/or microlaryngeal instrumentation is performed until the Teflon is encountered—recognized by its characteristic “sparkle” when vaporized by the laser.

granuloma (pink) at the medial edge of the vocal fold, from superior to inferior. Note the lateral extension of the excision infraglottically

glottic space (Fig. 24.3). The most medial portion of the granuloma should be first obliterated in an even fashion from superior to inferior. 6. The mucosa/lamina propria portion of the vocal fold that is retracted for preservation and exposure purposes can be intermittently redraped to assess the morphology of the infraglottic and true vocal fold.

 

Chapter 24

Fig. 24.8  Postoperative photograph after typical endoscopic Teflon Fig. 24.6  Immediately after CO2 laser ablation, showing infraglottic

contour

granuloma removal. Note reduction of convex bulge compared to preoperative (Fig. 24.1) and intact tissue at free edge of vocal fold

24.6

Postoperative Care and Complications

■ The most feared complication is a laser fire. Laser precautions must be followed, especially the use of a laser-protected tube and oxygen concentrations of 35% or less. ■ Voice rest should be between 3 and 7 days, depending on the clinical situation. ■ PPIs and pain medicine. Antibiotics are optional. ■ There is a small risk of igniting the granuloma with the CO2 laser, but this is minimized to a negligible level using lower-power setting. ■ Because the Teflon is often exposed with this approach, there can granulation tissue formation post operatively. This is managed conservatively with PPIs and observation. It should resolve over several weeks. Preserving intact mucosa on the free edge and infraglottic surface of the vocal fold will minimize this complication.

Fig. 24.7  Postoperative result

7. An adequate amount of Teflon should be removed to create

an anatomically correct infraglottic anatomy (inverted cone) and a straight free edge of the vocal fold (Fig. 24.5, 24.6). 8. Completion of the procedure is achieved when the vocal fold soft tissue is redraped over the residual Teflon mass operative site. Sutures can be place at the cordotomy site as needed; however, this is usually not necessary. 9. Completed excision, showing relatively symmetric appearance of the operated an uninvolved vocal fold (Figs. 24.7, Fig. 24.8).

Key Points ■ Teflon granuloma typically present many years after injection, with slowly worsening dysphonia that may progress to airway difficulties. ■ Although complete removal of Teflon granuloma is frequently not possible using an endoscopic approach, symptomatic improvement can be achieved. ■ The goal of endoscopic treatment for Teflon granuloma of the larynx is to recontour a straight edge to the involved vocal fold.

153

154

Endoscopic Management of Teflon Granuloma

 

Selected Bibliography 1 2

24

Dedo HH (1992) Injection and removal of Teflon for unilateral vocal cord paralysis. Ann Otol Rhinol Laryngol 101:81–86 Nakayama M, Ford CN, Bless DM (1993) Teflon vocal fold augmentation: failures and management in 28 cases. Otolaryngol Head Neck Surg 109:493–498

3

Ossoff RH, Koriwchak MJ, Netterville JL et al (1993) Difficulties in endoscopic removal of teflon granulomas of the vocal fold. Ann Otol Rhinol Laryngol 102:405–412

Chapter 25

Endoscopic Excision of Saccular Cyst

25.1

Fundamental and Related Chapters

Please see Chaps. 10, 11, 12, 13, and 43 for further information.

25.2

increased incidence of dilated saccules in patients with squamous cell carcinoma of the larynx. Fine cut (1–1.5 mm) CT scan of the larynx with contrast is recommended to confirm the diagnosis, and to define the extent of the cyst (Fig. 25.3).

Disease Characteristics and Differential Diagnosis

The normal saccule arises as a diverticulum originating at the anterior portion of the ventricle, and extending upward into the supraglottis. It is sandwiched between the false vocal fold medially and the aryepiglotticus muscle and thyroid cartilage laterally. The saccule contains numerous mucus-secreting glands, and acts as a reservoir, expressing secretions onto the vocal folds due to the squeezing action of the surrounding supraglottic musculature. A saccular cyst is a mucous-filled dilation of the laryngeal saccule, and can be categorized as congenital or acquired. Two anatomic types of saccular cysts exist: anterior and lateral. Anterior saccular cysts tend to be smaller in size, and project into the laryngeal lumen in the anterior ventricular region. Lateral saccular cysts are typically larger and present as a bulge in false vocal fold and/or aryepiglottic fold. (Figs. 25.1, 25.2) In rare cases, the cyst can extend into the neck through the thyrohyoid membrane, although this is more typical of a laryngopyocele. Although most saccular cysts are benign in nature, there is an

Fig. 25.1  Saccular cyst, anterior

25

Fig. 25.2  Saccular cyst, lateral

Fig. 25.3  CT scan of bilateral saccular cysts

156

Endoscopic Excision of Saccular Cyst

25.3

Surgical Indications and Contraindications

Indications for excisional intervention include: 1. Hoarseness 2. Airway compromise 3. Concern of malignancy (especially in patient with smoking history) In nonsmoking asymptomatic patients, and medically infirm patients for whom elective surgery is contraindicated, observation is acceptable. Periodic reexamination of the larynx with photodocumentation and/or CT scanning may be warranted to monitor for any changes of the cyst. Relative contraindications include: ■ Pediatric cases (external approach favored) ■ Extension of the cystic mass into the neck (external approach recommended)

25.4

Surgical Equipment

Equipment needed includes: ■ Standard laser microlaryngoscopy set (Chap. 13) ■ Laryngeal bipolar device (Instrumentarium, Montreal, Quebec, Canada) ■ Lindholm or bivalue type laryngoscope ■ CO2 laser

 

25.5

Surgical Procedure for Saccular Cyst

The following procedure is adapted from Hogikyan et al.: 1. Intubation with 5 or 5.5 laser-protected ETT 2. Expose supraglottis on involved side widely (Lindholm or bivalve laryngoscope often needed) (Fig. 25.4) and place in suspension. The distal tip of the Lindholm laryngoscope rests in the vallecula to achieve wide supraglottic exposure. 3. Observe standard laser precautions (see Chap. 13, “Principles of Laser Microlaryngoscopy”) a) Moist eye pads, and towels covering patient fully b) Moist Cottonoid placed above ETT balloon c) O2 concentration 35% or less d) Protective eyewear for OR personnel 4. A curvilinear laser mucosal incision is made over the lateral aspect of the false vocal fold. A lateral relaxing incision may be required into the aryepiglottic fold in some cases, if lateral extension is extensive (Fig. 25.5). 5. The lateral extension of the cyst is dissected, retracting the mucosa medially, and using blunt dissection with a 5French suction (a 30° dull flap elevator can be used, but is likely to cause perforation of the cyst, which may complicate the resection) (Fig. 25.6). This lateral dissection can extend to the thyroid ala, and branches of the superior laryngeal vasculature may cause troublesome bleeding. Suction and bipolar laryngeal cautery are often useful, as the laser may be ineffective in stopping bleeding from larger vessels such as these. 6. The dissection is continued around the inferior aspect of the cyst, using blunt dissection with 5-French suction, and scissors as needed (Fig. 25.7).

25

Fig. 25.4  Lindholm laryngoscope (Karl Storz, Tuttlingen, Germany)

Fig. 25.5  Incision locations

 

Chapter 25

7. Taking care to protect the underlying true vocal fold using

platform suction, the anterior and posterior cuts are made with the laser (Fig. 25.8). These cuts encompass the full extent of the cyst, and include the attached mucosa of the ventricle and false vocal fold (FVF) with the specimen, to prevent recurrence. A suture is occasionally needed to reattach the false vocal fold laterally, but trimming of redundant mucosa is often all that is needed.

8. Excision of anterior saccular cysts utilizes the same ap-

proach and techniques as described above. These lesions are usually easier to remove because of their size and favorable location.

25.6

Postoperative Care and Complications

■ Consider overnight admission for airway observation/ precautions in cases where extensive dissection and suspension were used. ■ Postoperative care should include PPIs (to reduce the chance of granuloma formation), pain medicine, and a normal diet as tolerated. ■ Adverse outcomes ■ Cyst recurrence is a risk with endoscopic excision, and great care must be taken to include all of the ventricular mucosa with the specimen by removing the entire inferior FVF and ventricle. ■ In cases of recurrence, an open approach is indicated for re-excision. Care should be taken to avoid dissection into the paraglottic space at or below the level of the true vocal fold. Fig. 25.6  Exposed cyst after initial incisions

Fig. 25.7  Blunt dissection of cyst with suction

Fig. 25.8  Final cuts of cyst, including inferior false vocal fold

157

158

Endoscopic Excision of Saccular Cyst

Key Points ■ Saccular cysts of the larynx in the adult can usually be managed endoscopically. ■ Saccular cysts in infants and children are generally approached externally. ■ Two anatomic types of saccular cysts occur ■ Anterior ■ Smaller in size ■ Presents as a ventricular mass in the anterior half of the larynx ■ Lateral ■ Larger ■ Presents as a bulge in the FVF/ aryepiglottic fold ■ Endoscopic CO2 laser and cold dissection are used to remove the cyst. ■ The dissection should include a complete removal of the FVF and underlying ventricle, to reduce the chance of recurrence.

25

 

Selected Bibliography 1

2 3

Danish MN, Meleca RJ, Dworkin JP, Abbarah TR (1998) Laryngeal obstructing saccular cysts: a review of this disease and treatment approach emphasizing complete endoscopic carbon dioxide laser excision. Arch Otolaryngol Head Neck Surg 124:593–596 DeSanto LW, Devine KD, Weiland LH (1970) Cysts of the larynx: classification. Laryngoscope 80:145–176 Hogikyan ND, Bastian RW (1997) Endoscopic CO2 laser excision of large or recurrent laryngeal saccular cysts in adults. Laryngoscope 107:260–265

Chapter 26

26

Anterior Glottic Web

26.1

Fundamental and Related Chapters

Please see Chaps. 1, 4, 10, and 13 for further information.

26.2

Disease Characteristics and Differential Diagnosis

An anterior glottic web formation (Fig. 26.1) can occur from either congenital or acquired causes. A congenital anterior glottic web is quite rare, and the symptoms are usually identified at birth or in a young child if the web is large, causing stridorous breathing. Smaller congenital webs are often identified later in life and are associated with exercise restriction and/or dysphonia. Acquired anterior glottic webs are the most common type of glottic web, and these typically occur from a traumatic injury to the larynx, be it surgical, iatrogenic, external trauma, or intubation related. Anterior glottic webs range in size from being extremely small (a microweb) to encompassing the entire length of the membranous vocal folds. Obviously, the symptoms, severity, and surgical procedures will vary significantly based on the etiology and size of the web. Anterior glottic webs should be evaluated in two specific dimensions: from an anterior–posterior dimension and in a

superior–inferior plane. The latter can often involve web formation from the glottis to the supraglottis and/or web formation from the glottis into the subglottis. A variety of conditions are associated with anterior glottic webs; specifically, laryngeal framework stenosis should be carefully examined and considered when evaluating a patient with an anterior glottic web. This can involve supraglottic stenosis, thyroid cartilage constriction resulting in glottic stenosis, and subglottic stenosis from cricoid cartilage deformation and loss of normal dimensions, specifically in the anterior–posterior plane. Vocal fold scar is frequently associated with an anterior glottic web because of the traumatic nature of the etiology of most of these conditions. Differential diagnosis for an anterior glottic web is: ■ Wegner’s granulomatosis ■ Sarcoidosis ■ Amyloidosis

26.3

Surgical Indications and Contraindications

Indications include: ■ Airway restriction ■ Abnormally elevated phonatory pitch ■ Dysphonia Contraindications include: ■ No functional voice limitations and no airway restriction ■ Uncontrolled LPR ■ Active RRP without any airway restriction

26.4

Surgical Equipment

Equipment needed includes: ■ Standard phonomicrosurgery set (see Chap 10, Table 10.1) ■ Standard laser microlaryngoscopy set (see Chap. 13) ■ Silastic sheet and/or premade laryngeal keel Fig. 26.1  Anterior glottic web

160

Anterior Glottic Web

■ Endo-extra laryngeal needle passer (Richard Wolf Medical, Knittingen, Germany) or 18-g angiocatheter/2-cm 18-g needle (Fig 27.7) ■ 0 Prolene suture ■ Silicone surgical button(s) ■ Mitomycin C (optional)

 

26.5

Surgical Procedure

Fig. 26.2  Endoscopic assessment of superior–inferior extent of glottic

The two approaches most often used for the release and removal of an anterior glottic web are endoscopic flap or endoscopic placement of a keel. The endoscopic flap approach is best used for smaller anterior glottic webs and involves the asymmetric division of the anterior glottic web, with utilization of the web for mucosal coverage on one side of the anterior commissure. This operation involves delicate surgical handling. Elevation and preservation of the anterior glottic web mucosa is performed, and then the flap is sutured over one side of the anterior commissure. For larger anterior glottic webs and for patients that do not have adequate tissue for an endoscopic flap, release of the anterior glottic web and endoscopic placement of a keel is required. Patients undergoing this procedure need to be informed of the need for two surgical procedures (placement of keel and removal of keel.) They also need to be prepared for moderate pain and discomfort as well as globus sensation for the 7- to 10-day period that the keel is in position. 1. Endoscopic flap for anterior glottic web a) Laryngoscopic exposure of the anterior glottic web and the anterior commissure region with suspension laryngoscopy (see Chap. 10, “Principles of Phonomicrosurgery”) b) Visualize and assess superior and inferior depth of anterior glottic web and plan incision location(s) using angled telescopes (Fig. 26.2). c) Incise the anterior glottic web in an asymmetric fashion at either the free edge of the vocal fold or onto the superior surface of the vocal fold that will then be incorporated into the flap (Fig. 26.3).

Fig. 26.3  Incision for asymmetric division of anterior glottic web

Fig. 26.4  Elevation of the anterior glottic web flap and release of web/

web

26

scar up to inner aspect of the thyroid cartilage

 

Chapter 26

d) Preservation of flap mucosa, complete release of the an-

terior glottic web all the way up to the anterior commissure/thyroid cartilage is then performed using cold-steel instrumentation or the CO2 laser (Fig 26.4). e) Often demucosalization of the undersurface of the flap and the subglottis in the region of the anterior commissure and anterior third of the vocal fold is then required. It can be done with either cold steel or a CO2 laser using a defocused beam on low-power settings (Fig. 26.5). f) The endoscopic flap can now be draped down into the subglottis and secured in place with a single 5.0 or 6.0 absorbable suture. It is a rare endoscopic flap that does not need suturing to stay in the proper location. Tissue glue has not been adequate, in the authors’ past experience, to secure the endoscopic flap into location (Figs. 26.6. 26.7). g) The application of mitomycin C onto the contralateral anterior commissure and anterior third of the vocal fold in the demucosalized area is optional (see Chap. 29). 2. Release of the anterior glottic web with endoscopic keel placement a) Suspend the laryngoscope with adequate false vocal fold retraction and complete exposure of the anterior glottic web and anterior commissure. It is important to suspend the laryngoscope with adequate space above the anterior commissure for placement of the superior position of the planned keel (approximately 3–4 mm above the level of the glottis). b) Visualize the anterior glottic web with 30 and 70° telescopes. During this visualization it is important to evaluate the web in a cephalocaudal dimension given that this will determine the minimum length of the planned keel (Fig. 26.2).

Fig. 26.5  Demucosalization of the undersurface of the flap

c) Release or excision of the anterior glottic web can be

done either with a CO2 laser (smallest spot size and low power) or with straight-up scissors and/or a sickle knife. When incising the anterior glottic web, it is important to put tension on the vocal folds with lateral retraction and stay in the midline between the two vocal folds to minimize any further lamina propria damage. Cold-steel excision is preferable to minimize laser surgery-related scar formation (Fig. 26.8). d) After excision or release of the anterior glottic web up to the anterior commissure, the CO2 laser can then be used to make an approximately 1-mm deep groove into the inner aspect of the thyroid cartilage, extending 3–4 mm above the anterior commissure and 4–5 mm below the anterior commissure. This groove will be used for placement of the keel in an anterior-most location (Fig. 26.9). e) Thirty and 70° telescopes can then be used to visualize the superior and inferior extent of the anterior glottic web release and determine the superior–inferior extent of the intended keel. When visualizing this area with a 30 or 70° telescope, the telescope should be passed to the superior-most location to which the keel will need to be secured, and then the telescope shaft can be marked at the location of the junction of the shaft and the proximal laryngoscope. The 30° telescope is then moved to the inferior limit of the planned keel location. The telescope is held at this position; a mark on the telescope shaft can be placed at the junction of the shaft and the proximal laryngoscope. The distance between the two marks on the telescope shaft is measured and this distance will be used to determine the superior–inferior length of the keel (Fig. 26.10).

Fig. 26.6  Inferior reflection of flap to cover one side of the anterior

commissure

161

162

Anterior Glottic Web

Fig. 26.7  Securing the endoscopic flap with suture placement

 

Fig. 26.9  CO2 laser vaporization of a 1-mm thyroid cartilage groove at

the anterior commissure

f) After trimming the keel to the required superior–infe-

26

Fig. 26.8  Midline division of the anterior glottic web down to inner

aspect of the thyroid cartilage

rior dimension as well as the anterior–posterior dimension, the keel can be placed with a heavy cup forceps into the larynx to evaluate the appropriate size and fit. g) A 0 Prolene suture can then be passed from the subglottis to the anterior neck with the Lichtenberger endo-extralaryngeal needle passer. This can be done with microlaryngoscopy or endoscopically with a 30° telescope. A clamp should be placed on the free end of the suture that comes out of the anterior neck (Fig. 26.11). Alternative Method i. Have an assistant pass an 18-g angiocatheter or 2.5cm needle from the anterior neck to the desired location in the anterior subglottis during simultaneous microlaryngoscopy or telescopic visualization of the larynx. Once the needle is in the proper location into the subglottis, then a 0 Prolene suture can be passed in through the tip of needle and out through the neck where it is secured with a clamp. h) Pass the free end of the suture through the laryngoscope. Secure the keel at two locations along the spine of the keel with the suture. The placement of the suture through the keel will ultimately determine the exact location of the keel in the larynx. Thus, it is helpful to place the keel into the appropriate location and obtain endoscopic visualization with the 70° telescope of where the fixation sutures should be placed onto the keel. i) Load the suture coming from the keel into the endo-extra laryngeal needle passer and place down the laryngoscope to pass the suture from the region superior to the anterior commissure to the anterior neck (Fig. 26.11).

 

Chapter 26

Alternative Method i. After passing the suture through the keel, place the 18-g angiocatheter or 2.5-cm needle through the anterior neck into a location above the anterior commissure with simultaneous microlaryngoscopy or telescopic visualization. ii. Pass a 0 Prolene suture into the shaft of the angiocatheter/needle until an assistant can see the suture emerging from the angiocatheter. The assistant can then remove the angiocatheter or needle and clamp the suture that has been passed from the larynx to the anterior neck. j) Guide the keel into position in the endolarynx as an assistant applies equal tension to the sutures coming out of the anterior neck. k) Place a moderate and equal amount of tension on the two sutures coming out of the anterior neck and confirm the proper location of the keel using 30 and 70° telescopic visualization. l) If the keel is not in the proper location from either a superior, inferior, or lateral perspective, then the passing of the sutures and placement of the sutures through the keel should be repeated. m) Secure the endoscopic keel in place by tying the sutures coming out of the anterior neck over surgical buttons with a simultaneous visualization of the keel during the suture tying procedure (Fig. 26.12). 3. Keel removal (10–14 days post-placement) a) Apneic anesthesia is the preferred method of anesthesia for this procedure, given that endotracheal intubation can complicate the endoscopic keel removal and injure the operative site. b) Direct laryngoscopy is then performed, and a 0° telescope is used to visualize the endolarynx, specifically the

superior portion of the keel. A large cup forceps is then used to grasp the keel. Once the endoscopist is confident that he has a firm grasp of the keel, the anterior neck sutures can be cut and the keel can then be removed via the laryngoscope. c) After adequate mask ventilation of the patient, a repeat direct laryngoscopy and endoscopic visualization of the operative site is performed. If there is severe granulation tissue or a reformation of the anterior glottic web, then the endoscopic glottic web procedure can be repeated.

Fig. 26.10  30° telescope is used to measure the length of the keel from

superior to inferior

Fig. 26.11  Passing inferior fixation suture from endolarynx through the anterior neck and place-

ment of suture through keel

163

164

Anterior Glottic Web

 

Complications comprise: ■ Anterior glottic web reformation ■ Dislodgement of keel ■ Scar or erosion of the vocal fold from malposition of the keel ■ Granulation at the keel suture location

Key Points

Fig. 26.12  Visualization of proper placement of the keel with 30 and

■ Anterior glottic web most commonly is an acquired condition from surgical trauma. ■ Anterior glottic web surgery is indicated for airway restriction or symptomatic dysphonia. ■ Endoscopic flap release of anterior glottic web can be done successfully with good laryngeal exposure and a small glottic web. ■ Release of anterior glottic web and placement of endoscopic keel requires skill from the surgeon and can be successfully performed if attention to technical details are observed.

70° telescopes, with keel secured together over button on the neck

Also at this juncture, if indicated, mitomycin C can be applied at the operative site. These decisions are made based on the amount of mucosalization that has occurred at the anterior glottis.

26.6

Postoperative Care and Complications

Postoperative care includes: ■ ■ ■ ■ ■ ■

26

Intravenous antibiotics (perioperatively only) Intravenous steroids perioperatively Laryngopharyngeal reflux disease treatment Pain medicine as needed Overnight observation in the hospital Reevaluation of the patient in approximately 8–10 days in the office with flexible laryngoscopy or indirect laryngoscopy to determine the amount of mucosalization that has occurred underneath the keel

Selected Bibliography 1 2

3 4

5 6

7

8

Benninger MS, Jacobson B. Vocal nodules, microwebs and surgery (1997) J Voice 11:238–246 Casiano RR, Lundy DS (1998) Outpatient transoral laser vaporization of anterior glottic webs and keel placement: risks of airway compromise. J Voice 12:536–539 Dedo HH (1979) Endoscopic Teflon keel for anterior glottic web. Ann Otol Rhinol Laryngol 88(Pt. 1):467–473 Ford CN, Bless DM, Campos G, Leddy M (1994) Anterior commissure microwebs associated with vocal nodules: detection, prevalence, and significance. Laryngoscope 104(Pt 1.):1369–1375 Hsiao TY (1999) Combined endolaryngeal and external approaches for iatrogenic glottic web. Laryngoscope 109:1347–1350 Liyanage SH, Khemani S, Lloyd S, Farrell R (2006) Simple keel fixation technique for endoscopic repair of anterior glottic stenosis. J Laryngol Otol 120:322–324 Milczuk HA, Smith JD, Everts EC (2000) Congenital laryngeal webs: surgical management and clinical embryology. Int J Pediatr Otorhinolaryngol 52:1–9 Schweinfurth J (2002) Single-stage, stentless endoscopic repair of anterior glottic webs. Laryngoscope 112:933–935

Part B Phonomicrosurgery for Benign Laryngeal Pathology

III Laser Microlaryngeal Surgery (Airway/ Neoplastic Conditions)

Chapter 27

Bilateral Vocal Fold Paralysis

27.1

Fundamental and Related Chapters

Please see Chaps. 3, 5, 9, 10, 13, and 28 for further information.

27.2

Disease Characteristics and Differential Diagnosis

Patients with bilateral vocal fold paralysis (BVFP) generally fall into two categories, (1) iatrogenic recurrent laryngeal nerve injury (typically from a thyroidectomy), or (2) progressive neurological disorder (Shy-Drager Syndrome, syringomelia, Guillian-Barré syndrome, etc.). In contrast to unilateral vocal fold paralysis, with which the patient principally complains of voice and swallowing difficulties, bilateral vocal fold paralysis (BVFP) causes airway restriction and not vocal dysfunction. In patients with BVFP, treatment is directed at maximizing the airway, while attempting to limit the negative effects of treatment on vocal function. It can be difficult to distinguish BVFP from posterior glottic stenosis. In some ways, the distinction is not essential, because posterior transverse cordotomy and/or partial arytenoidectomy are often effective for both conditions. However, a correct diagnosis greatly facilitates patient counseling and appropriate treatment, therefore a careful examination to evaluate cricoarytenoid joint fixation and posterior glottic stenosis should be carried out prior to surgical intervention (see Chap. 28, “Posterior Glottic Stenosis”). The most reasonable approach to patients with bilateral vocal fold paralysis is a step-wise approach to enlarge the glottic airway. The least aggressive and safest procedures are the posterior transverse cordotomy (PTC) or medial arytenoidectomy (MA). After these procedures, an extended version of either (or a combination) can be performed, or a total arytenoidectomy. Please note the procedure historically called a total arytenoidectomy does not involve complete anatomic removal of the arytenoid cartilage. Its aim is to remove all arytenoid cartilage that effects the airway. Selection of the side to perform surgery for bilateral vocal fold paralysis is based on a variety of factors. The most important factor for selection is presence of any purposeful motion either adductory or abductory. If there is no motion of either vocal fold, then laryngeal electromyography can assist in determining which side has the worst neuromuscular status and thus is the best location for the surgical procedure. In addition to these methods, palpa-

27

tion of the cricoarytenoid joint as described below is helpful to determine which cricoarytenoid joint has the worst range of motion and mobility and would then be best choice for surgical procedure to widen the posterior glottic airway.

27.3

Surgical Indication and Contraindications

An indication for surgery is symptomatic airway obstruction. Contraindications to treatment of BVFP include: ■ Rapidly progressive neurologic disorder ■ Unrealistic patient expectations (improvement in both airway and voice) Relative contraindications to treatment include: ■ Presence of aspiration ■ Compromised pulmonary status ■ Diabetes (more true for open procedures than endoscopic) ■ Previous radiation therapy to the neck/larynx Treatment options for BVFP include: ■ Tracheotomy ■ Microlaryngoscopy with laser posterior transverse cordotomy ■ Microlaryngoscopy with laser medial arytenoidectomy ■ Microlaryngoscopy with laser total arytenoidectomy ■ Endoscopic suture lateralization ■ Open arytenoidectomy In general, rapidly progressive neurologic disorders (such as Shy–Drager) tend to be treated with tracheotomy, due to comorbid conditions. However, most other causes of BVFP can be treated more conservatively with endoscopic techniques. Posterior transverse cordotomy or medial arytenoidectomy are generally the ideal endoscopic treatment options, because voice results tend to be better, and aspiration is less likely, as compared with total arytenoidectomy. Endoscopic suture lateralization is useful if temporary treatment is warranted. Open arytenoidectomy is reserved for cases where endoscopic techniques have failed or are impossible due to anatomic limitations, and thus is rarely required.

168

Bilateral Vocal Fold Paralysis

27.4

Surgical Equipment

Equipment includes: ■ ■ ■ ■

Laser microlaryngoscopy equipment (Chap. 13) Laryngeal bipolar/monopolar cautery (not essential) Mitomycin C (0.4 mg/ml) Also for suture lateralization only: ■ Endo-extralarnygeal needle carrier by Lichtenberger (Richard Wolf Medical, Knittingen, Germany) ■ Silicone buttons ■ 0 or 2.0 Prolene sutures

27.5

Surgical Procedure

1. Palpation of cricoarytenoid joint

Direct laryngoscopy should be performed. It is best to perform cricoarytenoid joint palpation without an endotracheal tube in place. Anesthesia should induce complete muscle paralysis and the posterior larynx is viewed with microlaryngoscopy or a 0° endoscope. Care should be taken to ensure that suspended laryngoscope is positioned cephalad in the larynx to avoid the laryngoscope limiting the range of motion of the arytenoid cartilages. Palpation of the cricoarytenoid joint is performed by using a sturdy instrument such as a large cup forceps and placing it adjacent to the vocal process and pushing the vocal process laterally swiftly. With this maneuver, the surgeon can gauge the degree of effort required to displace laterally the vocal process as well as the speed of the recoil of the tissue in a medial direction

 

(Figs. 27.1, 27.2). During this maneuver, careful evaluation of the posterior commissure should be done. If the entire posterior commissure moves with lateralization of the vocal process, then this suggests that posterior glottic stenosis may be present. This same procedure should be done on the contralateral side and used to compare the degree of stiffness and range of motion of both cricoarytenoid joints. This maneuver can be helpful in selecting which side is optimal for surgery to improve the posterior glottic airway. One should select the arytenoid with the worst cricoarytenoid joint mechanics to operate on. 2. Posterior transverse cordotomy a) Intubation with 5.0 or 5.5 laser safe endotracheal tube (ETT) Alternately, a subglottic jet catheter (Hunsaker tube, Medtronic Xomed, Jacksonville, Fla.) can be used. b) Expose larynx with laryngoscope and place into suspension. i. Ensure that the ETT is in posterior commissure, and that there is still good vocal process visualization with the ETT in a posterior position. If the ETT obstructs the surgical site, then the EET can be moved anteriorly with the laryngoscope securing the ETT anteriorly (see Chap. 19, “Vocal Fold Granuloma”). ii. It is often helpful to angle the laryngoscope toward the side where the cordotomy is being performed to maximize the exposure of the lateral aspect of the true vocal fold/false vocal fold (see Chap. 19, Fig. 19.2). c) Laser precautions are implemented (see Chap. 13, “Principles of Laser Microlaryngoscopy”). d) Laser incision

27

Fig. 27.1  Palpation of a mobile (nonfixed) cricoarytenoid joint: lateral

displacement of arytenoid with blunt instrument

Fig. 27.2  Release of arytenoid, resulting in recoil of arytenoid medi-

ally. This would be observed in a patient with BVFP

 

Chapter 27

i. A CO2 laser setting typically is 4 W, superpulse with

a very small spot size. An intermittent firing of 0.1-s on/0.5-s off time will also minimize collateral thermal damage. ii. A platform suction device (or a moist Cottonoid) is placed below the surgical site to protect distal structures. iii. The vocal process location is confirmed by palpation. iv. Incision is started just anterior to vocal process, being careful not to expose the cartilage, to avoid granulation tissue postoperatively. v. Laser char (carbonaceous debris) should be removed by rubbing a saline soaked Cottonoid over the surgical site periodically. The CO2 laser is ineffective in a heavily charred area or bleeding operative site. e) Extension of cordotomy i. Once the entire vocal fold is separated from the vocal process, the cordotomy is extended into the false vocal fold tissue. ii. Frequently, a branch of the superior laryngeal artery is encountered, and troublesome bleeding can occur. iii. Suction and bipolar laryngeal cautery are effective in stopping the bleeding. iv. A complete cordotomy extends laterally 3–4 mm into the false vocal fold tissue/musculature (see Figs. 27.3, 27.5, shaded portion no. 1). v. Confirmation of complete cordotomy is achieved via endoscopic evaluation with a 0 and/or 30° telescope, confirming that the cordotomy site is flush with the lateral subglottic wall.

Fig. 27.3  Lateral extent of transverse cordotomy at both the level of

true and false vocal fold

vi. The residual vocal fold will retract anteriorly and ap-

pears shortened (Fig 27.4).

vii. The degree of lateral extension of the cordotomy can

be adjusted based on (1) tissue response to the initial cordotomy and (2) the amount of airway improvement needed by the patient. f) Application of LTA i. 4% lidocaine is sprayed on the vocal folds/trachea to minimize laryngospasm postoperatively. g) Application of mitomycin C (optional) i. Topical mitomycin C is placed (typically 0.4 mg/ml) via a soaked pledget for 5 min. 3. Medial arytenoidectomy a) Placement of laser laryngoscope i. Place laser laryngoscope (with built-in suction) to allow exposure of the posterior membranous vocal fold, arytenoid cartilage and posterior glottic space on the intended side of the surgical procedure. b) Laser safety precautions i. All laser safety precautions should be put into place prior to starting the use of the laser (see Chap. 13, “Principles of Laser Microlaryngoscopy”). c) Laser incision i. The CO2 laser setting should involve a small spot size (0.25–0.4 μm) at a setting of 2–4 W, super-pulse mode, and used to obliterate the medial-most portion of the arytenoid cartilage for approximately 2–3 mm in width. ii. The anterior–posterior dimensions of this area of obliteration should be posterior to the tip of the vocal process preserving all or most of the vocal process. iii. The area of the obliteration should not extend to the posterior arytenoid tissue and should spare adjacent mucosa in the intra-arytenoid area (Fig. 27.5, shaded portion no. 2). iv. Titration of the amount of arytenoid cartilage that is obliterated is based on the amount of airway im-

Fig. 27.4   Surgical result immediately after a right posterior transverse

cordotomy; note how the residual vocal fold retracts anteriorly and appears very thick and shortened

169

170

27

Bilateral Vocal Fold Paralysis

provement that is required by the patient and tissue response after the initial aspect of the medial arytenoidectomy. v. This is a clinical judgment and should initially be done in a very conservative fashion with an expectation that some patients may require repeat surgery to further enlarge the posterior glottic airway to a satisfactory level. If adequate surgical enlargement of the posterior glottic airway is not obtained with a conservative medial arytenoidectomy, then further arytenoid lateral to the initial defect can be removed all the way to the lateral aspect of the cricoid ring resulting in a total arytenoidectomy (see below). vi. To further improve the posterior glottic airway, the area of ablation can be taken anteriorly to include the vocal process and a partial posterior cordectomy to the level of the lateral ventricle (see Fig. 27.5, shaded portion no. 3). vii. Remove all laser char from the operative site with suction and moist cotton pledget. viii. Obtain hemostasis with epinephrine-soaked (1– 10,000 concentration) pledget. ix. Apply mitomycin C to the operative site (0.4 mg/ml for 5 min) (optional). x. Spray the endolarynx with 4% plain lidocaine. xi. Suction esophagus and stomach with oral gastric tube placement. 4. Total arytenoidectomy a) Follow the preparatory steps listed above for medial arytenoidectomy. b) Continuous CO2 laser ablation of arytenoid tissue until the operative defect is flush with the walls of the cricoid ring, both posteriorly and laterally. Tissue removal posteriorly should not remove any interarytenoid mucosa. Evaluation of this goal can be done by: i. Placement of a curved elevator on the lateral aspect of the subglottis and then slowly drawing the instrument in a cephalad direction feeling for a glottic level “overhang” of arytenoid tissue. If there is an “overhang,” additional arytenoid tissue can be removed (Fig. 27.6). ii. In addition, the endoscopic evaluation of the posterior glottic airway with a 70° telescope, can identify if there is any residual arytenoid overhang that needs further laser ablation to maximize the glottic airway to complete the total arytenoidectomy procedure 5. Endo-extralarnygeal suture lateralization (based on the technique of Lichtenberger) a) Special consideration i. This procedure is best suited as a temporizing measure for airway improvement in early BVFP cases, ideally in the first 2 months after onset. b) Indications: i. Early, symptomatic BVFP (first 2 months) with uncertain prognosis for recovery c) Contraindications i. Recent trauma to the posterior glottis from indwelling endotracheal tube ii. Indwelling tracheostomy tube d) Procedure

 

Fig. 27.5  Diagram of different degrees of arytenoid removal (medial,

total) compared to transverse cordotomy (shaded area no. 1). Laser ablation of the medial arytenoid for medial arytenoidectomy is shown in shaded area no. 2. Laser ablation of total arytenoidectomy is shaded area no. 3

Fig. 27.6  Palpation of residual arytenoid overhang

 

Chapter 27

i.

Suspension laryngoscopy is performed (jet ventilation is initiated or a small 5.0 or 5.5 endotracheal tube can be used). ii. The skin overlying the neck on the side of the proposed suture lateralization is prepped and draped in a sterile fashion. iii. The most medialized vocal fold is selected in this procedure. An endo-extralaryngeal needle carrier device (Richard Wolf; Fig 27.7) is loaded with a 2.0 or 0 Prolene suture. Under microscopic or telescopic visualization, the needle is positioned below the posterior vocal fold at a point just anterior to the vocal process (Fig 27.8). Using the carrier device, the needle is pushed through the larynx until the tip of the needle appears externally through the skin of the neck. The needle is grasped, and the suture is advanced through the skin and temporarily secured with a clamp (Fig 27.9). iv. The proximal end of the same Prolene suture is then threaded through the free needle, which is designed to be used with the endo-extralaryngeal needle carrier. The procedure as in step (iii) is performed at the same location of the posterior glottis, this time at a level slightly superior to the true vocal fold (Fig 27.10). The needle is again advanced externally through the skin of the neck (Fig 27.11). A second lateralization suture is placed in a similar fashion, 1–2 mm anterior to the first suture. v. Traction is now placed on the two sutures to create lateralization of the posterior vocal fold and expansion of the static airway dimensions (Fig 27.12). vi. A 2-cm horizontal incision is made in the neck. The sutures are then pulled deep to the skin incision. The two ends of the suture are then tied with a surgeon’s knot over the sternohyoid muscle, using a silicone button as an anchoring point (Fig 27.13). vii. The skin incision is closed in a standard fashion. A permanent version of this surgery can be performed by combining this suture lateralization technique with an ipsilateral partial submucosal laser resection of the TA/LCA complex and/or a partial arytenoidectomy. This technique is illustrated in Chap. 28, (“Posterior Glottic Stenosis”).

27.6

Fig. 27.7  Endo-extralaryngeal needle carrier device (Richard Wolf)

Fig. 27.8  Infraglottic placement of suture just below the level of the

vocal process

Postoperative Care and Complications

Care immediately postoperatively includes: ■ Twenty-four hour observation in a monitored setting may be indicated, although these procedures can be performed on an out-patient basis, especially if a stable tracheotomy is present. ■ Voice rest is not essential. ■ Proton-pump inhibitor(s) ■ Pain medications ■ Corticosteroid taper ■ Antibiotics, as per the surgeon’s discretion

Fig. 27.9  The suture is grasped by an assistant and pulled through the

skin

171

172

Bilateral Vocal Fold Paralysis

Fig. 27.10  The same initial suture is now placed above the vocal fold

(through the ventricle) at the region of the vocal process

 

Fig. 27.11  One completed lateralization suture. This sequence will

be repeated once more, slightly anterior to the previous suture placement

Fig. 27.13  The two sutures are

brought deep to the skin through a separate incision and tied over the strap muscles, using a silicone button

Fig. 27.12  After completion of the suture lateralization. Note lateral-

ization of the vocal fold with two sutures slightly anterior to the vocal process

27

During the (expected) postoperative course, the patient will experience significant worsening of the voice, which will improve over a 2- to 3-month period and then stabilize. Followup at 2–3 week intervals for reexamination and reassurance is important during the healing phase. The expected final result

is a small posterior glottal notch in the case of posterior transverse cordotomy (Fig. 27.14). Although the notch may appear to have only increased the airway 2–3 mm, this results in significant improvement in the patient’s airway, and only mild worsening of the patient’s voice. Complications related to posterior transverse cordotomy, medial, and total arytenoidectomy: 1. Granuloma formation a) Granuloma formation at the operative site is not uncommon, and should be treated by maximizing antireflux medication. b) The granuloma tend to resolve over time, but may need to be excised if still present 3–4 months after surgery. c) These granulomas may also cause return of airway symptoms, and must be monitored carefully.

 

Chapter 27

Key Points

Fig. 27.14  Long-term postoperative result after a right transverse cor-

dotomy

2. Excessive scar tissue obliterating operative site a) Occasionally, the operative site heals completely, without

the characteristic “notch.”

b) The operation can be repeated on the same side with re-

application of mitomycin C.

c) It is quite rare to need additional surgery after a second

surgical procedure. Complications related to suture lateralization include: a) Trauma to the posterior vocal fold from excessive tension on the lateralization suture. b) The suture may “cut into” the vocal fold, separating the muscular vocal fold from the vocal process. c) This complication can be avoided by: i. Not operating on vocal folds after “fresh” ETT trauma ii. Placing the first suture anterior to the vocal process, thus avoiding the temptation to lateralize the vocal process/arytenoid tissue. The sutures must be removed promptly if significant vocal fold trauma is present.

■ Bilateral vocal fold paralysis should be differentiated from posterior glottic stenosis, even though static glottic enlargement procedures such as medial arytenoidectomy, posterior transverse cordotomy and total arytenoidectomy are often helpful for both conditions. ■ Patients undergoing glottic enlargement procedures for bilateral vocal fold paralysis must be counseled regarding the exchange of improved airway for decreased voice quality and volume. ■ A variety of surgical procedures are available for treatment of bilateral vocal fold paralysis. The most conservative, limited procedure should be selected initially, and then further surgery and more extensive surgery can be tailored to the patient’s airway and voice needs. ■ Pre-, intra- and post-operative angled telescopic (30 and 70°) evaluation of the posterior glottic airway is an essential aspect of surgery for bilateral vocal fold paralysis. ■ All laser char should be removed from the operative site at the end of the surgical procedure to minimize post-operative granulation tissue formation. ■ Post-operative reflux treatment should be implemented to reduce post-operative granulation formation.

Selected Bibliography 1

2

3

4 5

6

Lichtenberger G, Toohill RJ (1997) Technique of endo-extralaryngeal suture lateralization for bilateral abductor vocal cord paralysis. Laryngoscope 107:1281–1283 Bosley B, Rosen CA, Simpson CB, McMullin BT, GartnerSchmidt JL (2005) Medial arytenoidectomy versus transverse cordotomy as a treatment for bilateral vocal fold paralysis. Annals of Otology, Rhinology & Laryngology 114:922–926 Hillel AD, Benninger M, Blitzer A et al (1999) Evaluation and management of bilateral vocal cord immobility. Otolaryngol Head Neck Surg 121:760–765 Dray TG, Robinson LR, Hillel AD (1999) Idiopathic bilateral vocal fold weakness. Laryngoscope 109:995–1001 Crumley RL (1993) Endoscopic laser medial arytenoidectomy for airway management in bilateral laryngeal paralysis. Ann Otol Rhinol Laryngol 102:81–84 Dennis DP, Kashima H (1980) Carbon dioxide laser posterior cordectomy for treatment of bilateral vocal cord paralysis. Ann Otol Rhinol Laryngol 98:930–934

173

Chapter 28

Posterior Glottic Stenosis: Endoscopic Approach

28.1

Fundamental and Related Chapters

Please see Chaps. 6, 9, 10, 13, 27, and 29 for further information.

28.2

Diagnostic Characteristics and Differential Diagnosis

Posterior glottic stenosis (PGS) presents as progressive airway obstruction, which develops 4–8 weeks after extubation from a period of extended mechanical ventilation (Fig. 28.1). PGS has been reported as a complication that can occur after intubation times as short as 4 days and has been linked to LPR. Often the patient complains of dysphonia after extubation. Examination will frequently reveal granulation tissue in the area of the arytenoid cartilage or over the interarytenoid cleft. This tissue prevents vocal fold approximation for voice production, and the voice is breathy or whispered. The granulation tissue itself can grow to obstruct the glottis. When this occurs, the patient is often seen by the otolaryngologist. Prompt evaluation, diagnosis, and debridement of the granulation tissue can be associated with reduction in mature scar tissue formation and lessens the overall risk of the stenosis of the airway. Frequently, however, patients are not seen acutely and as the granulation tissue resolves, mature scar tissue develops which impairs vocal fold

Fig. 28.1  Posterior glottic stenosis

28

mobility and leads to “mature” PGS. The diagnosis is often complicated by the presence of a tracheotomy, which increases the bacterial count in the tracheobronchial tree and may exacerbate problems with granulation tissue development. Since the patient breathes through the tracheotomy, the effect of the granulation tissue obstructing the airway goes unnoticed until it has had a chance to mature and form a scar contracture. This process typically occurs over 4–8 weeks. Even minimal injury to the mucosa over the cricoarytenoid (CA) joint can be associated with loss of cricoarytenoid joint function for vocal fold abduction. In an animal model, laser depithelialization over the CA joint was associated with a 25% reduction in vocal fold abduction after healing. Deeper injuries were associated with a greater reduction in motion and injuries into the cricoarytenoid joint capsule were associated with fusion of the arytenoids to the cricoid. The differential diagnosis of posterior glottic stenosis is: ■ Bilateral vocal fold paralysis ■ Cricoarytenoid joint ankylosis (e. g., autoimmune from rheumatoid arthritis) ■ Interarytenoid synchiae Severe injury with erosion of the CA joint from pressure due to prolonged intubation can lead to CA joint fusion. This is usually noted in the endoscopic exam, which reveals a normal posterior glottis associated with CA joint ankylosis. Often this finding can be appreciated on careful flexible laryngoscopy examination in the office under topical anesthesia. In the PGS patient, there is also a history of relatively recent intubation. Laryngeal electromyography (EMG) can be used to distinguish PGS from immobility due to previous bilateral neurological injury or bilateral paralysis (see Chap. 2, “Principles of Clinical Evaluation for Voice Disorders”). In PGS, the EMG activity of the thyroarytenoid–lateral cricoarytenoid muscle complex will be normal, while in bilateral paralysis, even of chronic origin, there will be evidence of old neurological injury with partial recovery. EMG activity in bilateral paralysis will show reduced interference pattern often with reduced recruitment and large polyphasic motor unit potentials. Frequently, there will be active recruitment of additional motor units with voluntary activity, but this will not be normal in amount and the amplitude of the individual potentials will be increased. Severe scarring with CA joint fixation can be distinguished from loss of mobility due to mucosal scar contraction only via an endoscopic examination and exploration. Therefore, the initial management strategies in all patients with suspected PGS should include diagnostic and staging endoscopy, with planned palpation and potential mucosal flap elevation (see

176

Posterior Glottic Stenosis: Endoscopic Approach

also Chap. 27, “Bilateral Vocal Fold Paralysis”). If mucosal scar contraction is the sole reason for loss of vocal fold abduction, then mucosal flap elevation will be associated with at least temporary improvement in vocal fold abduction and airway. The patient will notice an immediate improvement in their ability to breathe in the recovery room. If this improvement does not occur, then it is unlikely that restoration of active CA joint function will be achieved, and management then needs to proceed to either (1) ablative endoscopic procedures such as posterior transverse cordotomy, partial arytenoidectomy, total arytenoidectomy, suture lateralization or (2) open approaches with posterior glottic grafting (see Chaps. 27 “Bilateral Vocal Fold Paralysis” and 46, “Glottic and Subglottic Stenosis: Cricotracheal Resection with Primary Anastomosis”).

28.3

Surgical Indications and Contraindications

Indications for surgery include: ■ Airway obstruction due to PGS ■ Patient desire for tracheotomy decannulation Relative contraindications include: ■ Presence of aspiration ■ Compromised pulmonary status ■ Diabetes (more true for open procedures than endoscopic) ■ Previous radiation therapy ■ Unrealistic patient expectations (improvement in both airway and voice) ■ Uncontrolled laryngopharyngeal reflux

28.4

Surgical Equipment

Equipment needed for surgery includes: ■ Standard laser microlaryngoscopy set (Chap. 13) ■ Mitomycin C (0.4 mg/ml)

28.5

Surgical Procedure

1. Intubate with laser safe endotracheal tube through existing

28

tracheotomy, perform new tracheotomy, or expose larynx with suspension laryngoscope and commence jet ventilation (see Chap. 13,” Principles of Laser Microlaryngoscopy”). 2. Suspension laryngoscope details The procedure is begun by obtaining exposure with the largest possible laryngoscope. If the patient does not have a tracheotomy, then jet ventilation can be used to support respiration.

 

a) Posterior commissure exposure is usually obtained with-

out the need for anterior counter pressure.

b) To help spread the vocal folds apart, it may be beneficial

to insert the tip of the laryngoscope through the vocal folds. This needs to be done with extreme caution or not at all if the patient does not have a tracheotomy. c) If the patient does not have a tracheotomy, then inserting the tip of the laryngoscope through the vocal fold or over manipulation may cause postoperative edema requiring tracheotomy. Therefore, in patients without tracheotomy, manipulation, even palpation of uninvolved tissue needs to be minimized. d) After exposure is obtained, the posterior commissure is examined with 0, 30, and 70° angles telescopes. The mucosal integrity in terms of granulation tissue and scarring is assessed. 3. Visualize the operative field with the binocular operating microscope. a) High magnification will help to evaluate mucosal integrity. 4. Assess passive cricoarytenoid (CA) joint mobility (see Chap. 27, “Bilateral Vocal Fold Paralysis”). a) Palpate the arytenoids. b) Pushing lightly on the laryngeal surface of the mid body of the arytenoid should result in translocation or lateralization of the ipsilateral vocal process and vocal fold (see Chap. 27, Figs. 27.1 and 27.2). c) If joint mobility is impaired, then this maneuver will result in minimal vocal process displacement, and the entire larynx will move. d) After assessment of the posterior commissure mucosa and passive CA joint mobility, decisions regarding intervention can be made. 5. Surgical options a) Interarytenoid synchiae i. If a bridge of mucosa between the arytenoids is identified, then this should be excised and removed (Fig. 28.2). ii. Mitomycin C may be applied to the raw surfaces to reduce the risk of reformation of the scar band. iii. If this procedure results in restoration of passive mobility, then the procedure is likely to be successful, and the case should be terminated. iv. Approximately 50% of patients with an interarytenoid synchiae will regain mobility after this type of intervention. If mobility is not restored, then it is likely that injury process has resulted in exposure of the cricoarytenoid joint, with remodeling and possible fusion of the arytenoid to the cricoid. Thus, a glottic enlargement procedure will be needed such as a posterior transverse cordotomy (PTC) or medical arytenoidectomy (MA) (see Chap. 27), or permanent suture lateralization as described in this chapter. b) Posterior scar—microtrap-door flap i. Through palpation of the CA joints, the joint with the best mobility should be identified. ii. The laser or a knife is used to make an incision in the mucosa over the contralateral arytenoid starting

 

Chapter 28

Fig. 28.2  Interarytenoid synchiae, with dashed line indicating surgical

Fig. 28.3  Initial incision for microtrap-door flap

Fig. 28.4  Ablation of posterior glottic scar, with CO2 laser

Fig. 28.5  Draping of microtrap-door flap

plane of division

near the vocal process, extending over the body and into the interarytenoid cleft over the interarytenoidius muscle (Fig. 28.3). iii. Scissors or the CO2 laser is used to separate a flap of epithelium and submucosal tissue from the underlying scar.

iv. The underlying scar tissue is vaporized or excised

(Fig. 28.4).

v. Troublesome bleeding is stopped by applying epineph-

rine (1:10,000) on 0.5 × 3-cm Cottonoids. These are held in place for 1–3 min until the bleeding stops.

177

178

Posterior Glottic Stenosis: Endoscopic Approach

vi. The flap is elevated and the scar removed until mo-

bility is restored or the limits of the dissection are reached. Often the flap is elevated over the contralateral CA joint and 4–5 mm below the vocal folds in the interarytenoid cleft. vii. The flap is then repositioned over the ipsilateral CA joint (Fig. 28.5). viii. Sutures may be required to hold the flap in place.

 

ix. Mitomycin C (0.4 mg/ml) may be applied to the

exposed CA joint to lessen scar tissue formation in this region. x. If joint mobility is not obtained, then it is unlikely that the procedure will be successful, and consideration should be given to additional procedures that enlarge the posterior glottis, such as PTC, MA, total arytenoidectomy (see Chap. 27), or irreversible suture lateralization as depicted in this chapter. These procedures are best used when attempts at restoration of joint mobility have failed and the cartilaginous glottis is relatively well preserved. If the cartilaginous portion of the arytenoid has been resorbed by the healing process, then identification of the vocal process will be difficult. Since the area is filled in with scar tissue, incision in this area will usually result in scar reformation, without significant airway improvement. c) Permanent suture lateralization This technique, as described by Lichtenberger, is more appropriately performed in cases of BVFP. Only in carefully selected cases, and when the surgeon has extensive experience in the endoscopic management of PGS should one attempt this treatment for PGS. That being said, this procedure, especially if performed bilaterally can be successfully used in recalcitrant cases of PGS that do not respond to other methods such as PTC and subtotal arytenoidectomy. xi. The skin overlying the neck is prepped and draped in a sterile fashion.

Fig. 28.6  Outline of extent of excision in permanent suture lateraliza-

tion technique

28 Fig. 28.7  CO2 laser excision of lateral arytenoid and lateral vocal fold

tissue

Fig. 28.8  After completed excision, with extension of the excisional

margin below the free edge of the vocal fold

 

Chapter 28

xii. As depicted in Fig. 28.6, the procedure involves a

subtotal arytenoidectomy, as well as a partial removal of lateral vocal fold musculature. xiii. Grasping the mucosa overlying the arytenoid, the CO2 laser is used to excise the lateral aspect of the arytenoid, extending the incision anteriorly into the lateral aspect of the vocal fold for a distance of 3–4mm beyond the vocal process. The vocal process and medial aspect of the arytenoid, along with the mucosa overlying these structures are preserved (Fig. 28.7). xiv. The excision of arytenoid and lateral vocal fold musculature should continue inferiorly such that the defect extends infraglottically below the free edge of the vocal fold (Fig. 28.8). xv. Two sutures are used to lateralize the posterior vocal fold, as described in Chap. 27. “Bilateral Vocal Fold Paralysis”. Traction is placed on the sutures by an assistant, while the posterior glottic scar is divided with a CO2 laser (Fig. 28.9). xvi. The sutures are then secured over a silicone button, or a modified curved plastic oral airway device (with drill holes) (Fig. 28.10). xvii. Often, the same process is repeated on the contralateral side to obtain maximal airway results.

28.6

Postoperative Care

Relative to the postoperative course are the following: ■ Voice rest is not necessary. ■ The patient is encouraged to ambulate and plug their tracheotomy (if present) while awake if possible. ■ Regular diet may be resumed when the effects of anesthesia are resolved ■ LPR medical therapy is essential

Fig. 28.9  After suture lateralization, traction is placed on the sutures,

while the posterior glottic scar is divided with the CO2 laser

■ The patient is reevaluated in the office at 1 month, with flexible laryngoscopy. If mobility of one or both arytenoids has been achieved, then consideration for decannulation can be undertaken. ■ With the suture lateralization technique: The patient is brought to the operating room 3–4 weeks later for removal of sutures. Mitomycin C may be placed in the posterior commissure as well as conservative removal of any granulation tissue at that time.

Key Points ■ PSG needs to be distinguished from bilateral true vocal fold paralysis. Ninety-five percent of the time a history of previous prolonged intubation, followed by a 4- to 8-week time course of progressive airway obstruction, is associated with stenosis. Careful physical examination will document abnormalities of the cartilaginous glottis in over 80% of these patients. ■ Laryngeal electromyography may be undertaken if the airway is safe or tracheotomy has been performed. EMG will usually show normal activity in PGS patients. ■ Direct laryngoscopy with palpation can be used to confirm the suspected diagnosis. ■ At the time of direct laryngoscopy, attempts to release the posterior scar band through simple excision or mucosal flaps can be undertaken. ■ Surgical success is usually associated with an immediate noticeable improvement in passive mobility of one or both vocal folds. Patients will also notice improvement in respiratory status immediately after the operation.

Fig. 28.10  Final result, with lateralization sutures tied over a modified

oral airway device external to the skin of the neck

179

180

Posterior Glottic Stenosis: Endoscopic Approach

■ Endoscopic attempts to restore CA joint mobility will fail if the causative injury has resulted in cartilaginous disruption with loss of the normal arytenoid structure or fusion of the arytenoids to the cricoid ring. ■ Destructive procedures such as irreversible suture lateralization, posterior transverse cordotomy, partial arytenoidectomy, or total arytenoidectomy (Chap. 27, “Bilateral Vocal Fold Paralysis”) may be used but are usually less successful in patients with PGS than patients with bilateral vocal fold paralysis. This is due to erosion of the posterior cartilaginous glottis with loss of the normal dimension and preexisting scar tissue, which predisposes to recurrent scar formation. ■ Mitomycin C may be beneficial in reducing scar tissue reformation.

 

Selected Bibliography 1

2

3

4

5

28

Koufman JA, Aviv JE, Casiano RR, Shaw GY (2002) Laryngopharyngeal reflux: position statement of the committee on speech, voice, and swallowing disorders of the American Academy of Otolaryngology-Head and Neck Surgery. Otolaryngol Head Neck Surg 127:32–35 Courey MS, Bryant GL Jr, Ossoff RH (1998) Posterior glottic stenosis: a canine model. Ann Otol Rhinol Laryngol 107 (Pt. 1):839–846 Lichtenberger G (1999) Endoscopic microsurgical management of scars in the posterior commissure and interarytenoid region resulting in vocal cord pseudoparalysis. Eur Arch Otorhinolaryngol 256:412–414 Dedo HH, Sooy CD (1984) Endoscopic laser repair of posterior glottic, subglottic and tracheal stenosis by division or microtrapdoor flap. Laryngoscope 94:445–450 McIlwain JC (1991) The posterior glottis. J Otolaryngol 20(Suppl.):1–24

Chapter 29

Subglottic/Tracheal Stenosis: Laser/Endoscopic Management

29.1

Fundamental and Related Chapters

Please see Chaps. 6, 9, 10, 13, 45, 46, and 47 for further information.

29.2

Disease Characteristics and Differential Diagnosis

Subglottic stenosis (SGS) (Fig. 29.1) and tracheal stenosis (TS) are terms that after often used interchangeably to describe symptomatic airway narrowing below the vocal folds. Strictly speaking, the “subglottic region” refers to the infraglottic airway from the free edge of the true vocal folds down to the inferior border of the cricoid cartilage. From a practical point of view, many cases of upper-airway stenosis overlap the subglottis/upper tracheal boundary, rendering anatomic distinctions impractical. Subglottic/tracheal narrowing is usually caused by scarring within the lumen of the airway. This must be distinguished from collapse secondary to weakened or absent cartilaginous framework (usually tracheal), or external airway compression. In addition, narrowing of the airway from neoplastic conditions (e. g., chondrosarcoma of the cricoid) can be confused clinically with scar in the subglottis. A more complete differential diagnosis is included in Chap. 6, “Glottic and Subglottic Stenosis: Evaluation and Surgical Planning”.

29.3

29

Surgical Indications and Contraindications

Indications include endoscopic treatment of subglottic/tracheal stenosis for cases of symptomatic cicatricial narrowing of the upper airway (Fig. 29.2). Absolute contraindications to laser excision/dilation of SGS include airway narrowing due to external compression, and tracheomalacia, or significant cartilage collapse (Fig. 29.3). Relative contraindications include: ■ Extensive length of stenosis > 2–3 cm ■ Absence of identifiable airway lumen ■ Stenosis involving the trachea at the level of the tracheostomy tube

Fig. 29.2  Diagram of tracheal stenosis due to intraluminal scar forma-

Fig. 29.1  Subglottic stenosis

tion. Cartilaginous tracheal arches are intact. Arrow depicts the region of stenosis adjacent to the tracheo-esophageal party wall, where care must be taken during laser radial incisions, to avoid esophageal lumen entry

182

Laser Treatment for Subglottic Stenosis

Fig. 29.3  Tracheal airway narrowing due to collapse of cartilaginous

framework (commonly seen after tracheotomy). Note the limited amount of airway expansion that could be achieved intraluminally

29.4

Surgical Equipment

Equipment needed for surgery includes: ■ Standard laser microlaryngoscopy set (Chap. 13) ■ 3.5 or 4.0 endotracheal tube wrapped with Cottonoid externally (for mitomycin C application)

29.5

29

Surgical Procedure

The example given below is typical for SGS/TS treatment in the absence of a tracheostomy tube. 1. The patient is anesthetized via mask induction, and the table is turned 90° to allow the surgical team to obtain visualization of the upper and lower airway. Endotracheal intubation (which can be traumatic to the stenotic region) is avoided. 2. The tooth guard is placed, and suspension laryngoscopy is established. The laryngoscope/subglottiscope should be positioned proximal to the vocal folds initially (for evaluation and mapping of the stenosis), and jet Venturi ventilation (with 100% O2) initiated through the laryngoscope channel. 3. “Mapping” of the stenosis is carried out as follows: a) The 0° telescope is advanced to the level of the vocal folds, and a mark is made on the telescope shaft where it intersects the proximal end of the laryngoscope (Fig. 29.4, “a”). b) The telescope is then advanced to the upper edge of the stenotic region, and another mark is made (Fig. 29.4, “b”). c) The telescope is then placed at the distal edge of the stenosis for the final mark (Fig. 29.4 “c”).

 

Fig. 29.4  Mapping of the stenosis using a 0° telescope. The marks are

made on the telescope and measurements are taken directly off the telescope

d) The diameter of stenotic region is estimated in millime-

ters (the telescope diameter can be used as a guide).

e) The remainder of the trachea and proximal bronchial tree

is visualized (and additional sites of stenosis mapped, if appropriate). f) A ruler is placed along the telescope: i. The measurement from “a” to “b” represents the proximity of the stenosis from the true vocal folds (useful for treatment planning if external procedures are entertained). The measurement from “b” to “c” represents the length of the stenosis (in general, 1–2 cm is ideally suited for endoscopic treatment). 4. Pre-laser precautions (see Chap. 13, “Principles of Laser Microlaryngoscopy”) a) Protect the patient i. Moistened eye pads ii. Wrap the head in moist surgical towels. b) Protect the endotracheal tube (if used) i Use a laser-safe tube. ii O2 concentration of 30% or less iii Protect tube balloon by covering with a moist Cottonoid. iv If jet ventilation is used, then make sure that it is suspended during laser firing (note: 100% O2 concentrations are used with jet ventilation). c) Protect OR personnel i Safety eye wear 5. Laser radial incision (CO2 laser settings 4–8 W, superpulse, or intermittent pulse) The laryngoscope should be advanced past the true vocal folds (for protection), and positioned just above the stenotic region. The platform suction device is placed through the stenosis and used to protect the distal tissues while the laser

 

Fig. 29.5  Schematic view of laryngotracheal region. Note placement

of laryngoscope distal to the vocal folds for protection. Platform suction is placed underneath the stenotic shelf providing protection of distal trachea

incisions are made. The platform suction device is engaged by “hooking” the stenotic “shelf ” that characterizes most upper airway stenosis (Fig. 29.5). As most stenotic lesions are asymmetrical, the initial laser radial incision is used to open the most severely affected portion, usually the region that has the most extensive shelf. While the laser is being fired, jet ventilation is suspended. The incision should begin centrally and extend in a radial fashion, like the spokes on a bicycle wheel. It is important to keep the incision precise (narrow), so that a maximal amount of surrounding mucosa is preserved, which will promote more rapid re-epithelialization. The incision should be extended through fibrous scar tissue only. When characteristic “sparking” of the tissue is encountered (indicating the presence of cartilaginous framework), the laser incision is terminated. Further extension of the incision could expose cartilage leading to granulation/further scarring and/or cartilage loss. 6. Additional laser radial incisions are made. The orientation of the incision is commonly compared to the hands of a clock. In the case of a perfectly symmetric stenosis, a maximum of four laser radial incisions are typically made at 12, 3, 6 and 9 o’clock (Fig. 29.6). Again, it is important to maintain a strip of uninjured mucosa between the incisions to facilitate re-epithelialization. From a practical point of view, most stenotic lesions are asymmetric, and two to three strategically placed laser radial incisions in the stenotic region with preservation of a normal quadrant of airway are often all that is needed (Fig. 29.7). Caution must

Chapter 29

Fig. 29.6  Perspective view of laser radial incisions. Note planned inci-

sions at 12, 3, 6, and 9 o’ clock, with sparing of intervening mucosa

Fig. 29.7  Example of predominantly right sided SGS with only three laser radial incisions needed at 12, 3, and 6 o’ clock

be exercised when making laser incisions in the trachea at 6 o’clock due to the risk of esophageal entry along the party wall (see Fig. 29.2, arrow). 7. The laryngoscope is advanced distally and resuspended to expose the more inferior extent of the stenosis. The 0° telescope (30° telescopes are helpful as well) is then passed through the stenosis to evaluate the extent of the

183

184

Laser Treatment for Subglottic Stenosis

 

Fig. 29.8  Schematic illustration of airway after laser radial incisions (left), during rigid broncho-

scopic dilation (center), and after serial dilations are complete (right)

29

laser incisions. The laser radial incisions are extended distally, if indicated. Failure to extend the laser radial incisions through the entire distal aspect of the stenosis is a common error. This is likely due to the inherent limitations of a fixed visual field used in microlaryngoscopy. The dynamic view provided through the telescope provides a better view of this distal stenotic region. 8. Rigid dilation of stenosis Refixed-wire balloon dilators (Boston Scientific, Boston, Mass.) are much easier and expeditious for dilatation compared with rigid dilatation. a) A series of rigid ventilating bronchoscopes (nos. 5–9) is now used to gradually dilate the airway (Fig. 29.8). Prior to dilation, each bronchoscope should be connected to the anesthesia circuit via flexible rubber tubing, so that endotracheal ventilation can be performed during dilation. This is an important step due to the accumulation of CO2 that tends to occur during prolonged jet ventilation. b) Generally, a no. 5 bronchoscope is used initially, placing the bronchoscope directly through the laryngoscope opening, and advancing past the stenosis. Surgical lubricant placed on the tip of the bronchoscope is sometimes helpful. The bronchoscope is then rotated 90° to achieve maximal dilation from its eccentric shape. c) Serial dilations are then carried out using progressively larger bronchoscopes, stopping with the largest size that can be comfortably advanced past the stenosis. However, bronchoscopes sized no. 6 and larger will not pass through most other laryngoscopes; therefore, they may be passed using a sliding Jackson laryngoscope or “freehand” without the aid of laryngoscopic guidance. A better suited alternative is the use of a large bore Lindholm laryngoscope (Karl Storz, Knittigen, Germany), which will allow passage of all bronchoscope sizes (see Fig. 25.4) Clinically successful results usually occur if dilation to #7 or greater bronchoscope is achieved, although dilation to #6 in females is sometimes adequate. 9. Suspension laryngoscopy with application of mitomycin C (0.4 mg/ml)

Fig. 29.9  Cottonoid-wrapped ETT segment (saturated in mitomycin

C) in place, allowing jet ventilation to proceed

a) Application of mitomycin C to the surgical site is an im-

portant adjunct in the endoscopic treatment of airway stenosis. Usually a concentration of 0.4mg/ml is used, but concentrations of up to 10mg/ml (supersaturated) may occasionally be employed if a tracheostomy tube is in place. Two options for mitomycin c application can be utilized: i. A mitomycin c–saturated Cottonoid is placed on the surgical site, taking care that the entire surgical site is in contact with the pledget. The Cottonoid is left in place for 4–5 min, under apneic conditions, and then removed. The time can be split up if the patient desaturates during the mitomycin-application period. ii. A Cottonoid-wrapped 3.5 or 4.0 ETT segment (2– 3 cm in length) can be saturated with mitomycin and

 

Chapter 29

placed into the airway in contact with the surgical site (Fig. 29.9). This seems to provide better contact with the surgical site as well as a providing an airway for jet ventilation during the 4–5 min of treatment. The device is removed prior to returning the patient to the anesthesia team. 10. The patient is returned to the care of the anesthesia team. Jet ventilation can be continued until the team is prepared to switch to mask ventilation. The patient is awakened using mask ventilation and an oral airway preferably, although other nontraumatic techniques such as laryngeal mask ventilation are acceptable. Intubation is not recommended at the termination of the case, in an effort to avoid any further trauma to the operative site. If tracheostomy is present distal to the stenotic region, then the case is significantly simplified—the airway is maintained with standard general anesthesia delivered through the tracheostomy site with a laser safe tube. The tube need only be removed briefly for endoscopic viewing of the entire upper airway at the beginning of the case, and again for dilation at the end of the case. An apneic technique is used during tube removal for the tracheal evaluation and dilation aspect of the procedure.

29.6

Postoperative Care and Complications

Postoperatively, management includes: ■ The patient is observed overnight in an ICU or stepdown unit. With experience, and especially with patients who are having repeated endoscopic treatments, such monitoring may not be necessary. ■ Chest x-rays should be obtained if the patient has any unexpected findings postoperatively, such as SpO2 values less than 95%, shortness of breath, chest/pleuritic pain, or subcutaneous crepitance in the neck. ■ Perioperative steroids are important: ■ 10 mg Decadron intravenously ■ Oral steroid-taper ■ Additional postoperative meds: ■ PPIs for at least 2 months, until healing is complete ■ Antibiotics for 5–7 days (optional) ■ Pain medications (usually from tongue compression) ■ Cough suppressants (Tessalon Perles 100 mg three times daily, as needed) Complications can include: ■ Laser fire ■ Tracheal penetration with pneumomediastinum/pneumothorax ■ Late postoperative edema/granulation/fibrinous exudates with airway obstruction ■ Tracheoesophageal fistula (exceedingly rare) ■ Reccurent stenosis

29.7

T-Tube Stenting of SGS

Placement of a T-tube represents an “intermediate” step between endoscopic and open treatments for SGS/tracheal stenosis. T-tube placement is indicated for tracheotomized patients with subglottic/tracheal narrowing (from any cause) who have failed serial CO2 radial incisions/dilation treatment. T-tube placement is contraindicated for patients on ventilatory support. The open-ended design does not allow positive pressure ventilation through the external limb of the T-tube. SGS involving the infraglottic aspect of the vocal folds (undersurface) is not well-suited for T-tube stenting (and is a relative contraindication), because the proximal limb of the T-tube will likely either interfere with vocal fold closure or lead to granulation tissue formation and obstruction of the proximal T-tube.

29.8

Surgical Equipment

Surgical equipment needed includes the following: 1. All of the equipment listed for CO2 laser radial incisions and dilation 2. Commercially produced standard T-tube stents: a) Hood adult sizes 10–16 (size indicates outer diameter in millimeters) b) Montgomery adult sizes 10–16 (size indicates outer diameter in millimeters) 3. One of the following to occlude/bypass the proximal end of the T-tube for ventilation: a) Fogarty catheter with 3- to 5-ml balloon capacity b) Hemostat/clamp c) Small-diameter ETT (4.0) 4. Connector piece from a small bore (4.5–6.0) ETT (i. e., the detachable piece of the ETT in which you connect your ventilation circuit). Ensure that this piece fits snuggly into the ventilation port of the T-tube to be used.

29.9

Surgical Procedure

A preexisting tracheostomy is required to perform T-tube placement. 1. Steps 1–8 of CO2 laser radial incisions and dilations are first performed (as outlined in Sect. 29.5), until an adequate airway caliber is obtained. 2. Suspension laryngoscopy is performed, and an assistant places a rigid endoscope, connected to a camera/monitor to visualize the airway during the placement of the T-tube stent, and to assist in positioning the stent (Fig. 29.10). 3. An appropriate T-tube stent is selected according to the diameter of the airway after dilation. In general, sizes 11–14 (Hood) are used. The stent is sterilized prior to placement (Fig. 29.11). 4. A nasogastric (NG) tube is placed through the external limb of the T-tube, and up through the proximal (shorter limb). A

185

186

Laser Treatment for Subglottic Stenosis

Fig. 29.10  An assistant provides visualization (with a 0° telescope) of

Fig. 29.11  T-tube stent prior to placement

Fig. 29.12  An NG tube is placed through the external limb of the T-

Fig. 29.13  The proximal end of the T-tube is passed into the

clamp is placed at the external limb of the tube, which fixes the T-tube to the indwelling NG tube (Fig. 29.12). The tip of the NG tube is then placed through the tracheal stoma and advanced into the proximal trachea. Working through the laryngoscope, the assistant grasps the NG tube with a large laryngeal cup forceps/grasper. The NG tube is pulled into the upper trachea, seating the proximal end of the T-tube in the airway (Fig. 29.13). 5. The distal end of the T-tube is crimped (Fig. 29.14) with a hemostat, and advanced through the stoma, and into the distal

tracheal airway (Fig. 29.15). This step may be difficult, and might need to be attempted a few times before the T-tube can be successfully positioned in the distal airway. 6. The assistant uses the rigid telescope to visualize the entire length of the T-tube to insure patency and adequate positioning in the airway (Fig. 29.16). The T-tube should not be kinked, twisted, partially occluded, or “loose” in the airway. In addition, the proximal end of the T-tube should not come within 5 mm of the undersurface of the vocal folds. The distal end should not come in contact with

the airway during T-tube placement

tube, up through the proximal (shorter limb), and clamped in place

29

 

airway and the NG tube is grasped by the assistant via endoscopic visualization

 

Fig. 29.14   The distal end of the tube is crimped with a curved clamp

Fig. 29.16  The assistant passes the telescope through the T-tube into

the distal trachea to insure good placement and patency of the lumen of the tube

the carina. A properly seated T-tube should fit snuggly in the airway and maintain its shape/patency regardless of patient position/neck movement. If the above conditions are not met, then T-tube placement will ultimately fail due to granulation tissue formation and occlusion of the tube. A good indicator of successful T-tube placement is the ability of the patient to maintain good air exchange with the T-tube capped at the end of the surgical case and in the recovery room. 7. Once the T-tube is positioned, the patient must be ventilated until he/she is able to breathe spontaneously.

Chapter 29

Fig. 29.15  The clamped distal end of the tube in advanced into the

distal trachea through the stoma

Options include: a) LMA (laryngeal mask ventilation) b) Occlusion of the proximal end of the T-tube with a endoscopically positioned Fogarty catheter. A connector from an ETT is placed into the external limb of the T-tube for ventilation distally (Fig. 29.17). c) Occlusion of the proximal end of the T-tube using a hemostat/clamp placed through the stoma at the proximal end of the T-tube (care must be taken not to also occlude the external limb). Again, a connector from an ETT is placed into the external limb of the T-tube for ventilation distally (Fig. 29.18). 8. Once the patient is breathing spontaneously, without ventilatory support, the external limb of the T-tube should be capped (closed), so that the patient is now moving air oronasally. Inability to cap the T-tube (for any reason) when the patient is fully awake and recovered from anesthesia, is cause for concern. An uncapped T-tube can lead to drying/crusting of airway secretions within the tube, and ultimately luminal obstruction of the stent. Successful maintenance of long-term T-tube stent in the airway cannot be achieved unless the tube is capped during the majority of the patient’s waking hours. Patients with coexisting obstructive sleep apnea can often uncap the T-tube at night, as long as humidified air is used by the bedside.

187

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Laser Treatment for Subglottic Stenosis

Fig. 29.17  Occlusion of the proximal end of the T-tube with a Fogarty catheter to allow venti­

lation

29

Fig. 29.18  Occlusion of the proximal end of the T-tube with a curved clamp to allow ventilation

 

 

Chapter 29

Complications include the following:

29.10 Postoperative Care Postoperatively: 1. Observation of the patient in a monitored setting for 24 h (ICU or step-down unit) 2. Ten milligrams intravenous Decadron preoperatively, and every 8 h (×2) during hospitalization – Consider prednisone/methylprednisone oral taper at dis­ charge 3. Additional postoperative medications: – PPIs for at least 2 months, until healing is complete – Antibiotics for 5–7 days (optional) – Pain medications (usually from tongue compression) – Cough suppressants (Tessalon Perles 100 mg three times a day, as needed) 4. Tracheostomy tube at bedside, one size smaller than that of

the T-tube:

T-tube size

Tracheotomy tube size (Shiley)

10

2

11

2

12

4

13

4

14

6

15

6

16

8

5. Humidified air at bedside, especially during sleep 6. Suctioning of the upper and lower limb of the T-tube every

8 h and as needed • An excellent nursing/patient instruction manual is included with the Hood T-tube package 7. Prior to discharge from the hospital, educated patient/caregivers regarding emergency measures in the event that the T-tube becomes obstructed at home: • Uncap T-tube first; if this does not improve breathing, then suction upper and lower limb of T-tube/irrigate with 2 ml normal saline. • If still unable to move air adequately, then grasp and pull firmly on external limb of T-tube to remove it. • Come to the Emergency Department immediately; page the surgeon. A tracheostomy tube can be placed through the stoma as a temporizing airway until arrangements to replace the T-tube (in the OR) can be made. 8. Follow up in the office frequently in the first 2 months postoperatively (every 1–2 weeks depending on patient’s reliability/family support/anxiety level) • The inside of the T-tube should be inspected each visit, using a flexible laryngoscope to insure upper and lower limb patency and to check for reactive granulation tissue. Crusting in the external limb can be cleaned with a cerumen loop. • Review importance of suctioning/cleaning of tube and humidification

■ T-tube occlusion due to poor position/incorrect size of T-tube ■ Granulation tissue at proximal or distal end of T-tube ■ This presents within the first 2 months postoperatively, and must be dealt with by either removal/ cryotherapy of the granulation tissue, or by replacing the stent with a more appropriate T-tube. Patients are at higher risk for this complication if the T-tube is “modified” by cutting off a portion of the proximal or distal tube. This modification replaces the inert, smooth “factory” edge of the tube with a sharper, reactive surface—often resulting in granulation tissue formation at the tube/tissue interface. If customization of the T-tube cannot be avoided, it is important to bevel and smooth the cut edges, as described by Montgomery et al. ■ Hoarseness/aphonia due to extension of the proximal end of the T-tube into or through the glottis ■ Edema and granulation tissue of the vocal folds can result, as well as incomplete glottal closure. If transglottic extension of the superior limb of the T-tube cannot be avoided, then the upper limb should be located at the ventricle/inferior false vocal fold level. ■ Accidental T-tube displacement/removal ■ The use of large bore suction catheters (10 French or greater) can lead to this. Nine French or less is recommended for cleaning/suctioning. ■ Cracking/splintering of the T-tube ■ Although uncommon, this can occur with prolonged (>3 years) T-tube placement. To avoid this, replacement of the T-tube should be performed every 2 years.

29.11 Special Considerations in T-Tube Stenting T-tube stenting of the airway is intended as long-term management strategy for patients with SGS/tracheal stenosis, who have failed endoscopic laser treatments. However, in select cases, removal of the T-tube can be attempted, after a minimum period of 1–2 years of stenting. The T-tube should be removed in the OR, and careful postoperative monitoring should be undertaken for at least 2–3 month/hs after stent removal to check for recurrence of stenosis.

Key Points ■ Endoscopic treatment of subglottic and tracheal stenosis is an excellent management option, and in most cases, is the first method attempted before embarking on open surgical treatment.

189

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Laser Treatment for Subglottic Stenosis

■ Absolute contraindications for endoscopic treatment of stenosis include airway narrowing due to external compression and tracheomalacia/cartilage collapse of the airway ■ Relative contraindications for endoscopic treatment of airway stenosis include extensive length of stenosis (greater than 2–3 cm in length), complete stenosis (no identifiable lumen), and stenosis at the level of the tracheostomy. ■ “Mapping” of the stenosis is an important part of the initial evaluation of airway stenosis, and is helpful for determining treatment planning. ■ The CO2 laser is generally the workhorse laser for endoscopic airway management. ■ Laser radial incisions are used to open the stenosis, while simultaneously preserving surrounding mucosa for re-epithelialization. ■ Topical application of mitomycin C after endoscopic treatment greatly increases the chance for success.

29

 

■ Placement of a T-tube stent represents a intermediate step between pure endoscopic treatment and open procedures for laryngotracheal stenosis. ■ A good indicator of successful T-tube placement is the ability of the patient to maintain good air exchange with the T-tube capped at the end of the surgical case. ■ Careful follow-up for cleaning and inspection of the T-tube in required in the first 2 months after T-tube placement.

Selected Bibliography 1

2

Montgomery WW, Montogomery SK (1990) Manual for use of Montgomery laryngeal, trachea and esophageal prostheses: update 1990. Ann Otol Rhinol Laryngol 99:2–28 Shapshay SM, Beamis JF, Hybels RL et al (1987) Endoscopic treatment of subglottic and tracheal stenosis by radial laser incisions and dilation. Ann Otol Rhinol Laryngol 96:661–664

Chapter 30

Carcinoma of the Vocal Fold

30.1

Fundamental and Related Chapters

Please see Chaps. 4, 10, and 13 for additional information.

30.2

Disease Characteristics and Differential Diagnosis

This chapter discusses the surgical treatment of squamous cell carcinoma of the glottis (T1N0M0). Nonglottic laryngeal sites of cancer and advanced laryngeal cancer disease that spreads from the level of the vocal fold to other sites are not discussed. Vocal fold cancer involves epithelial migration or invasion via malignant transformation into the lamina propria and muscle of the vocal fold. The most common symptoms associated with vocal fold carcinoma include hoarseness, change in pitch, and roughness of the voice. For most patients with early vocal fold carcinoma (Fig. 30.1), the more advanced head and neck cancer related symptoms of odynophagia, otalgia, neck mass, or dysphagia are rarely present. Early vocal fold carcinoma can occur unilaterally (T1aN0M0) or bilaterally (T1bN0M0). The specific anatomic sites of the vocal fold that are important to take into consideration when assessing early vocal fold carcinoma include the anterior commissure, laryngeal ventricle, infraglottis, and the arytenoids. The assessment of early vocal

30

fold carcinoma prior to surgical excision should ensure that the cancer has not spread laterally into the ventricle, the infraglottis, or the supraglottis. The spread of the cancer to the anterior or medial border of the arytenoid cartilage is somewhat controversial regarding resectability via a microlaryngoscopy approach. Normal vocal fold motion must be assured to confirmed early glottic disease. The most common method for excision of early vocal fold carcinoma is using the CO2 laser via a microlaryngoscopy approach. Cold-steel excision can also be used either in combination with CO2 laser or exclusively, depending on the location and depth of the cancer. The CO2 laser has the advantage of precision, small spot size and its hemostatic properties for excision of the vocal fold cancer. A cold-steel excision is best suited for relatively superficial lesions that have neither deep muscle involvement nor cartilage involvement (arytenoid). Differential diagnosis of early vocal fold carcinoma is: ■ ■ ■ ■ ■ ■ ■

Hyperkeratosis/dysplasia Carcinoma in situ Recurrent Respiratory Papillomatosis Verrucous carcinoma Spindle cell carcinoma Tuberculosis Fungal disease (histoplasmosis, blastomyocosis)

30.3

Surgical Indications and Contraindications

Indications for surgery include T1aN0M0 SCCa of the vocal fold. Contraindications include: ■ Inadequate microlaryngoscopic exposure of the entire vocal fold lesion ■ T2N0M0 staging with > 5-mm supraglottic or intraglottic extension, partial vocal fold fixation, or arytenoid involvement (note: patient counseling must include the treatment option of radiation therapy).

30.4

Surgical Equipment

Equipment needed includes: Fig. 30.1  Early carcinoma of the vocal fold

■ Standard laser microlaryngoscopy set (Chap. 13) ■ Tongue blade with fine gauge needles

192

Carcinoma of the Vocal Fold

30

Fig. 30.2  Vocal fold cancer seen via microlaryngoscopy with CO2 la-

ser created marks for proposed excision boundaries (anterior, posterior, and lateral)

30.5

Surgical Procedure

1. Exposure of vocal fold cancer via suspension microlar2.

3.

4. 5.

6.

yngoscopy should allow complete visualization of the lesion. Detailed and angled visualization with telescopes, specifically, 30 and 70° telescopes, is essential. Using this method, it is very important to evaluate the borders of the vocal fold cancer from an anterior–posterior, lateral, and infraglottic perspective. Implement all laser safety procedures including protection of the endotracheal tube cuff, patient head and neck protection, and eye protection for all individuals in the OR (see Chap. 13, “Principles of Laser Micro­laryngoscopy”). With vocal fold palpation, a decision should be made between using the CO2 laser and cold-steel excision. Using the CO2 laser on a single-fire setting, outline the area of excision anteriorly, posteriorly and laterally around the vocal fold cancer with approximately 1- to 2-mm margins of excision (Fig. 30.2). Using the CO2 laser on a repeat superpulse mode with a relatively small spot size (approximately 0.3 mm), incisions can be made around the vocal fold cancer in an anterior, lateral, and posterior dimension. Care should be taken to make these initial cuts perpendicular to the superior surface of the vocal fold, without any medial or lateral “skiving” of the incisions. Also, it is best to incise the anterior, posterior and lateral excision borders in a fairly

 

even fashion (similar depth) for best exposure during the excision (Fig. 30.3). 7. Complete the anterior, posterior, and lateral borders of the excision down to the appropriate depth that will allow complete excision of the cancer without excessive removal of normal deep laryngeal tissue. Once the anterior, posterior and lateral borders of the excision are completed, the cancer excision can be retracted with a triangular forceps or curved alligator medially for exposure of the inferior border for excision. 8. Prior to the release of inferior excision, it is important to make a mental note of the exact location of the retraction instrument on the specimen, specifically, which border and where on the border the instrument is. This is very helpful for the orientation of the cancer excision immediately after the release of the inferior attachment of the excision (Fig. 30.3). 9. With the cancer excision specimen retracted medially, straight-up scissors or the laser can be used to release the inferior border of the excision and remove the lesion for orientation (Fig. 30.3). This lesion can be placed on a tongue blade and fixed into position with anatomic orientation. The deep margin of the excision lays on the surface of the tongue blade and then the anterior, lateral, and posterior borders of the excision are noted on the tongue blade. Small-gauge pins are used to secure the excision specimen to the tongue blade (Fig. 30.4). It is best to physically review the preoperative cancer excision photographs and the tongue blade orientation with the pathologist immediately after the excision in the operating room. Serial sectioning (using routine histopathology processes) can be used to map the nature of the pathology throughout the specimen and especially at the margins. 10. Carefully evaluate the margins of the excision via highpower microlaryngoscopy and the angled telescopes, looking for other areas of abnormal epithelium or tissue that would require biopsy or further excision. 11. Microcup forceps can be used to take selected margins (lateral, anterior, posterior, inferior, deep) as indicated. These can be sent for frozen section analysis or permanent pathological evaluation. Frozen section processing of the excisional tissue is generally avoided due to inherent inaccuracies in determining margins in a small specimen, especially with laser artifacts.

30.6

Postoperative Care and Complications

Immediately postoperatively: ■ Same-day surgery discharge on an outpatient basis is typical for this type of vocal fold cancer excision. ■ No voice rest indicated. ■ Laryngopharyngeal reflux treatment with PPIs may reduce granuloma formation at the operative site. ■ Follow-up with patient, depending on the results of the final pathology report

 

Chapter 30

Fig. 30.4  Orientation and pinned vocal fold cancer excision specimen

on tongue blade

Fig. 30.3  Medial retraction of vocal fold cancer excision with expo-

sure of the inferior border for excision (with scissors in place for final excision)

Complications include: ■ Bleeding from the deep excision location ■ This can be treated with an application of topical epinephrine on a Cottonoid and/or using the CO2 laser with a defocused beam for coagulation purposes. ■ Granulation tissue at operative site ■ This granulation tissue commonly occurs within 2–4 weeks and will slowly involute over time. If the granulation tissue is slow to involute, causing significant dysphonia or breathing problems, then this can be re-excised either in the operating room or in an office-based setting. ■ Residual tumor/recurrence

Key Points ■ Exposure is essential to successful microlaryngoscopy excision of vocal fold carcinoma. ■ Orientation of the excision specimen on a tongue blade is extremely helpful to further management of any positive margins that occur on the final pathologic analysis and to minimize the amount of tissue that is damaged or removed during the treatment of early vocal fold carcinoma.

Selected Bibliography 1

2

3

4

Myers EN, Wagner RL, Johnson JT (1993) Microlaryngoscopic surgery for T1 glottic lesions: a cost effective option. Ann Otol Rhinol Laryngol 103:28–30 Zeitels SM (1993) Microflap excisional biopsy for atypia and microinvasive glottic cancer. Operat Tech Otolaryngol Head Neck Surg 4:218–222 Zeitels SM (1995) Premalignant epithelium and microinvasive cancer of the vocal fold: the evolution of phonomicrosurgical management. Laryngoscope 105(Pt. 2):1–51 Zeitels SM, Hillman RE, Franco RA, Bunting GW (2002) Voice and treatment outcome from phonosurgical management of early glottic cancer. Ann Otol Rhinol Laryngol 190(Suppl.):3–20

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Part B Phonomicrosurgery for Benign Laryngeal Pathology

IV Laryngeal Injection Techniques

Chapter 31

Vocal Fold Augmentation via Direct Microlaryngoscopy

31.1

Fundamental and Related Chapters

Please see Chaps. 5, 8, 10, 14, 32, 33, and 34 for further information.

31.2

Disease Characteristics

Vocal fold injection can be an extremely useful treatment method for a variety of voice disorders. There are different locations, injection materials and methods to perform vocal fold injection (see Chap. 14, “Principles of Vocal Fold Augmentation”). The advantage of injection augmentation versus open laryngeal procedures (laryngeal framework surgery) is the endoscopic and minimally invasive nature. Other advantages include a more direct visualization of the vocal fold pathology requiring treatment. Injection augmentation can be divided into two specific anatomic locations, with subsequent different indications, materials, and methodologies applied to all of these locations. A superficial or medial vocal fold injection is performed for the treatment of vocal fold scarring or focal loss of lamina propria.

This technique is discussed in Chap. 32, “Superficial Vocal Fold Augmentation via Microlaryngoscopy.” Injection augmentation can also be carried out in a deep or lateral vocal fold position. This injection location is used to augment globally the vocal fold for cases of significant glottal incompetence due to: ■ ■ ■ ■ ■ ■

Vocal fold paralysis Vocal fold paresis Vocal fold atrophy Sulcus vocalis Severe vocal fold scar Soft tissue loss of the vocal fold(s)

31.2.1 Material Selection The ideal vocal fold injection material would be readily available, inexpensive, easy to use and completely biocompatible. The search for such a material has been ongoing for close to a 100 years, and significant advances in vocal fold injection material availability and design have occurred in the last 10 years. The original injection material was paraffin, which resulted in a significant foreign body response and rejection. Similar responses have occurred with Silicone injections as well as more recently with Teflon® vocal fold injections. An additional requirement of all future vocal fold injection materials will be a matching of the biomechanical properties of the material with the biomechanical properties of either the superficial aspect of the vocal fold (superficial layer of the lamina propria) or the deep aspect of the vocal fold (vocalis, thyro-arytenoid and lateral cricoarytenoid muscle). The materials presently available for vocal fold injection include (see Chap. 14, “Principles of Vocal Fold Augmentation”): ■ ■ ■ ■ ■ ■ ■

Fig. 31.1  Deep vocal fold augmentation locations

31

Autologous fat ® Radiesse (calcium hydroxylapatite) Teflon Gelfoam® Radiesse Voice Gel® Bovine collagen–based products (Zyplast®, Zyderm®) Human collagen–based ®products (Cymetra®, Cosmoplast , Cosmoderm) ■ Hyaluronic acid–based products (Hyalaform®, Hyalaform Plus®, Restylane®, Perlane®) ■ Autologous fascia (minced)

198

31

VF Augmentation – Microlaryngoscopy

All of these materials other than Cymetra and other collagenbased produces have been designed and used for deep vocal fold augmentation. Bovine collagen, autologous collagen, and human-based collagen are all products that have been used in the past or are presently being used for superficial vocal fold augmentation (see Chap. 32, “Superficial Vocal Fold Augmentation via Microlaryngoscopy”).

31.3

Surgical Indications and Contraindications

Vocal fold augmentation is indicated for the patient with glottal incompetence; however, the degree, nature, and cause of the glottal incompetence need to be further elucidated. Incomplete vocal fold closure is divided into global or focal deficit of the vocal fold. Furthermore, the nature of the glottal incompetence can be identified as to either a lack of muscle bulk or of lamina propria (or both). For disorders that cause global glottal incompetence and/or lack of vocal fold bulk such as vocal fold paralysis, vocal paresis, and vocal fold atrophy, a deep vocal fold augmentation is the preferred injection approach. Prior to vocal fold augmentation, careful evaluation and consideration of the patient’s airway is warranted. Patients with poor abductory range of motion on the contralateral vocal fold or with poor bilateral vocal fold abduction are at significant risk for airway compromise postoperatively. This contraindication is especially true for vocal fold lipoinjection, which requires significant overinjection of the vocal fold (see Chap. 14, “Principles of Vocal Fold Augmentation”).

31.4

Surgical Equipment

Vocal fold augmentation via microlaryngoscopy requires following: ■ Standard phonomicrosurgery equipment (see Chap. 10) ■ Vocal fold injection needle and device Lipoinjection of the vocal fold requires: ■ Standard phonomicrosurgery set (See Chap. 10) ■ Brunings syringe vocal fold injection device with 18- and 19-g needles (Storz, St. Louis, Mo.) or Instrumentarium lipoinjection device (Instrumentarium Surgical Corp., Inc., Montreal, Quebec, Canada). ■ Liposuction device (large bore, low pressure) (Tulip™) or small “plastics” instrument tray for open harvest ■ Sterile funnel ■ Merocel™ sponges (Medtronic-Xomed, Jacksonville, Fla.) Endoscopic vocal fold injection requires the following: ■ Slotted small laryngoscope (anterior commissure laryngoscope; Pilling, Fort Washington, Pa.)

 

■ Vocal fold injection needle and device ■ Zero degree Hopkins telescope (4–5 millimeters in diameter and 30 cm long) ■ C-mount camera and video monitor

31.5

Surgical Procedure

Selection of the vocal fold augmentation technique is determined by the underlying etiology, the vocal fold injection location, comfort level of the surgeon, and the vocal fold injection material. The options for vocal fold injection methodology include percutaneous, transoral, endoscopic direct laryngoscopy, and via microlaryngoscopy (see Chaps. 33, “Peroral Vocal Fold Augmentation in the Clinic Setting” and 34, “Percutaneous Vocal Fold Augmentation in the Clinic Setting”).

31.5.1 Principles of Deep Vocal Fold Augmentation Principles of deep vocal fold augmentation comprise the following: 1. The vocal fold should be injected at the intersection of two anatomic landmarks: a) At the level of the vocal process b) At the transition zone from the superior surface of the vocal fold to the ventricle (superior arcuate line). The junction of these two anatomical locations is the optimal location for a deep vocal fold injection (Fig. 31.1). 2. The vocal fold injection needle should be angled slightly laterally and placed approximately 3–5 millimeters deep to the mucosa prior to the injection. Injection can then be done in a graded or step-wise fashion, observing the immediate impact of the vocal fold injection on vocal fold size, bulk, position, and glottic closure. Optimal needle placement is confirmed when the initial augmentation is seen at the level of the infraglottis. After reasonable infraglottic augmentation, further injection will often spread superiorly to augment the vocal fold at the level of the glottis or the injection needle can be withdrawn 1–2 mm to finish the vocal fold augmentation in the region of the midmembranous vocal fold (Fig. 31.2). 3. Often, a second injection site is required along the superior arcuate line in the region of the midmembranous vocal fold (Fig. 31.1). 4. It is important to remember that the best deep vocal fold injection is placed lateral within vocal fold, and this is optimally achieved with a slightly angled injection needle that is not completely parallel to the longitudinal axis of the laryngoscope (thus the advantage of using a slotted laryngoscope). This can be further enhanced by purposefully positioning the laryngoscope to visualize the lateral aspect of the vocal fold ventricle as opposed to the midline of the glottis.

 

31.5.2 Vocal Fold Augmentation via Microlaryngoscopy

Chapter 31

6. Over-correction as depicted on Fig. 31.7 should be

achieved.

7. Lidocaine is sprayed on the larynx after the vocal fold in-

jection is completed to help prevent postoperative laryngospasm.

Suspension microlaryngoscopy with general anesthesia can be used to perform vocal fold augmentation. The advantages of this approach are outstanding visualization and precise vocal fold injection placement. The disadvantage is the lack of an endpoint due to the inability to assess vocal fold closure. 1. Review of the preoperative videolaryngoscopy and/or videostroboscopy is an important start to vocal fold augmentation. 2. After adequate general anesthesia and complete muscle relaxation has been achieved by the anesthesiology team, a large bore laryngoscope is suspended, providing complete visualization of the vocal fold (see Chap. 10, “Principles of Phonomicrosurgery”). 3. Angled telescopes (0, 30, and 70°) are used to visualize the entire larynx in a “three-dimensional fashion,” which allows one to fully assess the lack of bulk and exact pathology that is to be corrected with the vocal fold augmentation (see Chap. 10). 4. Deep vocal fold augmentation should be performed at this vocal fold injection site approximately 3–5 mm deep to the mucosa, and the needle should be angled as lateral as possible as it is placed through the laryngoscope. To ensure a lateral vocal fold injection site, it is wise to position the laryngoscope with the suspension device angled in a lateral facing direction (Fig. 31.3). 5. Visualization of the vocal fold during the vocal fold injection allows one to determine the ideal amount and location of the injection by observing immediate changes in the vocal fold contour during and after the injection.

Endoscopic vocal fold injection is used for a deep vocal fold augmentation. This technique allows the surgeon a magnified, detailed view during vocal fold augmentation, with the patient awake. This allows visualization of vocal fold motion and closure before, during, and after the injection. This injection technique is also advantageous given that it allows the vocal fold injection to be performed with complete visualization of the procedure by both student and mentor simultaneously. Endoscopic vocal fold injection involves a deep vocal fold augmentation using a small slotted laryngoscope under a local anesthesia (with minimal intravenous sedation). A surgical telescope provides endoscopic visualization for the procedure. 1. Preoperative anesthesia is a crucial aspect of this procedure. Topical nebulized 4% plain lidocaine should be administered for 10–15 min prior to the operative procedure. Additional 4% plain lidocaine can be directly applied to the oropharynx and endolarynx via indirect laryngoscopy and/or direct laryngoscopy. Alternative anesthesia methods include trans-tracheal lidocaine injection and/or superior laryngeal nerve block (either percutaneous or via the pyriform sinus). 2. Preoperative anesthesia will allow the slotted anterior commissure laryngoscope (Pilling) to be passed through the

Fig. 31.2  Depth of injection needle for deep vocal fold augmentation

Fig. 31.3  Angled laryngoscope position for deep vocal fold augmenta-

31.5.3 Endoscopic Vocal Fold Injection

tion via microlaryngoscopy

199

200

31

VF Augmentation – Microlaryngoscopy

oral cavity and oropharynx and to pick up the tip of the epiglottis. With this visualization, 4% plain lidocaine can be applied directly to the endolaryngeal region and intended vocal fold. 3. After adequate laryngeal anesthesia is achieved and a small amount of intravenous sedation is given, the slotted laryngoscope is then advanced with the nondominant hand, immediately over the vocal fold to be injected and manually suspended. The laryngoscope is positioned to slightly retract the false vocal fold to allow complete visualization of the entire length of the membranous vocal fold and the ventricle of the intended site for injection.

 

4. A 0° telescope (30 cm, 4- to 5-mm diameter) is then passed

through the manually suspended laryngoscope. The vocal fold motion, closure pattern, and the glottal incompetence deficit are noted by visualization through either the endoscope or a camera attached to the endoscope (Fig. 31.4). 5. The injection device is then passed into the laryngoscope parallel with the endoscope, using the visualization achieved by the endoscope for guidance. Deep vocal fold injection is performed (Figs. 31.5, 31.6). 6. Once adequate vocal fold augmentation is obtained by direct visualization (Fig. 31.7), the needle can be retracted and kept sheathed within the laryngoscope, and vocal fold closure is visualized during the patient’s phonation. The need for any further injection is determined.

31.5.4 Lipoinjection of the Vocal Fold

Fig. 31.4  Overview of endoscopic vocal fold injection

Fig. 31.5  Endoscopic vocal fold injection method

Lipoinjection of the vocal fold is designed to be a deep/lateral vocal fold injection, resulting in medialization and augmentation of the vocal fold by deposition of autologous fat. Lipoinjection can be done via an endoscopically guided peroral approach or a microlaryngoscopy approach (see above). Given the viscous nature of the fat, a pressurized injection device such as a Brunings syringe or the lipoinjection device designed by Instrumentarium is required. Fat harvest for lipoinjection can be done either through open incision with harvesting subcutaneous fat or via liposuction. Liposuction is the preferred technique because it is expedient, less invasive, and provides perfectly sized injection material. For patients with only “modest” amounts of subcutaneous fat, open harvest is recommended. The most reasonable location for open harvest is in the infra-umbilical region or through a preexisting abdominal scar. The former area of the body typically has a plentiful amount of material and an incision immediately inside the umbilicus can be easily hidden. Fat harvest can be done under local or general anesthesia. 1. Open fat harvest a) The abdomen is prepped and draped in a sterile fashion. b) Local injection of lidocaine with epinephrine is done as a regional block for local anesthesia, or only at the proposed incision site for hemostasis if under general anesthesia. c) A curvilinear incision is made at the junction of the umbilicus and the infra-umbilical region, from approximately 4 to 8 o’clock. d) Subcutaneous elevation of the dermis proceeds in an inferior direction, releasing the subcutaneous fat off the subdermal plane. e) The fat is sharply dissected out with cold-steel instruments, taking care not to violate the skin above or the peritoneum below. f) Hemostatis is attained with electric cautery as needed, and tacking sutures are placed in the deeper aspect of the wound to the subdermal plane. g) The harvested fat is then carefully cut into small pieces with scissors, approximately 1 × 2 × 1 mm in size. (This aspect of the procedure is time consuming and laborious

 

but important. If the fat graft is not properly prepared, then it will not flow smoothly through the injection needle.) h) The fat graft material is then handled in a similar manner as the liposuction harvest material (described below). 2. Liposuction fat harvest for lipoinjection Liposuction should be performed using a large bore, lowpressure liposuction technique. Small-gauge and high-pressure liposuction devices should be avoided to minimize trauma to the fat during the harvest process. An excellent liposuction cannula is made by Tulip™ (San Diego, Calif.) that includes a 4.6-mm diameter, single-hole liposuction cannula with low-pressure suction applied to the cannula. Liposuction from the subcutaneous abdominal space can be done under general or local anesthesia. The latter requires local anesthesia injection in the area of the intended liposuction. a) The abdominal skin is prepped and draped in a sterile fashion. b) A small skin incision (approximately 5 mm) is made in the right upper quadrant of the abdomen. c) The liposuction cannula is passed through the skin and into the subcutaneous space, and negative pressure is applied to the liposuction cannula. d) The liposuction cannula is then moved rapidly in the subcutaneous space in a transverse direction across the patient’s abdomen, with great care taken to control the plane and location of the liposuction tip to avoid penetration into the peritoneum or the overlying skin. Pinching the skin to create “tunnels” helps develop a safe plane for fat harvest (Fig. 31.8). 3. Preparation of fat for lipoinjection Fat harvested by any method is covered with free fatty acids, blood, and serum. The free fatty acids are from ruptured lipocytes and induce an intense inflammatory response if not removed prior to lipoinjection. This inflammatory response will diminish the graft survival. The fat must be carefully and thoroughly rinsed and carefully handled prior to lipoinjection to maximize graft survival. a) Fat from either open or liposuction harvest is placed in a sterile funnel that is lined with strips of Merocel (Fig. 31.9). b) Suction tubing is applied to the downward spout of the funnel, and 2 liters of saline is used to rinse and irrigate the blood and fatty acids from the surface of the harvested fat. c) The fat is then transferred into a small dish with 100 U of regular insulin and soaked for 5 min (the insulin is theorized to stabilize the lipocyte cell membranes and thus improve cell survival during the transplantation process). d) To remove excess moisture, the fat is then placed on a dry Merocel sponge and partially dried by air for several minutes. e) The harvested material can then be loaded into the injection device in preparation for lipoinjection (Fig. 31.10). 4. Lipoinjection of the vocal fold The approach and exposure of the vocal fold and injection sites for Lipoinjection of the vocal folds are identical to all

Chapter 31

Fig. 31.6  Endoscopic vocal fold injection method

Fig. 31.7  Photo demonstrating the appropriate amount of overcorrec-

tion (15–30%, or an additional 0.1–0.2 ml of material) used for most injectables

previously described deep vocal fold injection techniques (see above). Great care should be taken to avoid injection of fat material into the: a) Ventricle b) Subglottis c) Superficial planes of the lamina propria Lipoinjection of the vocal fold should be performed with the goal of substantial overinjection of the vocal fold to allow for expected fat loss during the transplantation process (Fig. 31.11). Care should be taken to restrict lipoinjection unilaterally if the patient has vocal fold paralysis and poor abduction of the contralateral vocal fold. More aggressive lipoinjection can be carried out safely when both vocal folds are mobile. Often, bilateral lipoinjection patients with mobile vocal folds will be done to the extent that after immediate completion of the procedure the membranous vocal folds will be in complete approximation.

201

202

VF Augmentation – Microlaryngoscopy

31.6

31

Postoperative Care and Complications

The voice rest requirement of postoperative care for patients with deep vocal fold injection is highly variable. After lipoinjection of the vocal fold, 3–6 days of voice rest, and a course of oral steroids are recommended. Other deep vocal fold injections require significantly fewer days of voice rest or no voice rest. For nonautologous material injections (CaHA, Teflon, Gelfoam), a single dose of antibiotics is used, given that a nonhuman material is placed in the body. Complications of deep vocal fold injection include: ■ ■ ■ ■ ■ ■

Airway obstruction Infection at the injection site Overinjection Underinjection Allergic reaction Superficial injection

 

Airway obstruction is rare and can be treated with oral or intravenous steroids, antibiotics, airway observation, and humidification. If the airway obstruction is severe, then the treatment options include intubation to allow laryngeal edema to resolve or tracheotomy to bypass the airway obstruction. Swallowing difficulties can also occur from the irritation and pain associated with vocal fold injection. Most pain and swallowing difficulties are minor and are treated with Tylenol or nonsteroidal over-the-counter medicine. Complication of over- or underinjection for deep vocal fold injection can occur. Approximately 3–6 months should be allowed for the injected vocal fold material to settle completely before deciding whether excessive vocal fold injection material has been deposited. Removal of overinjected material can be done via suspension microlaryngoscopy, and performing a lateral cordotomy and cold steel dissection down to the injected material and removing the material partially to correct

Fig. 31.9  Fat in Merocel-lined funnel

Fig. 31.8  Liposuction technique

Fig. 31.10  Fat from lipoinjection needle

Fig. 31.11  The appropriate amount of overcorrection (100%) used for

autologous lipoinjection

 

Chapter 31

the over injection of material (see Chap. 12, “Management and Prevention of Complications Related to Phonomicrosurgery”). Accidental injection of augmentation material into the superficial aspect of the vocal fold is possible when a fine gauge needle is used and the depth of the injection is not controlled. One must take great care to control the depth of the injection needle. If superficial injection occurs, the material should be removed as soon as possible. The material can usually be easily removed via a microflap approach (see Chapter 10, “Principles of Phonomicrosurgery”).

Key Points ■ Vocal fold augmentation (deep) is a versatile and essential procedure for a variety of voice disorders associated with glottal insufficiency. ■ Vocal fold augmentation has an advantage of avoiding an open surgical procedure and involves a quick and prompt recovery. ■ Vocal fold augmentation (deep) can be performed via microlaryngoscopy (via general anesthesia) or endoscopically under local anesthesia. ■ Precise needle placement and careful attention to the vocal fold tissue during injection are critical to successful vocal fold injection.

2

3

4

5

6 7

8

9

10

11

Selected Bibliography 1

Brandenburg JH, Unger JM, Koschkee D (1996) Vocal cord injection with autogenous fat: a long-term magnetic resonance imaging evaluation. Laryngoscope 106(Pt. 1):174–180

12

13

Cantarella G, Mazzola RF, Domenichini E, Arnonr F, Maraschi B (2005) Vocal fold augmentation by autologous fat injection with lipostructure procedure. Otolaryngol Head Neck Surg 132:239–243 Chen YY, Pai L, Lin YS, Wang HW, Hsiung MW (2003) Fat augmentation for nonparalytic glottic insufficiency. ORL J Orothinolaryngol Relat Spec 65:176–183 Hsiung MW, Lin YS, Su FW, Wang HW (2003) Autogenous fat injection for vocal fold atrophy. Eur Arch Otorhinolaryngol 260:469–474 Laccourreye O et al (2003) Intracordal injection of autologous fat in patients with unilateral laryngeal nerve paralysis, long-term results from the patient’s perspective. Laryngoscope 113:541–545 Mikaelian DO, Lowry LD, Sataloff RT (1991) Lipoinjection for unilateral vocal cord paralysis. Laryngoscope101:465–468 Shaw GY et al (1997) Autologous fat injection into the vocal folds: technical considerations and long-term follow-up. Laryngoscope 107:177–186 Mikus JL, Koufman JA, Kilpatrick SE (1995) Fate of liposuctioned and purified autologous fat injections in the canine vocal fold. Laryngoscope 105:17–22 Nakayama M, Ford CN, Bless DM (1993) Teflon vocal fold augmentation: failures and management in 28 cases. Otolaryngol Head Neck Surg 109(Pt. 1):493–498 Remacle M, Lawson G, Delos M, Jamart J (1999) Correcting vocal fold immobility by autologous collagen injection for voice rehabilitation. A short-term study. Ann Otol Rhinol Laryngol 108:788–793 Rihkanen H (1998) Vocal fold augmentation by injection of autologous fascia. Laryngoscope 108(Pt. 1):51–54 Rosen CA (1998) Phonosurgical vocal fold injection: Indications and techniques. Oper Tech Otolaryngol Head Neck Surg 9:203–209 Schramm VL, May M, Lavorato AS (1978) Gelfoam paste injection for vocal cord paralysis: temporary rehabilitation of glottic incompetence. Laryngoscope 88(Pt. 1):1268–1273

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Chapter 32

Superficial Vocal Fold Injection

32.1

Fundamental and Related Chapters

Please see Chaps. 8, 10, and 23 for further information.

32.2

Disease Characteristics and Differential Diagnosis

Superficial vocal fold injection involves placement of a lamina propria replacement substance into the superficial aspect of the vocal fold to restore pliability. This procedure is done via highpowered microlaryngoscopy with a fine-gauge needle (27–30 g). This procedure is aimed at correcting vibra­tory deficits of the vocal fold(s), not providing global augmentation. The most commonly used materials presently available for superficial vocal fold injection are collagen based materials such as Cymetra, Zyplast, or Cosmoplast. These materials are all temporary in nature but can last up to 1 year. In addition, these materials may induce new, native extracellular matrix protein recruitment. It is likely that new lamina propria substitutes/replacement will be developed in the near future, which may be able to be delivered via a superficial vocal fold injection approach. Cross-linked hyaluronic acid-based substances have proven not to be of any value when placed superficially, and thus are contraindicated for this procedure. The best prediction of success is a positive saline-infusion trial. A saline-infusion trial involves superficial injection of saline or diluted epinephrine underneath the epithelium to determine if a substance such as collagen could be subsequently injected into the vocal fold in the area of the focal lamina propria defect or vocal fold scar. If the saline-infusion trial is positive, then it is best to wait several minutes and/or “milk” the saline out of the vocal fold and then proceed with the superficial vocal fold injection. If the scar is too severe in nature, then the saline will track to locations other than those desired, and the patient will not respond well to a superficial vocal fold injection. Superficial vocal fold injection is used in select cases of vocal fold scar. In addition, there are instances of a very focal defect of the lamina propria that would be suitable for augmentation via a superficial vocal fold injection approach.

32.3

32

Surgical Indications and Contraindications

Indications include: ■ Mild-to-moderate vocal fold scar ■ Focal lamina propria defect ■ A positive saline-infusion trial Contraindications include: ■ Need for global augmentation, such as seen in patients with vocal fold paresis, vocal fold paralysis, vocal fold atrophy ■ Negative saline-infusion trial ■ Sulcus vocalis (relative)

32.4

Surgical Equipment

Equipment needed comprises: ■ Phonomicrosurgery tray (see Table 10.1) ■ A fine-gauge injection needle and device (27 or 30 g) ■ Injection device can be designed from a fine-gauge butterfly needle, with the wings of the needle removed and cup forceps used to deliver the needle down to the vocal fold. Alternatively, an orotracheal injector with a disposable 27-g needle attached (Medtronic Xomed, Jacksonville, Fla.) serves the purpose for a superficial vocal fold injection extremely well.

32.5

Surgical Procedure

Superficial vocal fold injection via microsuspension laryngoscopy allows for the precise and controlled placement of vocal fold injection material (collagen, etc.) into the most superficial aspect of the vocal fold. This procedure is done with high power microlaryngoscopy and a fine-gauge injection needle (27–30 g). 1. Review most recent preoperative videostroboscopy immediately before or during the operation to identify the specific pathology and location that requires vocal fold injection.

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Superficial Vocal Fold Injection

2. Placement of a large-bore laryngoscope (see Chap. 10) 3. Vocal fold palpation with a slightly curved blunt instru-

32

ment is helpful to identify completely the area of the vocal fold pathology and the nature of the pathology (vocal fold scar). 4. If there is a concern or question about the exact nature and severity of the vocal fold scar, then often a preliminary injection with 1:10,000 epinephrine or saline placed superficially in the area of the pathology will clearly delineate the

 

area of the deficit as well as the severity of the scar (Fig. 32.1). 5. Under high-power magnification, the vocal fold injection is done using a 27- or 30-g needle. The entry site should be 3–5 mm away from the intended vocal fold injection deposition to prevent extrusion of the injection material. It is best to have the entry site away from the proposed area of infiltration and then tunnel the needle submucosally to the intended area of injection (Fig. 32.2). 6. The vocal fold injection needle should be as superficial as possible after its entry through the epithelium, and is often visible through the mucosa as the needle is tunneled forward to the vocal fold pathology site. 7. There is no preset volume of material to be injected. The defect to be addressed will determine the volume to be injected. Typically, these injections only require 0.2–0.4 ml of material (Fig. 32.3).

32.6

Postoperative Care and Complications

Postoperatively: ■ ■ ■ ■

No need for antibiotics No indication for steroids Voice rest for approximately 6 days Voice therapy can start shortly after the resumption of voice use.

Fig. 32.1  Saline-infusion trial

Fig. 32.2  Superficial vocal fold injection with needle tunneled to area

of intended deposit

Fig. 32.3  Appearance after superficial vocal fold injection

 

With regard to complications, if there is an overinjection of superficial vocal fold injection that is not resolved with a short period (approximately 1–2 months) and inhibits vocal fold function and voice quality, then the superficial material can be removed by making a small incision over the most lateral aspect of the injection location and removing part or all of the material.

Chapter 32

Selected Bibliography 1

2

Key Points

3

■ Superficial vocal fold injection can be done to correct mild vocal fold scar or a focal lamina propria defect. ■ Saline-infusion trial predicts the suitability for superficial vocal fold injection. ■ Collagen-based materials are presently best suited for superficial vocal fold injection. ■ In the future, new lamina propria replacement materials may be delivered via a superficial vocal fold injection approach.

4

Ford CN, Bless DM, Loftus JM (1992) Role of injectable collagen in the treatment of glottic insufficiency: a study of 119 patients. Ann Otol Rhinol Laryngol 101:237–247 Ford CN, Staskowski PA, Bless DM (1995) Autologous collagen vocal fold injection: a preliminary clinical study. Laryngoscope 105(Pt. 1):944–948 Kass ES, Hillman RE, Zeitels SM (1996) The submucosal infusion technique in phonomicrosurgery. Ann Otol Rhinol Laryngol 105:341–347 Zeitels SM, Vaughan CW (1991) A submucosal vocal fold infusion needle. Otolaryngol Head Neck Surg 105:478–479

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Chapter 33

Peroral Vocal Fold Augmentation in the Clinic Setting

33.1

Fundamental and Related Chapters

Please see Chaps. 5, 14, 31, and 34 for further information.

33.2

Disease Characteristics and Differential Diagnosis

Transoral vocal fold augmentation in the clinic setting is used to provide global vocal fold augmentation into the deep aspect of the vocal fold for patients with glottal insufficiency. Chapters 5 and 14 (“Glottic Insufficiency: Vocal Fold Paralysis, Paresis, and Atrophy” and “Principles of Vocal Fold Augmentation,” respectively) discuss the pertinent issues regarding glottal insufficiency and their subsequent treatment with vocal fold augmentation. Information regarding the specific indications and nature of the current materials available for augmentation are discussed in detail in Chaps. 5 and 14. The most common symptoms associated with patients with glottal insufficiency include the following: ■ ■ ■ ■ ■ ■

Dysphonia Decreased volume Vocal fatigue Odynophonia Dysphagia/Aspiration of liquids Compensated falsetto

Several advantages to performing peroral vocal fold augmentation in a clinic setting exist. The patient does not have to arrange transportation to and from the hospital nor undergo a general anesthetic, and does not have to be NPO before the surgical procedure. Furthermore, since the procedure is performed with the patient completely awake and in the upright position, vocal fold augmentation can be tailored to optimize the patient’s voice result by intermittently testing the voice throughout and at the completion of the procedure. All patients should be counseled prior to injection regarding the expected duration of augmentation from injection. Duration varies with technique as well as with the type of material injected.

33.3

33

Surgical Indications and Contraindications

Peroral vocal fold augmentation in the clinic setting is indicated in treatment of symptomatic glottal insufficiency due to any of the following factors: ■ ■ ■ ■ ■ ■

Unilateral vocal fold paralysis Vocal fold atrophy Vocal fold paresis Vocal fold scar Sulcus vocalis Soft tissue loss of the vocal fold(s)

Injection in the clinic setting can be used as a temporizing treatment to correct the patient’s glottal insufficiency or for permanent correction. A typical example is a patient with idiopathic unilateral vocal fold paralysis who presents early (1–3 months after onset) in the course of the disease. If the patient is aspirating, or significantly dysphonic and has significant vocal demands, then temporary augmentation via peroral vocal fold augmentation in the clinic is an excellent option. This addresses the patient’s vocal/swallowing needs, while allowing for spontaneous recovery of function and avoids a surgical procedure in the hospital or general anesthesia. Vocal fold augmentation can also be offered to a patient as a minimally invasive opportunity to “test drive” their voice after correction of glottic insufficiency. This may help the patient decide if a permanent treatment option for their glottic insufficiency is desirable. This approach is referred to as a trial vocal fold augmentation. Contraindications involve: ■ Unstable cardiopulmonary status ■ Inability to tolerate procedure under local anesthesia (i. e., hyperactive gag response or high level of anxiety) ■ Use of anticoagulants (aspirin, nonsteroidal anti-inflammatories, Coumadin) ■ Ideally, the patient should be taken off any anticoagulant medication prior to any planned injection; however, clinical experience has shown that the procedure can be performed if medically unable to stop anticoagulant therapy. ■ Inability to visualize the larynx adequately during the time of injection ■ This may occur if the patient has significant hooding of the arytenoid or severe supraglottic constriction.

210

Peroral VF Augmentation – Clinic

33.3.1 Suitability for Peroral Vocal Fold Augmentation in the Clinic Setting

33

In order to be a suitable candidate for peroral vocal fold augmentation: ■ The patient must tolerate a flexible laryngoscopy endoscopic exam, without excessive gag. Monitoring with a flexible endoscope is key to maintaining visualization, and a hyper-responsive gag may render any procedures impossible. However, it should be noted that gagging with a mirror or rigid peroral endoscope is not a contraindication. ■ The patient must have an adequate oral opening (at least 2-cm intermaxillary distance). ■ The patient must be able to remain reasonably still and upright in the exam chair for the duration of the procedure (typically 5–15 min). Patients with severe torticollis or head tremor are sometimes difficult to treat.

33.4

Surgical Equipment

Surgical equipment needed (Fig. 33.1): ■ ■ ■ ■ ■ ■ ■ ■ ■

Flexible laryngoscope (fiberoptic or distal chip) C-mount camera (attaches to flexible scope) Videomonitor for visualization 3–6 ml of 4% lidocaine Curved Abraham cannula for delivery to topical lidocaine Cetacaine spray (benzocaine/tetracaine topical) Oxymetazoline and/or 2% Pontocaine (for nasal decongestant and anesthesia) Cotton nasal pledgets Disposable nebulization device

Fig. 33.1  Equipment used for transoral vocal fold augmentation in the

clinic (cotton pledgets, 4% plain lidocaine, Neosynephrine, Bioform injection needle filled with Radiesse, Abraham cannula, drip catheter)

 

33.5

Surgical Procedure

Peroral vocal fold augmentation comprises the following: 1. Topical anesthesia nasal/oropharynx a) Topical oxymetazoline/Pontocaine 2% spray to nasal cavities (medication-soaked cotton nasal pledgets placed intranasally are also very helpful). b) Topical Cetacaine spray to oral cavity (palate/posterior pharynx) 2. Videomonitoring/topical anesthesia of larynx a) A video camera is attached to a flexible laryngoscope (distal chip flexible laryngoscope system preferred) is inserted through the nasal cavity (typically the side opposite the intended vocal fold to be injected) by an assistant, employing a “videocart system.” The scope is generally maintained slightly below the palate so that the tongue base and larynx can be easily viewed on the video monitor. b) Four percent lidocaine drip onto larynx under flexible laryngoscope guidance (3–6 ml) The patient is bent forward at the waist with the neck extended in a “sniffing” position to maximize laryngeal exposure. The tongue is grasped with gauze with the surgeon’s left hand. A 3-ml syringe of 4% lidocaine attached to an Abraham cannula is passed from the oral cavity into the pharynx under flexible laryngoscopy guidance. Approximately 1 ml is deposited over the tongue base, and 2–4 ml are dripped onto the vocal folds during phonation, producing the characteristic “laryngeal gargle” (Fig. 33.2). The maximum recommended dose of 4% lidocaine is approximately 7–8 ml (4.5 mg/kg; approximately 300 mg in 70-kg patient). The initial dose is usually followed by a brisk cough, as the anesthetic is aspirated and then distributed over the laryngotracheal mucosa. Absence of the laryngeal gargle and cough may indicate that the patient has swallowed the anesthetic, and additional topical applications may be indicated until the desired effect is obtained.

Fig. 33.2  “Laryngeal gargle” of 4% lidocaine delivered via an Abraham

cannula

 

Fig. 33.3  Nebulization of 4% plain lidocaine for laryngeal anesthesia

Fig. 33.4  Drip catheter for applying 4% plain lidocaine to larynx via

flexible laryngoscope with a working channel

An alternative method to obtain anesthesia of the larynx involves nebulization of lidocaine, using a simple disposable nebulization device (frequently used in the hospital for respiratory therapy) and an external source of pressurized air (often from an oxygen tank). Four percent plain lidocaine can be nebulized and inhaled peroral by the patient (Fig. 33.3). This method of anesthesia provides a simple and less physician-involved method for obtaining laryngeal anesthesia. Typically, 4–5 ml of plain lidocaine is nebulized over a 5- to 10-min period to achieve anesthesia of the larynx and pharynx. After the nebulization process, a curved Abraham cannula can be used to supplement any further need for laryngeal anesthesia on an as-needed basis and to test for complete anesthesia of the larynx and, specifically, the vocal folds. Another technique to deliver anesthetic agent to the larynx is using a small Silastic, flexible cannula through the working channel of the flexible laryngoscope or an Endosheath™ with a working channel (Medtronic Xomed, Jacksonville, Fla.). This Silastic catheter (Olympus America, PW-2L-1.B, Center Valley, Pa.) is passed through the working channel

Chapter 33

of the flexible laryngoscope and used to deliver 4% plain lidocaine to the endolarynx during sustained phonation to achieve the “laryngeal gargle” as described above (Fig. 33.4). This catheter allows direct application of the anesthesia to the specific areas intended for the vocal fold injection and is very well tolerated by patients. 3. Transoral passage of the needle into the endolaryngeal region a) The two most commonly used needles for peroral vocal fold augmentation in a clinic setting are the orotracheal injector device (Medtronic Xomed) and the injection needle developed by Bioform Medical (Bioform Medical, San Mateo, Calif.). Each of these injection devices use fine-gauge needles (27- and 25-g, respectively.) The former device is curved for transoral injection, and the latter is malleable and can be bent to the appropriate dimensions and curvature needed for transoral vocal fold augmentation. In preparation for vocal fold injection, the intended injection material should be attached to the injection needle and “primed” to eliminate the dead space within the needle. b) The patient holds his/her own tongue with gauze, or the surgeon grasps the tongue with the left hand. The needle is passed through the oral cavity and then advanced into the oropharynx under direct visualization from the flexible laryngoscope. The patient is instructed to phonate /a/ as the needle enters the oral cavity, which results in palatal raising, clearing the path into the oropharynx. The assistant should position the fiberoptic scope just above the palate, until the needle is visualized in the oropharynx. c) The needle is then guided into the oropharynx and the endolarynx under endoscopic visualization, as the assistant follows closely behind with the flexible laryngoscope (Fig. 33.5). The assistant must be adept at manipulating the flexible scope; consistent visualization of the needle can be challenging in a narrow airway with copious secretions. The flexible scope should be positioned a few millimeters above the true vocal folds, providing a clear, well-illuminated view before, during, and immediately after the injection (Fig. 33.6). 4. Vocal fold injection a) For unilateral vocal fold paralysis, the injection should be placed at two sites (Fig. 33.7): (1) the posterior aspect (lateral to the vocal process) and (2) the midmembranous vocal fold. b) The initial injection should be at the posterior aspect of the vocal fold, where, typically, the most correction is needed. c) The depth of injection should be into the substance of the vocal fold in a lateral position (see Chap. 14, “Principles of Vocal Fold Augmentation”). Care should be taken to avoid superficial placement into Reinke’s space, which will result in a stiff vocal fold and poor voice quality (Fig. 33.8). d) If the subglottis begins to bulge during injection, then the needle should be withdrawn slightly. Once the posterior vocal fold is adequately medialized, a smaller additional amount can be deposited at the mid vocal fold, if needed.

211

212

Peroral VF Augmentation – Clinic

 

33

Fig. 33.5  Transoral vocal fold augmentation in the clinic. Surgeon on

Fig. 33.6  Flexible laryngoscope image during peroral injection aug-

Fig. 33.7  Injection location(s) for deep vocal fold augmentation

Fig. 33.8  Injection depth for deep vocal fold

the left with the assistant on the right and patient holding her own tongue

e) If the injected substance extrudes from the puncture

hole, then the material can be cleared by instructing the patient to cough or clear their throat (this is rarely a problem when a fine-gauge needle is used). f) The injection should be carried out in a stepwise fashion, checking for improvement in the patient’s voice periodically. For most injectables, the medialized vocal fold should be overinjected (past midline) to a variable degree, depending on the specific nature of the material and the primary goal

mentation. The scope should be positioned a few millimeters above the true vocal folds, providing a clear, well-illuminated view

of the procedure (long duration of the temporary agent versus immediate need for optimal voice function.) In general, the vocal fold is medialized until the voice is maximally improved, and then an additional 0.1–0.2 ml is injected to achieve overcorrection. This overcorrection is necessary, because all injectables have a small aqueous component that will be absorbed 3–5 days after injection. The total amount necessary for unilateral augmentation is typically less than 1 ml, but amount injected should be determined by the sound of the voice and appearance of the vocal fold, not by the volume injected.

 

Chapter 33

For patients with a bowed vocal fold due to atrophy/paresis or presbylaryngis, the injection differs slightly from the previous technique. These cases typically require injection principally in the midportion of the vocal fold, where the maximal glottal gap usually occurs. In severe cases of muscular atrophy, the posterior vocal fold can be augmented to fill in the atrophy that occurs just anterior to the vocal process. Again, overcorrection is the rule, even in the case of bilateral injections. Airway compromise should not be a concern, because the posterior (respiratory) glottis remains patent and in cases of vocal fold atrophy both vocal folds are usually fully mobile.

33.6

Postoperative Care and Complications

Postoperative care includes: ■ Immediately after vocal fold injection in the clinic, patients should be observed for a short period to monitor for any complications of the vocal fold injection, most notably, airway difficulties. ■ Patients need to be instructed that they should not take anything orally for approximately 2 hours after vocal fold injection to allow adequate time for the local anesthesia to wear off. In addition, patients should take care as they resume oral intake to ensure that all aspects of the anesthesia are gone. ■ The use of strict voice rest after vocal fold injection is not standardized and is often determined by the size of the vocal fold injection needle used and the individual surgeon’s preferences. Given that most vocal fold injections are now performed with a fine-gauge needle, prolonged voice rest (exceeding 24 hours) is most likely not indicated. Some surgeons use no voice rest; others will use a 24-hour period of voice rest. The rationale for voice rest after vocal fold injection is to minimize loss of the injected material being extruded through the injection site(s) if immediate phonation is allowed. ■ Antibiotics and steroids associated with the vocal fold injection are not typically indicated for this procedure. ■ Patients should be instructed that, because of the vocal fold edema associated with the procedure, as well as possibly the overinjection of the augmentation material, optimal voice quality is typically not achieved for 1–2 weeks after vocal fold injection. Complications of peroral vocal fold injection include inappropriate placement of the vocal fold injection material comprise: ■ Either too superficially into Reinke’s space ■ Very lateral into the paraglottic space ■ Inferior into the subglottis

If these inappropriate locations of vocal fold injection are recognized during the procedure, then often the material can be “milked” out of the vocal fold with the use of an Abraham cannula, applying gentle lateral pressure to the vocal fold. If this is not possible, then it would be advisable that the vocal fold material, if permanent in nature (such as calcium hydroxylapatite) be removed under microlaryngoscopy with general anesthesia in the near future.

Key Points ■ Peroral vocal fold augmentation in a clinic setting provides the patient an opportunity for permanent or temporary vocal fold augmentation under local anesthesia, obviating a trip to the operating room and general anesthesia. ■ Appropriate patient selection is the key to successful peroral vocal fold augmentation. Patients should be cooperative and should not have a hyperactive gag reflex. ■ Adequate anesthesia can be easily obtained for peroral vocal fold augmentation, with topical lidocaine and does not necessitate nerve blocks or sedation (orally or intravenously). ■ Peroral vocal fold augmentation offers the unique advantage of having the patient unsedated and positioned in an upright position to monitor voice quality and vocal fold closure pattern during the injection. This allows for customization and maximum control of the vocal fold augmentation to optimize postoperative voice quality and function.

Selected Bibliography 1

2

3

4 5

Arad-Cohen A, Blitzer A (1999) Office-based direct fiberoptic laryngoscopic surgery. Oper Tech Otolaryngol Head Neck Surg 9:238–242 Bové MJ, Jabbour N, Krishna P, Rosen CA et al (2007) Operating room versus office-based injection laryngoplasty: a comparative analysis of reimbursement. Laryngoscope 117:226–230 Chu PY, Chang SY (1997) Transoral Teflon injection under flexible laryngovideostroboscopy for unilateral vocal fold paralysis. Ann Otol Rhino Laryngol 106:783–786 Simpson CB, Amin MR (2004) Office-based procedures for the voice. Ear Nose Throat J 83(Suppl.):6–9 Simpson CB, Amin MR, Postma GN (2004) Topical anesthesia of the airway and esophagus. Ear Nose Throat J 83(Suppl.):2–5

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Chapter 34

Percutaneous Vocal Fold Augmentation in the Clinic Setting

34.1

Fundamentals and Related Chapters

Please see Chaps. 5, 14, 31, and 33 for further information.

34.2

Disease Characteristics and Differential Diagnosis

Percutaneous vocal fold augmentation in the clinic setting is used to provide global vocal fold augmentation into the deep aspect of the vocal fold for patients with glottal insufficiency. Chaps. 5 and 14 (“Glottic Insufficiency: Vocal Fold Paralysis, Paresis, and Atrophy” and “Principles of Vocal Fold Augmentation,” respectively) discuss the pertinent issues regarding glottal insufficiency and their subsequent treatment with vocal fold augmentation. The most common symptoms associated with patients with glottal insufficiency include the following: ■ ■ ■ ■ ■ ■

Dysphonia Decreased volume Vocal fatigue Odynophonia Dysphagia Compensatory falsetto

A variety of major advantages to performing percutaneous vocal fold augmentation in the clinic setting exist. Specifically, it is a significant advantage to the patient, given that the patient does not have to arrange transportation to and from the hospital nor undergo a general anesthetic, and does not have to be NPO before the surgical procedure. Furthermore, since the procedure is performed with the patient completely awake and in the upright position, vocal fold augmentation can be tailored to optimize the patient’s voice result by intermittently testing the voice throughout and at the completion of the procedure. Information regarding the specific indications and nature of the current materials available for augmentation are discussed in detail in Chaps. 5 and 14. Awake, percutaneous vocal fold augmentation in the clinical setting is a viable option for many patients with glottal insufficiency. Vocal fold augmentation using a percutaneous approach in the clinic or at the bedside has been successfully performed with a number of different materials and can be performed with either temporary or permanent augmentation materials. See Chap. 14 for a discussion of different augmentation materials.

34

A variety of percutaneous vocal fold augmentation approaches exist for in-office procedures. These percutaneous approaches include: ■ Transthyroid cartilage ■ Transcricothyroid membrane ■ Transthyrohyoid membrane The transthyroid cartilage and cricothyroid membrane approaches are very similar. Ossification of the thyroid cartilage can prevent passage of the injection needle through the thyroid cartilage and thus, a cricothyroid or thyrohyoid approach may be required. All of these approaches require anesthesia of the overlying skin, a skilled endoscopist as an assistant, and a 23to 25-g needle (1.5 in. long). The thyrohyoid approach can be used for vocal fold augmentation as well as for injection of therapeutic substances such as cidofovir and Botox. The transthyrohyoid approach was developed by Milan Amin, M.D., and is as well tolerated as other percutaneous approaches, but provides unique visualization and precision compared to transthyroid cartilage and cricothyroid approach.

34.3

Surgical Indications and Contraindications

Percutaneous vocal fold augmentation in the clinic setting is indicated in the treatment of symptomatic glottal insufficiency (dysphonia and/or dysphagia) due to any of the following factors: ■ ■ ■ ■ ■ ■

Unilateral vocal fold paralysis Vocal fold atrophy Vocal fold paresis Vocal fold scar Sulcus vocalis Soft tissue loss of the vocal fold(s)

Injection in the clinic setting can be used as a temporizing treatment to correct the patient’s glottal insufficiency or for permanent correction. A typical example is a patient with idiopathic unilateral vocal fold paralysis who presents early (1–3 months after onset). If the patient is aspirating, or dysphonic and has vocal demands, then temporary augmentation via a percutaneous vocal fold augmentation in the clinic is an excellent option. This addresses the patient’s vocal/swallowing

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Percutaneous Augmentation

needs, while allowing for spontaneous recovery of function without having to perform a surgical procedure in the hospital with general anesthesia. Vocal fold augmentation can also be offered to a patient as a minimally invasive opportunity to “test drive” their voice after correction of glottic insufficiency. This may help the patient decide if a permanent treatment option for their glottic insufficiency is desirable. This approach is referred to as a trial vocal fold augmentation. Contraindications comprise: ■ Unstable cardiopulmonary status ■ Inability to tolerate procedure under local anesthesia (i. e., high level of anxiety) ■ Use of anticoagulants (aspirin, nonsteroidal anti-inflammatories, Coumadin) ■ Ideally, the patient should be taken off any anticoagulant medication prior to any planned injection; however, clinical experience has shown that the procedure can be performed if medically unable to stop anticoagulant therapy. ■ Inability to visualize the larynx adequately during the time of injection ■ This may occur if the patient has significant hooding of the arytenoid or severe supraglottic constriction. ■ Poorly defined or obstructing neck landmarks

34.3.1 Suitability for Percutaneous Vocal Fold Augmentation in the Clinic Setting To be a suitable candidate: ■ The patient must tolerate a flexible laryngoscopy endoscopic exam without excessive gag. Monitoring with a flexible endoscope is key to maintaining visualization, and a hyper-responsive gag may render any procedures impossible. However, it should be noted that gagging with a mirror or rigid transoral endoscope is not a contraindication. ■ The patient must be able to remain reasonably still and upright in the exam chair for the duration of the procedure (typically 5–15 min). Patients with severe torticollis or head tremor are sometimes difficult to treat.

34.4 ■ ■ ■ ■

Surgical Equipment

Skilled endoscopist to assist surgeon Flexible laryngoscope (chip-tip preferred to fiber optic) Videomonitor for visualization Local anesthetic (1% Lidocaine with epinephrine) to anesthetize skin over the cricothyroid membrane and thyroid ala on the side to be injected

 

■ Local anesthetic/decongestant mix (e. g., oxymetazoline and 2% Pontocaine) for nasal passage in order to facilitate flexible laryngoscopy ■ Injection material (see Chap. 14) ■ Alcohol prep pad or topical prep solution such as povidone–iodine

34.5

Surgical Procedure

1. Percutaneous vocal fold augmentation in the clinic setting in

a transthyroid cartilage or transcricothyroid membrane approach. a) The area overlying the injection site may be cleaned with an alcohol prep pad or povidone–iodine prep. b) The patient is positioned in the sitting position with the neck in neutral position and the head slightly extended on the neck (i. e., the sniffing position). c) It is important to anesthetize both the skin over the area to be injected as well as the upper airway in preparation for flexible laryngoscopy. To anesthetize the skin and subcutaneous tissues, approximately 0.5 ml of local anesthetic is sufficient. The skin and subcutaneous tissues overlying the cricothyroid membrane are injected as well as the area over the inferior aspect of the thyroid ala on the side(s) intended for injections. Overinjection of this area with anesthetic may transiently impair cricothyroid function, thus clouding the picture of paresis/paralysis at the time of injection. d) The nasal cavity is anesthetized and decongested as is customary for the surgeon. Topical anesthesia to the endolarynx (see Chap. 33, “Peroral Vocal Fold Augmentation in the Clinic Setting”) is helpful per the surgeon’s preference but is usually not necessary for the percutaneous approach. e) Flexible laryngoscopy is performed by the assistant and the preprocedure diagnosis/diseases are confirmed. Ideally, the tip of the scope is maintained over the contralateral arytenoid, as posteriorly as possible to avoid stimulating the supraglottic structures. This position allows for some visualization of the infraglottic surface of the vocal fold to be injected. f) The cricothyroid membrane is palpated by the injecting surgeon. In many patients, it is possible to see (endoscopically) the depression of the underlying mucosa during this maneuver (Fig. 34.1). This is very helpful in estimating the height of the vocal fold relative to the cricothyroid membrane. If the impression from the palpating finger is not seen, then this maneuver may be performed with the injection needle without penetrating into the airway. g) The vertical and horizontal distance from this point to the midpoint of the membranous vocal fold is estimated by the surgeon. The needle (23 or 25 g, or 1.5 in. long) is placed along a vertical line approximately 6–12 mm from the midline; this distance depends on the size of the

 

Fig. 34.1  Palpation of cricothyroid space during simultaneous flexible

laryngoscopy

Fig. 34.2  Transthyroid cartilage placement of injection needle into

vocal fold

Chapter 34

217

larynx. The needle should be oriented perpendicularly in relation to the thyroid ala. h) The needle is placed against the thyroid ala at the desired vertical level along this line. In most females and younger males, gentle steady pressure will allow the needle to pass through the cartilage (Fig. 34.2). Care should be taken not to “past point” as the needle is passed through the thyroid cartilage. This will avoid entering the airway. If the needle meets significant resistance, then the needle is kept in the same line and “walked” down the thyroid ala until the inferior aspect of the thyroid cartilage is reached. The needle is then advanced medially, again perpendicular to the thyroid ala for approximately 3–4 mm through the junction of the thyroid ala and the cricothyroid membrane. At this point, the tip of the needle is in the infraglottic vocal fold and is directed nearly straight up, vertically (Fig. 34.3). All attempts should be made to avoid entering the airway. The needle may be seen indenting the infraglottic mucosa or penetrating the floor of the ventricle. To facilitate identifying where the needle has entered into the endolarynx, the needle can be moved back and forth rapidly several times over a short distance. The tip of the needle is then redirected if found not to be located in the membranous vocal fold. i) Once the needle location is confirmed, vocal fold injection is started slowly. Good visualization of the vocal fold is essential at this stage. As the material is injected, the vocal fold will swell. The endpoint for injection will be determined by the endoscopic appearance of the vocal fold as well as by the patient’s voice. Depending on the

Fig. 34.3  Transcricothyroid

membrane placement of injection needle into vocal fold

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Percutaneous Augmentation

nature of the injectate, modest to moderate overcorrection is often desirable (see Chap. 14). The patient may immediately notice the improvement in the voice—it is important in most cases to overcorrect past this point, if possible, to allow for a longer duration of overall benefit for temporary augmentation materials (see Chap. 14). j) If the contour is not ideal (focally overinjected) immediately after injection, then a hard cough may “straighten out” the vocal fold as seen during the endoscopy. k) In the case of bilateral vocal fold pathology, there is generally no limitation to treating both sides at the same setting. 2. Thyrohyoid approach to the larynx (of Milan Amin, M.D.) a) Spray (topical 50:50 mix of oxymetazoline/Lidocaine spray to nasal cavities) b) Inject skin and subcutaneous tissues overlying the thyrohyoid notch using a 25-g needle with 1% lidocaine with 1:100,000 epinephrine. c) Ensure the patient is positioned sitting upright with neck extended to expose the thyrohyoid notch. d) An assistant passes the flexible laryngoscope through the nasal cavity (usually left side) and positions the scope so the tongue base and larynx are clearly visualized. e) A 25-g needle (1.5 in. long) and syringe with topical 4% Lidocaine is passed into the airway above the vocal folds via the thyrohyoid membrane. The needle is passed immediately above the thyroid notch and directed acutely downward until the needle enters the airway in the area of the petiole. Proper positioning is confirmed by flex-

Fig. 34.4  Needle path for the thyrohyoid approach to the larynx

 

ible laryngoscopic guidance and the ability to draw back air into the syringe. Three milliliters of topical lidocaine is deposited in the larynx. Note that absence of a laryngeal gargle or cough suggests the patient swallowed the anesthetic, and additional 4% lidocaine may be needed. Adequate anesthesia is achieved after 3–5 min. Alternatively, topical laryngeal anesthesia may be administered through a working channel of the flexible laryngoscope if this is available or a peroral approach (see Chap. 33, “Peroral Vocal Fold Augmentation in the Clinic Setting”). f) Prepare implant/injectable material in appropriate syringe attached to a 25- or 23-g (1.5-inch needle) and “prime” the needle with material. g) The needle is passed in the midline just above the thyrohyoid notch in a downward, acute angle just under the patients’ chin. It may help to have the patient turn his/ her head slightly away from the surgeon to obtain the proper angle. The tip of the needle passes through the pre-epiglottic space and enters the larynx at the petiole of the epiglottis (Figs. 34.4, 34.5). h) Under direct guidance on the monitor, the assistant advances the flexible scope to follow the needle as it is guided to the appropriate injection site(s) (Figs. 34.6, 34.7). If necessary, bilateral vocal fold injection is achieved by backing the needle out slightly (without removing it) and redirecting the needle tip under direct visualization to the other side.

Fig. 34.5  Placement of needle through thyrohyoid membrane (endo-

scopic view)

 

Chapter 34

Fig. 34.6  Injection location for deep vocal fold

34.6

Postoperative Care and Complications

Postoperative care includes: ■ Immediately after vocal fold injection in the clinic, patients should be observed for a short period to monitor for any complications of the vocal fold injection, most notably, airway difficulties. ■ Patients need to be instructed that they should not take anything orally for approximately 2 h after vocal fold injection to allow adequate time for the local anesthesia to wear off. In addition, patients should take care as they resume oral intake to insure that all aspects of the anesthesia are gone. ■ The use of strict voice rest after vocal fold injection is not standardized and is often determined by the size of the vocal fold injection needle used and the individual surgeon’s preferences. Given that most vocal fold injections are now performed with a fine-gauge needle, prolonged voice rest (exceeding 24 hours) is most likely not indicated. Some surgeons use no voice rest; others will use a 24-hours period of voice rest. The rationale for voice rest after vocal fold injection is to minimize loss of the injected material being extruded through the injection site(s) if immediate phonation is allowed. ■ Antibiotics and steroids are not typically indicated for this procedure. ■ Patients should be instructed that, because of the vocal fold edema associated with the procedure, as well as the overinjection of the augmentation material, optimal voice quality is typically not achieved for 1–2 weeks after vocal fold injection.

Fig. 34.7  Injection depth for deep vocal fold augmentation

Complications comprise: ■ Injection should be aborted at the first sign of airway embarrassment or unexpected vocal fold swelling. Dramatic swelling may occur if air is inadvertently injected. ■ Bleeding into the airway occurs in many patients. It is typically minimal though when it leads to coughing, the endolarynx may be covered with a thin film of blood and limit visibility. The patient is asked to gargle (if possible) and the procedure is usually continued. ■ Hematoma in the skin overlying the injection site

Key Points ■ Percutaneous vocal fold augmentation in the clinic setting is an excellent alternative for patients who prefer not to undergo general anesthesia or will not tolerate transoral vocal fold injection in the clinic setting for either temporary or permanent vocal fold augmentation. ■ Providing the patient with information and supportive reassurance before and during the procedure is very important. ■ Identification of the needle in the mid to posterior membranous vocal fold is essential for successful percutaneous vocal fold augmentation in the clinic setting. ■ Patient positioning, skilled endoscopy of the assistant, and knowledge of multiple approaches to the vocal fold will provide the highest chance of success for vocal fold augmentation.

219

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Percutaneous Augmentation

 

Selected Bibliography 1 2

34

3

Amin, MR (2006) Thyrohyoid approach for vocal fold augmentation. Ann Otol Rhinol Laryngol 115:699–702 Berke GS, Gerratt B, Kreiman J, Jackson K (1999) Treatment of Parkinson hypophonia with percutaneous collagen augmentation. Laryngoscope 109:1295–1299 Chhetri DK, Blumin JH, Shapiro NL, Berke GS (2002) Officebased treatment of laryngeal papillomatosis with percutaneous injection of Cidofovir. Otolaryngol Head Neck Surg 126:642–648

4

5

6

Grant JR, Hartemink DA, Patel N, Merati AL (2006) Acute and subacute awake injection laryngoplasty for thoracic surgery patients. J Voice. 2006 Oct [Epub ahead of print] Lipton RJ, McCaffrey TV, Cahill DR (1989) Sectional anatomy of the larynx: implications for the transcutaneous approach to endolaryngeal structures. Ann Otol Rhinol Laryngol 98:141–144 Rosen CA, Thekdi AA (2004) Vocal fold augmentation with injectable calcium hydroxylapatite: short-term results. J Voice 18:387–391

Chapter 35

Botulinum Toxin Injection of the Larynx

35.1

Fundamental and Related Chapters

Please see Chaps. 7, 33, and 34 for further information.

35.2

Disease Characteristics and Differential Diagnosis

35.2.1 Botulinum Toxin Fundamentals Botulinum toxin is a naturally occurring clostridial neurotoxin that reversibly inhibits release of acetylcholine into the synaptic cleft of the neuromuscular junction, thereby causing flaccid paralysis. Clinically, this results in a reversible, dose-dependent weakening of injected muscles. In addition to its muscle weakening effect, botulinum toxin has been hypothesized to have an effect on efferent feedback to the central nervous system, although whether this is by means of a direct effect on intramuscular gamma motor neurons or an indirect consequence of muscle weakening remain matters of speculation. This efferent effect may be an important part of the broad success of botulinum toxin in the treatment of dystonia, particularly in comparison to surgical denervation. Although seven different serotypes of botulinum toxin are known, only two are available for clinical use, type A (Botox®, Allergan, Irvine, Calif., and Dysport®, Ipsen, Ltd., Slough, UK) and type B (Myobloc®, Elan Pharmaceuticals, Dublin, Ireland). Type A appears to have a slightly longer duration of effect (approximately 90 days) than has type B, and the Botox preparation diffuses less from the point of injection than the other two, both factors with practical clinical consequences. Dose is expressed in mouse units (U) and differs substantially among the commercial preparations; the reader should note that dosages discussed in this chapter refer to Botox. Adverse effects of botulinum toxin treatment may result from overweakening of the intended target muscle as well as unintended weakening of surrounding muscles. Therefore, both appropriate dosing and the tissue distribution of the toxin are crucial. In general, dose is proportional to targeted muscle mass, although the range of therapeutic dosing is typically highly variable. There is no standard botulinum toxin dose for patients with spasmodic dysphonia. Some patients get the best results from a unilateral dose and others from bilateral treatment. In bilateral injections for adductor spasmodic dysphonia, for example, therapeutic doses range from 0.3 to 15 U per thyroarytenoid muscle, although most dysphonia is well controlled with doses of 0.625–2.5U. The distribution of

35

the toxin is affected by accuracy of needle placement as well as by volume of the injectate, which can be varied as necessary. Systemic effects from botulinum toxin are very unlikely, particularly at doses used to treat laryngeal diseases. Development of antibody resulting in clinical resistance to toxin is very rare with recent preparations of toxin, and may be tested for with an antibody assay, or, more practically, with an injection into an area where muscle effect is obvious, such as the forehead. Technical issues rather than resistance remain the most likely reason for an ineffective laryngeal injection. For a more in-depth description of the pharmacology of botulinum toxin, the reader is referred to article by Aoki cited in “Selected Bibliography,” below.

35.2.2 Spasmodic Dysphonia and Essential Tremor Dystonia is a chronic neurologic disorder of central motor processing characterized by task-specific, action-induced muscle spasms. Spasmodic dysphonia is a focal dystonia involving the larynx. It is usually classified into adductor, abductor, and mixed forms, the first two characterized by hallmark clinical features and the latter being a combination of the first two. Adductor spasmodic dysphonia, the more common form, causes inappropriate glottic closure and as a result, produces strangled breaks in connected speech. Abductor spasmodic dysphonia, in contrast, causes inappropriate glottal opening that produces breathy breaks and hypophonia. Although clinical features are not always typical, the classification of spasmodic dysphonia into adductor and abductor varieties remains essential to treatment: Botulinum toxin is injected into the thyroarytenoid/lateral cricoarytenoid muscles (TA-LCA) in adductor spasmodic dysphonia, and into the posterior cricoarytenoid muscle in abductor spasmodic dysphonia. Essential voice tremor is an age-related disorder of involuntary muscle contraction, which can affect the voice to a debilitating extent in some patients. Clinical examination reveals rhythmic, oscillatory movement of the portions of the vocal tract (i. e., velum, base of tongue, pharynx, larynx, vocal folds), which typically involves a wide variety of muscles of the upper aerodigestive tract. No pharmacologic intervention has been documented to be effective in essential voice tremor, and botulinum toxin chemodenervation has provided symptomatic relief in selected patients. Administered much as in adductor spasmodic dysphonia, botulinum toxin symptom control is usually not as dramatic in essential tremor, probably due to differences in the pathophysiology of the two diseases. The

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Botulinum Toxin Injection of the Larynx

areas of tremor most responsive to the botulinum toxin injection from a symptom perspective are the true vocal folds and the false vocal folds.

 

35.3

Surgical Indications and Contraindications

Indications comprise:

35.2.3 Different Botulinum Toxin Injection Approaches

35

There are a variety of injection approaches to deliver botulinum toxin to the larynx: ■ Percutaneous injection with EMG guidance (most traditional) ■ Percutaneous with laryngoscopic guidance ■ Supraglottic botulinum toxin injection with laryngoscopic guidance Distinct advantages and disadvantages exist for these approaches (see below). Selection of the best injection approach is determined by surgeon’s training, equipment availability, patient’s disease characteristics and preference. Percutaneous injection under EMG guidance is the quickest and most precise method of botulinum toxin delivery into the larynx. However, this technique also has a learning curve and can take a considerable amount of time and practice to master. In addition, the technique requires the purchase of additional equipment (EMG machine) and moderate technical mastery of EMG interpretation. Given these barriers, some surgeons who perform laryngeal botulinum toxin injections on an infrequent basis may wish to consider an alternative method, a percutaneous or peroral injection technique, using laryngoscopic (visual) guidance. Given that this approach (without EMG guidance) is less precise, often the toxin dose used is slightly higher than EMG-guided percutaneous injection. Supraglottic botulinum toxin injection with laryngoscopic guidance for spasmodic dysphonia offers the advantages of: ■ More gradual/smooth onset of action ■ Smoothing of vocal fold “peaks and troughs” associated with true vocal fold injections ■ Less severe (minimal to none) breathy voice ■ Preserves singing voice/pitch control in many patients The disadvantages of this approach include a shorter duration (typically 6–8 weeks), less predictable voice results and more involved injection procedure. The unreliable voice results most likely occur from variable supraglottic muscular anatomy and variable needle location during the supraglottic injection. Supraglottic botulinum toxin injection with laryngoscopic guidance may be preferred in professional voice users afflicted with adductor spasmodic dysphonia, given the reduced number of days with a soft, weak, breathy voice.

■ Spasmodic dysphonia ■ Essential voice tremor ■ Vocal fold granuloma Muscle selection, injection strategies, and dosing involves the following: 1. Spasmodic dysphonia The standard treatment for adductor spasmodic dysphonia (SD) is bilateral EMG-guided, percutaneous injections of the TA-LCA muscles, using equal amounts of botulinum toxin, based on the understanding that the motor control disorder is bilateral and symmetric (see Blitzer et al. 1998). In patients with abductor spasmodic dysphonia, bilateral posterior cricoarytenoid muscles are treated, although injections are staggered for reasons of airway safety. For both forms of SD, the dose is adjusted based on the severity of the disease and on response to treatment, and the value of bilateral versus unilateral treatment is reassessed. It is clear from reports in the literature that unilateral injection may provide essentially equivalent symptomatic relief in patients with adductor spasmodic dysphonia, although the dose is usually increased and may not provide the same duration of benefit. A reasonable initial dose in adductor spasmodic dysphonia is 1.25 U per side, which represents a low-average dose. Dosing at subsequent treatment is adjusted based on patients response. For abductor spasmodic dysphonia, the first posterior cricoarytenoid (PCA) muscle is injected with 5 U; voice result and vocal fold mobility is evaluated 2 weeks later. The contralateral dose is determined in light of this, so that the dose in inversely proportional to the degree of muscle weakness observed. Asymmetric dosing is the rule in abductor spasmodic dysphonia. Botulinum toxin treatment results in an initial period of marked muscle weakness lasting several days, followed by a 3- to 4-month-long plateau of milder weakening, which constitutes the principal therapeutic effect. This effect probably occurs because of the two-stage mechanism of neural recovery from botulinum toxin administration. The transient, breathy dysphonia that usually follows bilateral TALCA injections is a clinical manifestation of this pattern, and is to some extent inevitable. In general, the length of the period of breathiness and the length of the therapeutic effect are approximately proportional, so that attempts to shorten the breathiness may compromise the duration of therapeutic effect. Naturally, patients prefer to minimize the frequency of their injections, but each will have a different tolerance for the initial breathy voice phase of their treatment. Dyspnea is the equivalent early treatment effect in abductor SD. Because this may be life threatening, only one side is treated at a time, to allow partial recovery of the first prior to denervation of its counterpart. Alternate explanations

 

Chapter 35

for greater difficulty and less satisfactory results in abductor SD patients are (1) the PCA muscle injection is technically more difficult and/or (2) some patients thought to have abductor SD have mixed SD, a combination of adductor and abductor SD. Even so, the potential for dyspnea imposes important treatment limitations in abductor spasmodic dysphonia, which may account for the generally less satisfactory results in these patients. 2. Essential voice tremor Essential voice tremor is typically treated with bilateral symmetric muscle injections of the TA-LCA muscles in the similar manner of adductor spasmodic dysphonia. These patients are more likely to be troubled by prolonged post­ injection breathiness; thus, a lower dose is preferred by most patients. Essential voice tremor usually involves the muscles of the upper aerodigestive tract more broadly, but no systematic attempt to treat other involved muscles, such as the strap muscles, has been made, and the functional requirements of swallowing prevent treatment of still others, such as pharyngeal constrictors. When the tremor is found to be predominantly at the level of the true and false vocal folds, botulinum toxin injection of the TA-LCA muscles and/or the supraglottis can be very effective. 3. Vocal fold granuloma Botulinum toxin injection has been advocated by some to weaken the vocal adductory force of the arytenoid to allow better healing and resolution of vocal fold granuloma. Botulinum toxin is injected into ipsilateral or bilateral TALCA muscles, in doses ranging from 1.25 to 20 U. Most often 5 U injected unilaterally is adequate. In most cases, a single application, either alone or in conjunction with surgical removal, has been sufficient to permit resolution of the granuloma. It should be noted that patients treated with this approach will have a severe breathy, weak voice for several months, and this may have a major impact on the functional voice capacity (work and social). Contraindications to injection include: ■ Pregnancy ■ Breast feeding ■ Impaired abduction of vocal fold for PCA injection (relative) ■ Neuromuscular diseases (e. g., myasthenia gravis) ■ Concurrent aminoglycoside treatment

35.4

Equipment

Equipment for botulinum toxin injection: ■ EMG device (AccuGuide® [Medtronic Xomed, Jacksonville, Fla.] is a hand-held device that offers principally acoustic output which may used as a lower-cost alternative to more expensive traditional electromyography machines.) ■ Botulinum toxin ■ Insulated 26-g needle electrode

■ Ground and reference electrodes ■ Tuberculin syringe ■ (Optional) local anesthetic for skin (1% lidocaine with 1:100,000 epinephrine) and tracheal use Additional equipment necessary for percutaneous injection with laryngoscopic guidance and/or peroral supraglottic injection with laryngoscopic guidance: ■ Flexible laryngoscope (with working channel or endosheath with channeled sheath (Vision Sciences, Orangeburg, New Jersey) ■ C-mount camera (attaches to flexible laryngoscope) ■ Videomonitor for visualization ■ Three to 6 ml of 4% plain lidocaine ■ 27-g needle, 37 mm in length (percutaneous injection with laryngoscopic guidance ■ Orotracheal injector device for peroral injection approach (Medtronic Xomed) ■ Cetacaine spray (benzocaine/tetracaine topical) ■ Curved Abraham cannula ■ Fine-gauge injection needle for use with working channel in flexible laryngoscope

35.5

Procedure

1. Botulinum toxin reconstitution and dilution

Botox is supplied as a freeze-dried powder in 100-U vials. It is reconstituted with preservative-free saline. The product insert provides dilution instructions to achieve a wide variety of concentrations (1.25–10 U/0.1 ml). Injection volume should be limited to minimize diffusion. Preferable volume is 0.1 ml per vocal fold; however, a volume of 0.2 ml is also acceptable. At that volume, there is virtually no risk of airway difficulty from vocal fold engorgement. A needle larger than 21 g should be used for reconstitution, dilution, and transfer from vial to injection syringe. After the correct dose is prepared, the insulated 26-g injection needle is attached to the syringe. 2. Percutaneous EMG-guided botulinum toxin injection a) Connecting EMG electrodes A ground and a reference electrode are attached to the patient’s skin at a convenient site so as not to obstruct the injection or inconvenience the injector. The insulated injection needle, which serves as a monopolar sampling electrode during the injection, is attached to an EMG recording device. b) Thyroarytenoid–lateral cricoarytenoid muscle complex localization and injection for Adductor SD The patient is positioned in a semirecumbent position, with the chin raised and the head back. If the neck is thin and laryngeal landmarks are easily palpable, then a shoulder roll may be omitted. If the neck is short and stocky, or the larynx is canted forward, then a shoulder roll is helpful. Alternatively, the headpiece of the chair can be positioned to allow neck extension (Fig. 35.1).

223

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35

Botulinum Toxin Injection of the Larynx

The patient is asked to breathe quietly and to try not to swallow during the procedure. Both skin and intratracheal anesthetic may be injected, the latter via a cricothyroid puncture. The anesthetic approach is highly variable among experienced clinicians. Some argue that the discomfort to the patient from the anesthetic injection is approximately equivalent to that from the toxin injection itself, while others will perform the skin injection (30-g needle using 1% lidocaine with 1:100,000 epinephrine and sodium bicarbonate).

 

It is helpful to bend the needle upward some 30–45°, especially when injecting the female larynx, as the shorter anterior–posterior distance requires a more acute angle of entry under the inferior rim of the thyroid cartilage. The needle is inserted into the cricothyroid space some 2–3 mm off the midline toward the side to be injected and advanced superiorly and laterally (Fig. 35.2). A more lateral entry point is used to attempt to avoid the airway, because traversing endolaryngeal mucosa is uncomfortable for the patient and may cause cough or even laryngospasm during the procedure. If it is possible to remain entirely submucosal, then the patient finds the procedure much less painful and stimulating to airway reflexes. Entry into the airway produces a characteristic “buzz” in the EMG signal, which should alert the injector to redirect the needle more laterally, or even begin again. The location where the needle penetrates the cricothyroid membrane from a superior–inferior perspective is determined by the surgeon’s preference. Some will enter the larynx at the junction of the inferior border of the thyroid cartilage and the membrane while others prefer to be at the halfway point of the membrane. The needle is maneuvered within the tissue until the tip lies in an area of crisp motor unit potentials. The patient is asked to phonate and a brisk recruitment and a full interference pattern confirms placement, and the botulinum toxin is injected. It is especially good to see

Fig. 35.1  Position of patient for percutaneous TA-LCA muscle botu-

linum toxin injection

Fig. 35.2  Insertion of needle through cricothyroid membrane into the

TA-LCA muscle complex for botulinum toxin injection

Fig. 35.3  Placement of EMG needle into the posterior cricoarytenoid

muscle, using a retrolaryngeal approach

 

Chapter 35

a characteristic prephonatory burst of EMG activity for optimal injection localization. c) Posterior cricoarytenoid muscle localization and injection for Abductor SD i. Retrolaryngeal approach The patient is seated upright, and the injector places his or her thumb at the posterior border of the thyroid cartilage on the side to be injected. Using counterpressure on the opposite side of the thyroid cartilage from the other four fingers, the larynx is gently rotated to expose its posterior aspect. The needle pierces the skin along the lower half of the posterior border of the thyroid cartilage and is advanced until it stops against the posterolateral surface of the cricoid. The needle is then pulled back slightly, and the patient is asked to sniff to confirm placement (Fig. 35.3). When this produces brisk recruitment, the toxin is injected. ii. Translaryngeal approach In this approach, the needle must cross the endo­lar­ yngeal mucosa so an intratracheal injection of 4% plain lidocaine is useful to prevent coughing and discomfort. The needle is inserted through the cricothyroid membrane in the midline, and directed posteriorly across the lumen of the glottis (identified by the characteristic airway buzz on EMG) angled toward the side to be injected. Using gentle pressure, it is pushed through the lamina of the cricoid cartilage until the opposite side is reached (due to cricoid cartilage calcification, this approach may not be possible in the older patient). The first electrical signal encountered on the far side represents posterior cricoarytenoid muscle. Placement is confirmed by muscle activation during sniffing, and the toxin is injected (Fig. 35.4). It is often useful (especially when learning the technique) to employ an assistant to provide flexible laryngoscopy visualization on a monitor during PCA injections (see Chap. 33, “Peroral Vocal Fold Augmentation in the Clinic Setting”). The surgeon should be aware that fragments of cartilage might plug the needle lumen as it crosses the cricoid, and expelling them to permit injection may require considerable force on the plunger of the syringe; a luer-lock syringe will prevent toxin leakage around the needle hub. d) Botulinum toxin injection with laryngoscopic guidance for Adductor SD i. Local anesthesia is obtained by performing a puncture through the cricothyroid membrane, and instilling approximately 3 ml of 4% lidocaine into the airway. ii. The nasal cavity is anesthetized and a flexible laryngoscope, attached to videomonitor, is inserted through the nasal cavity and advanced to a level slightly above the vocal folds. An assistant maintains the scope in position in order to provide constant visual feedback during the procedure. Alternatively, the surgeon may use a rigid telescope for laryngeal visualization (nondominant hand) while

Fig. 35.4  Placement of EMG needle into the posterior cricoarytenoid

muscle, using a translaryngeal approach

manipulating the needle with the other. The patient (or an assistant) must stabilize the tongue to facilitate good transoral visualization. iii. A 1-ml syringe filled with botulinum toxin is attached to a 27-g needle. The needle is placed through the cricothyroid membrane near the midline, using videomonitoring to confirm the location of the needle tip in the subglottic airway. iv. The needle is angled toward the posterior aspect of the vocal fold, piercing the infraglottic mucosa, and advancing the needle laterally into the adductor musculature of the vocal fold (TA-LCA complex) (Fig. 35.2). The posterior third of the membranous vocal fold is the targeted region for Botox placement. A similar injection is then performed on the opposite vocal fold through the same approach via the cricothyroid membrane. Visual confirmation, via the flexible laryngoscopic monitoring is used to confirm correct placement and to insure that inadvertent “loss” of the Botox does not occur. e) Supraglottic botulinum toxin injection with laryngoscopic guidance for Adductor SD. Supraglottic botulinum toxin injection with laryngoscopic guidance is effective for treatment of adductor spasmodic dysphonia as well as essential tremor involving the supraglottis. Two different injection approaches can be used to perform supraglottic botulinum toxin injection, (1) peroral approach or (2) an approach using a working channel of a flexible laryngoscope. Each of these two approaches are equally efficacious, and the decision to use one approach or the other is usually determined by the availability of the equipment to the surgeon. From a patient-comfort perspective, the injection through the working channel of a flexible laryngoscope is better tolerated.

225

226

Botulinum Toxin Injection of the Larynx

 

35

Fig. 35.5  False vocal fold site(s) for trans-oral botulinum toxin

Fig. 35.6  Characteristic submucosal bleb immediately after transoral

1. Topical anesthesia nasal/oropharynx a) Topical oxymetazoline/Pontocaine 2% spray to

curved needle. Disposable 27-g needles are used with this system. b) The needle is advanced into the oropharynx under direct visualization. The patient is instructed to phonate /a/ as the needle enters the oral cavity, which results in palatal raising, clearing the path into the oropharynx. The assistant should position the flexible scope just above the palate until the needle is visualized in the oropharynx. c) The injector is then advanced, and the needle tip is then guided into the hypopharynx, under endoscopic visualization, as the assistant follows closely behind with the flexible scope The assistant must be adept at manipulating the scope; consistent visualization of the injector can be challenging in a narrow airway with copious secretions. The flexible scope should be positioned a few millimeters above the false vocal folds providing a clear, well-illuminated, magnified view of the false vocal folds. 4. Laryngeal injection of Botox a) The needle is guided into the posterolateral and/ or mid-lateral false vocal fold under laryngoscopic visualization (Fig. 35.5). b) Botox is injected into a superficial (submucosal) plane, forming a characteristic bleb (Fig. 35.6). c) Five to 7.5 U are typically deposited in both false vocal folds (total of 10–15 U). An alternative way to perform supraglottic botulinum toxin injection with laryngoscopic guidance is to use a flexible laryngoscope with a working channel, or a flexible laryngoscope with an endosheath working channel apparatus. After adequate anesthesia to the larynx has been achieved

injection

nasal cavities

b) Topical Cetacaine spray to oral cavity (palate/pos-

terior pharynx)

2. Videomonitoring/topical anesthesia of larynx a) A video camera is attached to a flexible laryngo-

scope or a distal chip flexible laryngoscope, inserted through the nasal cavity (typically the left side) by an assistant, employing a “videocart system.” The scope is generally maintained slightly below the palate so that the tongue base and larynx can be easily viewed on the video monitor. b) Four percent lidocaine drip onto larynx under flexible guidance (3–5 ml; see Chap. 33) The patient is bent forward at the waist with the neck extended in a “sniffing” position to maximize laryngeal exposure. The tongue is grasped with a 4 × 4 gauze with the surgeon’s left hand. A 3-ml syringe of 4% lidocaine (40 mg/ml) attached to an Abraham cannula (Pilling, Fort Washington, Pa.) is advanced into the oropharynx. Approximately 1 ml is deposited over the tongue base, and 2–4 ml is dripped onto the vocal folds during phonation, producing the characteristic “laryngeal gargle”. The maximal recommended dose of 4% lidocaine is approximately 7–8 ml (4.5 mg/kg; approximately 300 mg for a 70-kg patient). 3. Peroral passage of the needle into the endolaryngeal region a) The Botox is drawn up in a 1-ml syringe, and secured into the orotracheal injector device (Medtronic ENT, Jacksonville, FL) with the

botulinum toxin injection

 

Chapter 35

via the approach described above, a fine-gauge injection needle can be passed through the working channel of the flexible laryngoscope (NM-9L-1, Olympus America, Center Valley, Pa.) and the supraglottic larynx can be injected with botulinum toxin as discussed above.

35.6

Postprocedure Care and Complications

Patients may be discharged immediately after the injection. Patients receiving TA-LCA injections should be cautioned regarding an initial period of (1) breathiness and (2) dysphagia, especially to liquids, as discussed above. Patient receiving their second posterior cricoarytenoid injection should be advised regarding dyspnea and stridor. Patients that received laryngeal anesthesia should be advised to retrain from any peroral intake for 2 hours (or until sensation returns to the larynx/pharynx) to avoid the risk of aspiration.

Key Points ■ Percutaneous, EMG-guided botulinum toxin injection ■ Effective administration of botulinum toxin depends on ■ Accuracy of injection ■ Minimizing diffusion to neighboring muscles ■ Appropriate dosing ■ When using EMG, confirmation of needle placement by muscle activation during appropriate activity (e. g., sustained “ee” or Valsalva for the thyroarytenoid, sniffing for the posterior cricoarytenoid) is essential to accuracy. ■ Diffusion is minimized by injecting a small volume of solution, ideally 0.1 ml. ■ Approximate dosing is determined by muscle mass and experience treating a given muscle. Precise dosing for each patient is determined by careful assessment of clinical result and adjustment of subsequent treatment. ■ Percutaneous injection of botulinum toxin with laryngoscopic guidance ■ Percutaneous injection of Botox under flexible (or rigid) laryngoscopic guidance is an ideal technique for the practitioner who performs



laryngeal injections infrequently because it is easier to master and relies on visual confirmation of the target, rather than blind needle placement. However, it does require an assistant to hold the flexible laryngoscope. ■ The response to botulinum toxin is similar with this technique when compared to EMG guided technique, except: ■ Higher doses are required ■ Delayed onset of action (up to 5 days) occurs ■ Toxin effect that is less consistent ■ Supraglottic botulinum toxin injection with flexible laryngoscope guidance ■ Supraglottic peroral Botox injection with flexible laryngoscopic guidance is indicated in selected patients with adductor spasmodic dysphonia (especially professional voice users and supraglottic-based essential tremor). ■ Advantages of supraglottic botulinum toxin (over EMG-guided approach) for spasmodic dysphonia ■ Smoothing of the vocal “peaks and troughs” associated with serial EMG-guided Botox injections ■ Less severe (minimal-to-no) breathy voice after injection ■ Disadvantages of supraglottic botulinum toxin for spasmodic dysphonia ■ Shorter duration of effect (6–8 weeks) ■ Variable patient response (variable supraglottic muscular anatomy)

Selected Bibliography 1 2

3 4

5 6

Aoki KR (2004) Pharmacology of botulinum neurotoxins. Oper Techniques Otolaryngol 15:81–85 Blitzer A, Brin MF, Stewart CF (1998) Botulinum toxin management of spasmodic dysphonia (laryngeal dystonia): a 12-year experience in more than 900 patients. Laryngoscope 108:1435–1441 Blitzer A, Sulica L (2001) Botulinum toxin: basic science and clinical uses in otolaryngology. Laryngoscope 111:218–226 Bové M, Daamen N, Rosen C et al (2006) Development and validation of the vocal tremor scoring system. Laryngoscope 116:1662–1668 Simpson CB, Amin MR (2004) Office-based procedures for the voice. Ear Nose Throat J 83(Suppl.):6–9 Sulica L, Blitzer A (2004) Botulinum toxin treatment of spasmodic dysphonia. Oper Tech Otolaryngol 15:76–80

227

Part C Laryngeal Framework Surgery

Chapter 36

36

Principles of Laryngeal Framework Surgery

36.1

Fundamental and Related Chapters

Please see Chaps. 1, 5, 8, 37, 38, 39, 40, 41, and 42 for further information.

36.2

Introduction

The general goal of laryngeal framework surgery is to improve phonatory glottal closure by altering vocal fold position. Medialization laryngoplasty, also called type I thyroplasty, is the most commonly performed laryngeal framework surgery, typically used to correct glottic insufficiency from a variety of causes, but most often from unilateral vocal fold paralysis. Whereas injection augmentation techniques principally improve glottal closure by expansion of the thyroarytenoid (TA) muscle, laryngoplasty techniques employ implant material in the paraglottic space to displace the affected vocal fold(s) medially into a more favorable phonatory position. These materials include Silastic, hydroxylapatite, polytetrafluoroethylene ribbon (GORE-TEX®) and titanium. Medialization laryngoplasty may be used in conjunction with an arytenoid repositioning procedure, an adjunctive technique that can be used to alter vocal fold height and tension by manipulating the arytenoid along its physiologic axis of rotation (see also Chaps. 40, “Arytenoid Adduction” and 41, “Cricothyroid Subluxation”).

36.3

Surgical Indications and Contraindications

36.3.1 Medialization Laryngoplasty The primary indication for medialization laryngoplasty (ML) is symptomatic glottic insufficiency. The goals of the surgery are to improve voice quality and protect the airway by achieving improved glottic closure during phonation and swallowing. Nevertheless, it is important to understand that vocal fold medialization does not always provide a sure remedy. In the presence of other motor or sensory deficits, as in a high vagal nerve lesion, the ability to close the glottis does not necessarily mean that this will occur appropriately during deglutition. Medialization is indeed likely to help, but many patients continue to have medically significant aspiration. Due caution is war-

ranted in making feeding recommendations after medialization in such individuals. A complete reevaluation of swallowing function is prudent after medialization in such patients. Medialization laryngoplasty has been advocated by some as a treatment for glottic insufficiency due to soft tissue loss in the aspect of the superficial vocal fold, such as is found in postsurgical scarring or sulcus vocalis. However, it is not well suited for these conditions, as it in no way addresses the lack of tissue pliability and may not yield significant voice improvement. It is worth noting that there is considerable evidence to suggest that at least part of the so-called “bowing” that has been accepted as the clinical correlate of vocal fold aging may also be due to changes in the lamina propria and loss of vocal fold muscle bulk, and thus medialization may represent only a partial solution. Indications for ML include: ■ Symptomatic glottic insufficiency (dysphonia and/or aspiration), especially if there is little chance of return of normal neurologic function Glottic insufficiency can be due to: ■ Unilateral vocal fold paralysis ■ Unilateral or bilateral vocal fold paresis ■ Vocal fold atrophy, including age-related atrophy Contraindications include: ■ Previous history of radiation therapy to the larynx (relative) ■ Malignant disease overlying the laryngotracheal complex ■ Poor abduction of the contralateral vocal fold (due to airway concerns) ■ Because medialization inevitably leads to some narrowing of the airway, patients with moderateto-severe bilateral vocal fold paresis may not be candidates for medialization. At least one vocal fold should have intact inspiratory vocal fold abduction for a medialization procedure to be considered

36.3.2 Arytenoid Adduction Arytenoid adduction and arytenopexy as described by Zeitels is an important adjunct in selected cases of vocal fold paralysis. The physiologic effects of arytenoid adduction are not completely understood, and some debate continues. However, there is consensus concerning the following basic premises.

232

Principles of Laryngeal Framework Surgery

Arytenoid adduction/re-position: ■ ■ ■ ■

36

Rotates the arytenoid cartilage Medializes and stabilizes the vocal process Lowers the position of the vocal process Lengthens the foreshorted vocal fold

In patients with vocal fold paralysis who have a lack of vocal process contact during phonation (large posterior gap) and those with vocal folds at different levels, arytenoid adduction should be considered in addition to medialization laryngoplasty. Videostroboscopy often provides valuable information about vocal process contact and vocal fold height, and therefore is useful preoperatively in assessing which patients may need an arytenoid adduction. A maximum phonation time of < 5 seconds has also been identified as a predictor of the need for arytenoid adduction in cases of vocal fold paralysis.

36.3.3 Cricothyroid Subluxation Cricothyroid subluxation was developed by Steve Zeitels to address the problems of a shortened vocal fold frequently seen in unilateral vocal fold paralysis. The concept of the procedure is to lengthen the vocal fold by increasing the distance from the cricoarytenoid joint (cricoid) to the anterior commissure (thyroid cartilage) by subluxing the cricothyroid joint on the side of the unilateral vocal fold paralysis. This results in a rotation of the anterior commissure away from the midline in a direction contralateral to the side of the unilateral vocal fold paralysis. Cricothyroid subluxation is an adjunct procedure to medialization laryngoplasty. This can be done with arytenoid adduction also, but is typically only used with medialization laryngoplasty. Cricothyroid subluxation addresses the commonly seen problem of a shortened vocal fold associated with unilateral vocal fold paralysis. The only other procedure that can lengthen a paralyzed vocal fold is arytenoid adduction (see Chap. 40, “Arytenoid Adduction”).

 

tion via Direct Microlaryngoscopy”; 33, “Peroral Vocal Fold Augmentation in the Clinic Setting”; and 34, “Percutaneous Vocal Fold Augmentation in the Clinic Setting”). Because medialization laryngoplasty is performed under local anesthesia, anxious/uncooperative patients, and pediatric patients are not ideally suited for this technique.

36.5

If the status of the nerve injury is unknown or LEMG data are equivocal or favorable for spontaneous recovery, then medialization surgery is best delayed until 6–12 months after nerve injury to allow for spontaneous recovery. The patient with troublesome symptoms may be treated by any of a number of temporary measures in the meantime principally injection augmentation (see Chaps. 31, “Vocal Fold Augmentation via Direct Microlaryngoscopy”; 33, “Peroral Vocal Fold Augmentation in the Clinic Setting”; and 34, “Percutaneous Vocal Fold Augmentation in the Clinic Setting”). Most surgeons advocate waiting at least 3 months after a known vagal or recurrent nerve transection before performing medialization laryngoplasty. Early or “primary” medialization (performed within the first 3 months after nerve injury) has fallen into disfavor, due to progressive atrophy of the vocal fold from ongoing nerve degeneration, which results in a return of glottal insufficiency weeks to months after medialization. In select cases, medialization between 3 and 9 months can be considered, especially if electromyography shows severe neuronal degeneration without evidence of neural recovery or the history strongly suggests nerve transection. In these cases, the patient should be counseled that the implant might need to be removed if vocal fold function returns. It is worth noting that in the very rare cases of recovery of vocal fold motion after laryngoplasty that have been observed, the implant does not appear to interfere with function, and has rarely required removal.

36.6 36.4

Patient Selection for Laryngeal Framework Surgery

Although any patient with symptomatic glottic insufficiency is technically a candidate for framework surgery, medialization laryngoplasty is not necessarily the best approach in every case. The ideal candidate for medialization laryngoplasty is a patient with moderate to severe glottic insufficiency (2–3 mm or greater glottic gap on phonation) manifested by weak, breathy dysphonia and/or dysphagia. Conversely, most patients with minor degrees of glottic insufficiency (<1-mm glottic gap on phonation) who have minimal voice symptoms (e. g., vocal fatigue) may be better suited for voice therapy and/or injection augmentation (see Chaps. 5, “Glottic Insufficiency: Vocal Fold Paralysis, Paresis, and Atrophy”; 31, “Vocal Fold Augmenta-

Timing of Medialization Laryngoplasty

Technical Notes and Pertinent Anatomic Landmarks for Medialization Laryngoplasty

Although many techniques and implant materials for medialization laryngoplasty exist, certain general principles of laryngeal anatomy can be universally applied. The level of the vocal fold lies closer to the lower border of the thyroid cartilage lamina than to the upper, and not at its midpoint, as is frequently (and erroneously) stated. It is important to place the thyroplasty window at the most inferior location possible. This will usually encompass the level of the vocal fold and make successful medialization possible with appropriate implant positioning. The inferior limit of placement is determined by the integrity of the cartilaginous strut below the window, which should be at least 3 mm high to prevent fracture, which destabilizes the implant in a way that usually prevents effective medialization. As

 

Chapter 36

233

Fig. 36.1  Gender differences in medial-

ization laryngoplasty. The more oblique angulation of the thyroid cartilage in females, along with the shorter length of the vocal folds requires that the medialization window be placed more anteriorly (5 mm in females, 7 mm in males)

Fig. 36.2  Diagram showing the incorrect

(left) and correct (right) method of exposing the inferior thyroid ala. On the left, the cricothyroid fibers have not been divided from the inferior border, and an incorrect, downwardly sloping line is used to trace the proposed horizontal plane of the vocal fold. On the right, a thorough dissection of the inferior thyroid ala allows the true horizontal plane of the vocal fold to be outlined, ensuring correct window placement. In this case, the inferior muscular tubercle (arrow) is ignored when determining the plane

a result of this limit, the implant often needs to be carved such that medialization occurs at the inferior limit of the window to avoid ventricular mucosa/false cord displacement. Another important anatomic consideration is the genderrelated differences in the configuration of the thyroid cartilage. In males, the vocal folds are longer, and the thyroid ala form a more acute angle when compared with the female larynx These anatomic differences require a more posterior location of the cartilaginous window in the male larynx to avoid excessive or disproportionate displacement of the anterior third of the vocal fold, which will result in strained or “pressed” voice. In general, the leading edge of the window is placed 7 mm back from the midline of the thyroid cartilage in males and 5 mm in females (Fig. 36.1). Many implants are shaped to medialize tissue in a plane exactly parallel to the long axis of the thyroplasty window; its orientation is thus an important factor for surgical success. The inferior border of the thyroid lamina is the most reliable guide to determining the plane of the long axis of the vocal fold. To accurately identify this plane, the inferior tubercle should be completely exposed and excluded from the determination of the plane along the long axis of the vocal fold (Fig. 36.2). Preserving some flexibility in medialization laryngoplasty technique to allow for individual variations in laryngeal anatomy is necessary to achieve consistently satisfactory surgical results. Being able to check on the result of medialization in-

traoperatively by means of flexible laryngoscopy, and auditory perceptual evaluation is essential to understanding the reason for a poor phonatory result in time to correct it, therefore, a flexible laryngoscope, its light source, a camera, and a monitor should be used for every case. Conflicting advice regarding the inner perichondrium has appeared in the literature. Maintaining the perichondrium intact effectively prevents medial migration and extrusion of the implant, and minimizes the possibility of endolaryngeal bleeding. Isshiki continues to advise its preservation in combination with Silastic and a cartilage island, as do McCullough and Hoffman when using expanded polytetrafluoroethylene ribbon. However, the medial projection of many preformed implants makes their insertion impossible unless the internal perichondrium is opened. In addition, an intact perichondrium tends to distribute the vector of medialization throughout the window, leading to less precise medialization. It is important to conceptualize medialization of the vocal fold in three dimensions. The most obvious dimension is medial/lateral, because the amount of medial displacement must be precisely determined to close the glottic gap. Just as important, however, is the anterior–posterior dimension. Anterior displacement must be avoided, while a well-defined “sweet spot” at the posterior aspect of the vocal fold is key to optimizing results. The superior–inferior dimension is often the least discussed, but no less important. This dimension is also

234

36

Principles of Laryngeal Framework Surgery

the most difficult to judge intraoperatively. A minor error in medialization within the superior–inferior plane can result in height mismatch during vocal fold closure. This mismatch is difficult to detect during intraoperative flexible laryngoscopy, and may only later be discovered with videostroboscopy post operatively. Details of technique specific to various implant materials and steps and modifications required to perform arytenoid repositioning surgery in conjunction with medialization laryngoplasty are covered elsewhere (see Chaps. 38, “Silastic Medialization Laryngoplasty for Unilateral Vocal Fold Paralysis”; 39, “GORE-TEX® Medialization Laryngoplasty”; and 40, “Arytenoid Adduction”)

Key Points ■ Medialization laryngoplasty and arytenoid adduction are the primary laryngeal framework techniques used to correct glottic insufficiency ■ The indications for laryngeal framework surgery include: ■ Unilateral vocal fold paralysis ■ Bilateral vocal fold atrophy/paresis ■ The ideal candidate for medialization laryngoplasty is a patient with moderate to severe glottic insufficiency (2- to 3-mm or greater glottic gap on phonation) manifested by weak, breathy dysphonia and/or dysphagia. Conversely, most patients with minor degrees of glottic insufficiency (<1-mm glottic gap on phonation) who have minimal voice symptoms (e. g., vocal fatigue) may be better suited for injection augmentation and/or voice therapy. ■ Medialization laryngoplasty can be performed with a variety of implant substances, including Silastic, GORE-TEX, Hydroxylapatite, and Titanium. ■ In unilateral vocal fold paralysis (UVFP), framework surgery is generally performed after a waiting period of 6–12 months to allow for spontaneous recovery. ■ Early medialization can be considered in select cases including: complete nerve transec-

 



tion, severe neuronal degeneration as seen with laryngeal electromyography, or in a clinical setting where there is little chance for recovery of vocal fold mobility (e. g., UVFP due to a malignancy). In these cases, a delay of 3 months from the time of injury is recommended to allow vocal fold atrophy to occur. Temporary vocal fold injection can be used acutely in these patients prior to proceeding with laryngeal framework surgery ■ The level of the vocal fold lies closer to the lower border of the thyroid cartilage lamina, and not at its midpoint. The thyroplasty window should be placed as inferior as possible. ■ Gender-related difference in the thyroid lamina requires a more posterior location for the medialization window in males. ■ The inner perichondrium of the thyroid lamina should be incised to gain access to the paraglottic space during medialization. An intact inner perichondrium limits the depth and precision of vocal fold displacement.

Selected Bibliography 1

2 3

4

5 6 7

Cohen JT, Bates DD, Postma GN (2004) Revision Gore-Tex medialization laryngoplasty. Otolaryngol Head Neck Surg 131:236–240 Isshiki N, Morita H, Okamura H, Hiramoto M (1974) Thyroplasty as a new phonosurgical technique. Acta Otolaryngol 78:451–457 Netterville JL, Stone RE, Luken ES, Civantos FJ, Ossoff RH (1993) Silastic medialization and arytenoid adduction: the Vanderbilt experience. A review of 116 phonosurgical procedures. Ann Otol Rhinol Laryngol 102:413–424 Netterville JL, Billante CR (2004) The immobile vocal fold. In: Ossoff RH, Shapshay SM, Woodson GE, Netterville JL (eds) The larynx. Lippincott, Williams & Wilkins, Philadelphia, pp 269–305. Rosen CA (1998) Complications of phonosurgery: results of a national survey. Laryngoscope 108:1697–1703 Woo P. Arytenoid adduction and medialization laryngoplasty (2000) Otolaryngol Clin N Am 33:817–839 Woodson GE, Picerno R, Yeung D et al (2000) Arytenoid adduction: controlling vertical position. Ann Otol Rhinol Laryngol 109:360–364

Chapter 37

Perioperative Care for Laryngeal Framework Surgery

37.1

Fundamental and Related Chapters

Please see Chaps. 1, 5, 8, 36, 38, 39, 40, and 41 for further information.

37.2

Perioperative Issues in Laryngeal Framework Surgery

Vocal fold edema may have a marked effect on voice quality and prolong recovery of normal voice, thus intravenous Decadron (10 mg) is given preoperatively, followed by two additional doses at 8 and 16 h postoperatively. In rare instances, a patient undergoing framework surgery may develop laryngeal edema to such a degree that partial or complete airway obstruction occurs. Patients undergoing bilateral medialization procedures and/or arytenoid adduction are at increased risk for this complication, as are those with a history of irradiation to the neck. Generally, maximal airway edema occurs within the first 24 h after surgery; however, edema may continue to progress up to 72 h postoperatively in rare cases. All cases are admitted for overnight observation, with pulse oximetry. Patients may be fed the evening of surgery, with the diet advanced to regular as tolerated. In cases of significant postoperative edema, a peroral corticosteroid taper may be used at discharge. Use of a surgical drain is not necessary in most medialization cases; however, with arytenoid adduction a drain is prudent. If a drain is placed, then it is typically removed the next morning before discharge. An intravenous antibiotic such as Ancef 1 gm is given preoperatively. Postoperative antibiotics are usually not necessary unless there is a history of irradiation to the neck, in which case a fluroquinalone may be use for 7–10 days postoperatively. Most patients have good-to-excellent voicing intraoperatively, but develop varying degrees of postoperative dysphonia as a result of edema or submucosal hemorrhage. Within hours, a good postoperative voice will become rough and hoarse. The patient should be warned of this before the surgery. The period of postoperative dysphonia is variable, but may last between 2 and 6 weeks. Rare cases may persist up to 3 months. Voice conservation is advocated; total voice rest is unnecessary.

37.3

37

Surgical Indications and Contraindications

The principal complications specific to medialization laryngoplasty include airway obstruction and implant extrusion. The results of a survey of American otolaryngologists performed in 1998 revealed incidences generally in line with those reported in various series. Medialization necessarily results in a narrowing of the glottic airway. In combination with postoperative edema or hematoma, this can result in significant airway obstruction—the

Fig. 37.1  Violation of ventricular mucosa at the anterior aspect of the

medialization window (cross-section). Note the close proximity of the ventricular mucosa to the thyroid lamina at the anterior aspect of the window

236

37

Perioperative Care for LFS

most dangerous postoperative complication of medialization laryngoplasty. Surgeons surveyed reported some airway compromise in 13.8% of cases. Usually, this was minor, and tended to occur more often after medialization laryngoplasty arytenoid adduction rather than medialization laryngoplasty alone. However, some 0.6% of patients undergoing medialization laryngoplasty and 2.2% of patients undergoing medialization with arytenoid adduction required intubation or tracheostomy. Extrusion of the implant was extremely rare (0.8%) and predominantly into the airway rather than transcutaneous, as one would expect on comparison of internal and external tissue covering of the implant. It is likely that at least some of the airway extrusions, particularly those that occur within a few weeks of surgery, are the result of intraoperative unidentified perforations through the mucosa. If perforation goes unrecognized at the time of surgery, then the implant is at risk for exposure and contamination. The implant then acts as a foreign body and may extrude, potentially precipitating an airway foreign-body emergency. The delicate ventricular mucosa is often located in close proximity to the inner aspect of the anterior thyroid ala, and can be easily torn when working at the anterior aspect of the window (Fig. 37.1). The key to preventing airway entry is to avoid undermining of the paraglottic space anterior to the window and to use care when removing the anterior portion of the cartilaginous window. If accidental mucosal violation does occur, then the tear can usually be closed with absorbable sutures. One can test that the closure is complete by flooding the operative field with irrigation and looking for air bubbles during a Valsalva maneuver. If the tear is successfully closed, then an implant can be safely placed in select cases. Securing the implant to the cartilage with sutures is thought to significantly reduce the risk of airway foreign body. In cases where delayed implant exposure within the airway is encountered, the patient should be taken back to the operating room for removal of the implant, either externally or endoscopically. In these cases, revision framework surgery should not be considered for at least another 3 months.

37.4

 

performed. There is some doubt that the vocal process of the arytenoid can be medialized effectively and consistently by a posterior extension of the medialization implant. Furthermore, the arytenoid and its vocal process move in three dimensions, a fact not always obvious during laryngoscopic examination, which renders height differences notoriously difficult to assess. A denervated vocal fold may thus rest at a different vertical position from its functioning counterpart. In fact, with muscle traction diminished or even absent, it may even lie outside of this trajectory, as in the case of a so-called prolapsed arytenoid, when the vocal process lies below the plane of glottic closure. Simple medialization cannot remedy a height mismatch. A height mismatch is often accompanied by unequal vocal fold tension, which causes the folds to react differently to phonatory air pressure, resulting in dysphonia. Undercorrection is another relatively frequent cause of poor results. This is especially likely to occur in cases that last longer than usual and allow normal intraoperative vocal fold edema to accumulate. Even mild edema can create enough medial displacement of the vibratory margin of the vocal fold to cause the surgeon to underestimate of the degree of medialization required. In these cases, the patient will report good voice immediately after surgery, only to fade 1–2 weeks later, when the edema begins to resolve. The key to avoiding this complication is to keep the time from intralaryngeal elevation until final implant placement as short as possible. The window should be probed, and medialization measurements should be obtained as soon as the window is opened. In addition, preoperative intravenous corticosteroids (Decadron, 10 mg) and application of epinephrine-soaked Cottonoids within the medialization window during implant carving can help lessen edema. It is important to recognize the onset of vocal fold edema intraop-

Suboptimal Results/Surgical Errors

An unsatisfactory voice result rather than any airway problem or extrusion is the most common cause of revision medialization surgery. Revision rates, reported to be 5.4% in the survey of complications, can reach 16%. When secondary procedures such as fat injection are included, revision rates have been reported to be as high as 33%. Certain causes of poor voice results occur regularly and with greater frequency than others in most reported series, as well as in the authors’ experience. These include: ■ ■ ■ ■

Persistent posterior glottic gap Undermedialization Superior implant malposition Anterior implant malposition

Persistent posterior glottic gap can account for up to 50% of revisions in cases in which arytenoid adduction has not been

Fig. 37.2  Flexible laryngoscopy demonstrating prolapse of the left

ventricular mucosa and false vocal fold from an implant that is placed “too high” (superior to the correct plane of the long axis of the vocal fold)

 

eratively. If more than 30–45 min elapse between the opening of the cartilaginous window and placement of the implant, then significant vocal fold edema may have developed. Clues that vocal fold edema has developed include: ■ The patient’s baseline voice (nonmedialized) sounds significantly better than it did before the case began. ■ Good voice quality is obtained during medialization with depth gauge immediately after opening the window, but cannot be replicated later (30 + min) in the case. When vocal fold edema is suspected, one must rely on visual clues more than auditory clues in determining the correct amount of medialization. In other words, it is more important to confirm a well-medialized vocal fold (using an indwelling flexible laryngoscope) in a patient with a mildly stained voice, rather than settling for a normal voice with a slightly undercorrected vocal fold. A subset of patients may be noted to have voice deterioration months to years after surgery. This is probably best explained by continued atrophy of the vocal fold musculature from prolonged denervation, or bilateral age-related atrophy. Implant malposition of the implant generally accounts for the balance of revisions. Netterville and Billante have identified placing the implant too far superior, which results in medialization of the ventricular mucosa or the false vocal fold, as the most common overall cause for revision. This can be avoided by placing the window no more than 3 mm above the inferior border of the thyroid ala, or as low as possible while maintaining a stable inferior frame of cartilage below the window. Also, one should carefully probe within the window to confirm the

Fig. 37.3  Flexible laryngoscopy demonstrating excessive medializa-

tion of the anterior third of the left vocal fold after medialization laryngoplasty

Chapter 37

plane of the true vocal fold prior to attempting the use of any depth-measuring devices. The image from an indwelling flexible laryngoscope is extremely useful to confirm the correct medialization plane; a bulging ventricular fold or everted ventricular mucosa (or, more rarely, subglottis) indicates an incorrect medialization plane (Fig. 37.2). Overmedialization of the anterior vocal fold, caused by too anterior a placement of the medialization implant, results in a distinctive pressed or strained vocal quality from early contact and “overclosure” of the anterior part of the membranous vocal fold during phonation (Fig. 37.3). To prevent this, glottic tissues overlying the anterior third of the window are generally not medialized. This is especially true in men, in whom the extremely thin glottic tissue overlying this area is prone to overmedialization from even small amounts medial displacement. It is not uncommon for a well-carved implant to cause a slight amount of unintended anterior medial displacement. If a pressed voice is noted after implant placement, forceps can be used to pull the anterior portion of the implant partially out of the window, and retest the voice. If the voice improves with this maneuver, reshaping of the anterior portion of the implant is necessary.

37.4.1 Revision Surgery The approach for revision surgery does not deviate much from that taken with primary surgery. The location of the original cartilaginous window from the previous surgery is not taken into consideration when planning the location of the revision window. The same meticulous exposure of the thyroid ala and precise measurements should be used to establish the “new” window location. The new window is then created, even if there is some overlap between this and the original window. In some cases, this may result in a larger window, or one with an irregular shape. As long as the revision implant occupies the new window location, and is secured within this space, the unusual window dimensions do not present a problem (Figs. 37.4, 37.5). Most implants can be removed easily as the new window is opened, using two single-prong hooks. Once the revised window is created, the fibrous capsule that has formed deep to the implant must be incised (Fig. 37.6). This fibrous tissue creates tethering of the thyroarytenoid muscle and must be incised along the perimeter of the window (Fig. 37.7). Finally, the paraglottic space is entered and undermined, similar to primary medialization techniques, to permit unencumbered medial displacement of the vocal fold. This is similar to the release of the internal perichondrium that is performed in most medialization surgery. The remainder of the surgical case proceeds in a similar fashion to primary medialization laryngoplasty. In many cases, the reason for failure may be related to vocal fold height differences, or lack of posterior glottic closure conditions that medialization surgery cannot correct. Therefore, it is not surprising that substantial number of medialization revisions require arytenoid adduction. If an adequate voice quality cannot be obtained by medial displacement of the vocal fold intraoperatively, then arytenoid adduction should be performed in conjunction with medialization.

237

238

Perioperative Care for LFS

 

37

Fig. 37.4  Original window/implant and the outline of the “new” ideal

Fig. 37.5  Combined revision window that is created. Note the secure

Fig. 37.6  Fibrous capsule within the paraglottic space after implant

Fig. 37.7  Sharp incision through the fibrous capsule along the margin

window dimension superimposed

removal. Note adherence of the capsule along the inner aspect of the thyroid lamina

position of the implant

of the window

 

37.5

Chapter 37

Long-Term Surgical Issues

Patients who have undergone successful medialization laryngoplasty, with or without arytenoid adduction often express concerns about the safety of endotracheal intubation for surgical procedures in the future. A waiting period of 6 months postsurgery (if the proposed surgery is elective) is advised. The anesthesiologist should place the smallest endotracheal tube that he or she feels is safe—ideally, size 6.0 or smaller—principally to avoid inducing laryngeal edema from a slightly constricted glottic aperture.

Selected Bibliography 1 2 3

4

5

Key Points

6

■ Corticosteroids should be given in the preoperative and immediate postoperative period to help minimize potential complications. ■ Major complications/ risk factors of framework surgery include: Complication

Risk factor(s)

Airway compromise/ obstruction

Arytenoid adduction Bilateral medialization Prior history of neck irradiation

Implant extrusion/exposure

Violation of airway mucosa

■ Suboptimal results with framework surgery are usually due to one or more of the following: ■ Persistent posterior glottic gap ■ Undermedialization ■ Implant malposition: ■ Anteriorly ■ Superiorly ■ Vocal fold height mismatch ■ A good voice after framework surgery that begins to “fade” or weaken 1–2 weeks postoperatively suggests undercorrection. ■ Revision surgery for medialization laryngoplasty failures often requires arytenoid adduction to achieve maximal voice results. ■ Endotracheal intubation is safe in patients who have undergone framework surgery in the past, but should be delayed until 6 months postoperatively, if possible. A smaller diameter ETT (6.0 or smaller) is recommended.

7 8 9

Anderson TD, Spiegel JR, Sataloff RT (2003) Thyroplasty revision: frequency and predictive factors. J Voice 17:442–448 Cohen JT, Bates DD, Postma GN (2004) Revision Gore-Tex medialization laryngoplasty. Otolaryngol Head Neck Surg 131:236–240 Cotter CS, Avidano MA, Crary MA, Cassisi NJ, Gorham MM (1995) Laryngeal complications after type 1 thyroplasty. Otolaryngol Head Neck Surg 113:671–673 Hong KH, Jung KS (2001) Arytenoid appearance and vertical height difference between the paralyzed and innervated vocal folds. Laryngoscope 111:227–232 Maragos NE (2001) Revision thyroplasty. Ann Otol Rhinol Laryngol 110:1087–1092 Netterville JL, Stone RE, Luken ES, Civantos FJ, Ossoff RH. Silastic medialization and arytenoid adduction: the Vanderbilt experience. A review of 116 phonosurgical procedures. Ann Otol Rhinol Laryngol 102:413–424 Rosen CA (1998) Complications of phonosurgery: results of a national survey. Laryngoscope 108:1697–1703 Weinman EC, Maragos NE (2000) Airway compromise in thyroplasty surgery. Laryngoscope 110:1082–1085 Woo P, Pearl AW, Hsiung MW, Som P (2001) Failed medialization laryngoplasty: management by revision surgery. Otolaryngol Head Neck Surg 124:615–621

239

Chapter 38

Silastic Medialization Laryngoplasty for Unilateral Vocal Fold Paralysis

38.1

Fundamental and Related Chapters

Please see Chaps. 1, 5, 9, 14, 36, 37, 39, 40, and 41 for further information.

38.2

Disease Characteristics and Differential Diagnosis

Patients with unilateral vocal fold paralysis (UVFP) typically complain of breathy dysphonia, vocal fatigue, and aspiration of liquids. The etiology of the paralysis is frequently vagal/recurrent laryngeal nerve injury secondary to iatrogenic causes or nonlaryngeal malignancy. Laryngoscopy generally shows an immobile vocal fold, although a slight amount of adduction can be present due to contralateral innervation of the interarytenoid muscle. The position of the paralyzed vocal fold can vary from median position to lateralized, and the height from slightly above to below the contralateral vocal fold. This variation of the position of the vocal fold is probably related to the degree of reinnervation that has occurred subsequent to the nerve injury, as well as the differing anastomotic connections between the RLN and SLN that are variable from patient to patient. Differential diagnosis of an immobile vocal fold includes vocal fold paralysis, cricoarytenoid joint fixation (usually due to trauma or rheumatologic disease), and cricoarytenoid dislocation (very rare, and almost exclusively related to severe external trauma—not intubation). Cricoarytenoid joint abnormalities can be differentiated from vocal fold paralysis using laryngeal electromyography and vocal fold palpation.

38.3

Surgery Indications and Contraindications

It is important to note that Silastic medialization laryngoplasty (ML) is designed to be a long-term treatment for symptomatic UVFP. Experimental and clinical evidence supports the efficacy of Silastic ML over a prolonged period. However, it should be noted that Silastic ML is fully reversible—that is, the implant can be removed if return of vocal fold mobility occurs, or if a revision surgery needs to be performed later. There is minimal tissue reactivity to Silastic over time; generally, a thin fibrous capsule surrounding the implant is all that is seen months to years after ML. Even though the implant can be removed, this

38

procedure should be used as a permanent treatment not a temporary method of medialization. Indications comprise: ■ Symptomatic glottic insufficiency (dysphonia, aspiration), especially if there is little to no chance of return of vocal fold motion Contraindications include: ■ Previous history of radiation therapy to the larynx (relative) ■ Malignant disease overlying the laryngotracheal complex ■ Poor abduction of the contralateral vocal fold (due to airway concerns) ■ Presence of lesion on the vocal folds

38.4

Surgical Equipment

No single implant material is superior to the others for performing ML. It is really a matter of surgeon preference and experience. We advocate hand carving of a medium-grade Silastic block (available from Medtronic ENT, Jacksonville, Fla.), using the surgical technique described by Netterville. This leads to precise medialization, superior voice results, and a better understanding of the dynamics of vocal fold medialization. However, other systems (such as the preformed implants in the Montgomery Thyroplasty Implant System (Boston Medical Products, Westborough, Mass.) or strip GORE-TEX® (W.L. Gore and Associates, Flagstaff, Ariz.) and VoCoM hydroxylapatite (Smith and Nephew, Bartlett, Tenn.) can be employed successfully as well. ■ ■ ■ ■

■ ■ ■ ■ ■

Netterville Medialization Tray (Medtronic ENT) Drill with 2- or 3-mm cutting burr Kerrison rongeurs tray (1- to 3-mm-sized tips) Medium-grade Silastic block (Medtronic ENT) ■ Partially preformed blocks are used in this procedure, referred to as “silicone strips” by the manufacturer Ruler (15-mm section of plastic ruler at tip of hemostat) Flexible laryngoscope C-mount camera with videocart/monitor Clear overdrape for laryngoscope (1010 drape) Local anesthetic (nasal and subcutaneous)

242

Silastic Medialization Laryngoplasty

 

38

Fig. 38.1  Diagram of typical prep/drape

for medialization laryngoplasty

4. 4. 5. 6.

Fig. 38.2  Horizontal skin incision: typically midthyroid cartilage and 5 cm in length

38.5

Surgical Procedure

7.

8.

1. The surgical region is liberally infiltrated with 1% lido-

caine with 1:100,000 epinephrine, from the hyoid down to the cricoid cartilage, on the side of the intended surgery. Typically, 15 ml are used. Preoperative intravenous Decadron (10 mg) is administered. 2. Four percent lidocaine and oxymetazoline nasal spray is applied to the most patent nasal cavity. 3. Placement of an indwelling flexible laryngoscope with videomonitoring of the larynx during the entire surgical case. The visual feedback of the larynx is invaluable when performing this surgery. One-inch tape is used to secure the flexible scope to a modified i.v. pole hanging above

9.

the patient’s head. The neck is then prepped and draped, including a clear overdrape to allow manipulation of the flexible laryngoscope during the case (Fig. 38.1). A horizontal incision is placed in a skin crease at the level of the midthyroid cartilage, typically 5–6 cm in length (Fig. 38.2). Subplatysmal flaps are raised to the hyoid superiorly and the upper portion of the cricoid below; retention hooks are used to secure the flaps out of the way. The midline raphae is divided between the strap muscles with cautery, exposing the laryngeal cartilage (Fig. 38.3). A single-prong hook is placed under the thyroid notch, and the larynx is retracted towards the side opposite the paralysis, bringing the entire hemilaryngeal cartilage into view (Fig.38.4). The outer perichondrium of the thyroid cartilage is then incised with a 15 blade, and a posteriorly-based flap is raised with a cottle or freer elevator. This requires serial release of the perichondrium superiorly and inferiorly (Fig. 38.5). The inferior border of the thyroid ala has muscle fibers from the cricothyroid muscle inserting onto it, so these must be divided (typically with bipolar cautery followed by 15-blade division). This exposes the inferior border, so that the correct orientation of the window can be properly determined (Fig. 38.6). The exposure of the inferior thyroid cartilage border must extend posterior to the muscular tubercle (an inferiorprojecting extension of the thyroid ala), as the angulation of this process can cause mistaken orientation of the medialization window. The downward projection of the muscular tubercle must be ignored when determining the horizontal plane of the inferior border of the thyroid cartilage (Fig. 38.7).

 

Chapter 38

Fig. 38.4  Single-prong hook under the thyroid notch to gain exposure

to thyroid ala

Fig. 38.3  Division of midline raphae of the strap muscles

Fig. 38.5  Posteriorly based outer perichondrial flap elevation

10. A window is outlined in the thyroid cartilage, measuring

6 × 13 mm, using the window-size gauge instrument. The window is placed 3 mm above the inferior border of the thyroid cartilage. Placement of the window any higher (superior) may result in medialization of the false vocal fold or ventricular mucosa, with poor voice results. The window is “set back” from the midline of the thyroid cartilage by a distance of 5 mm in women and 7 mm in men. This setback helps avoid medialization of the anterior vo-

Fig. 38.6  Bipolar cautery and sharp dissection are used to expose the

inferior border of the thyroid ala

cal fold, which may result in “pressed” voice (Fig. 38.8). After the window is outlined, one can pass a needle (21 gauge) through the anterior-superior corner of the proposed ML window during simultaneous flexible laryngoscopy. Care is taken to not “pass point” with the needle as it goes through the cartilage, thus avoiding the airway. The needle can usually be seen immediately or can be rapidly jostled to aid the identification of the needle location. The needle location can aid in optimal window localization. If

243

244

Silastic Medialization Laryngoplasty

 

Fig. 38.7  Diagram showing the incor-

rect (left) and correct (right) method of exposing the inferior thyroid ala. On the left, the cricothyroid fibers have not been divided from the inferior border, and an incorrect, downwardly sloping line is used to trace the proposed horizontal plane of the vocal fold. On the right, a through dissection of the inferior thyroid ala allows the true horizontal plane of the vocal fold to be outlined, insuring correct window placement. In this case, the inferior muscular tubercle (arrow) is ignored when determining the plane

38

Fig. 38.9  A small triangle of cartilage is removed from the posterior

window using a 15 blade and a Woodson elevator Fig. 38.8  Correct placement of the medialization window, 5–7 mm from the midline of the thyroid ala (5 mm in females, 7 mm males), and 3 mm above the inferior border. The window-size gauge instrument is 6 × 13 mm in area

the needle is seen too anteriorly or superiorly, the planned ML window can be adjusted appropriately. 11. The window of cartilage is then removed (with a 15 blade, Kerrison rongeur, or drill, depending on laryngeal calcification). In younger patients, the cartilage is soft, and can be removed with a 15 blade, being cautious to avoid penetration of the cartilage with resultant paraglottic bleeding. Often, a triangle of cartilage can be incised and then removed from the posterior superior aspect of the window using a Woodson elevator (Fig. 38.9). Once an entry point through the thyroid cartilage is established, a Kerrison rongeur can be used to complete the window (Fig. 38.10). When drilling the window, a 2- to 3-mm cutting burr is used, first outlining the perimeter of the window. Once the entire rectangular section of cartilage is thinned, a Woodson elevator can be used to gain entry into the paraglottic space (Figs. 38.11, 38.12).

12. The inner perichondrium that lies deep to the window is

removed, exposing the thyroarytenoid muscle fascia. Often this inner perichondrium is removed piecemeal with the Kerrison rongeur during primary cartilage removal of the window. However if it is intact, then it may be incised superiorly, posteriorly, and inferiorly (Fig. 38.13). A surgical plane is then developed, with the right-angle elevator within the paraglottic space (just superficial to the TA fascia) in all directions around the window except anterior (Fig. 38.14). Dissection anterior to the window may result in perforation into the airway through the very thin (and closely adherent) ventricular mucosa and should be avoided. Incising the inner perichondrium and establishing a surgical plane in the paraglottic space is important to successful medialization. An intact perichondrium remains tightly bound to the thyroid cartilage (even with undermining) and often provides great resistance to medialization; it is analogous to trying to displace a trampoline. In contrast, the paraglottic space allows for unencumbered medialization, once the inner perichondrium is incised.

 

Chapter 38

38.10  Kerrison rongeur is then used to remove the remainder of the

Fig. 38.11  A cutting burr is used to outline the window in cases where

Fig. 38.12  A Woodson elevator is then used to gain entry into the

Fig. 38.13  Release of the inner perichondrium, with a 15 blade supe-

cartilage

paraglottic space, when the cartilage is sufficiently thinned

the cartilage is calcified

riorly, posteriorly, and inferiorly

245

246

Silastic Medialization Laryngoplasty

 

38

Fig. 38.14  Undermining within the paraglottic space (deep to the in-

Fig. 38.15  Undermining the paraglottic space from below, to insure

13. The inferior paraglottic surgical plane should extend below

window to the point of maximal displacement (i. e., the tip of the depth gauge), which is referred to as the “A” measurement in the corresponding illustration. This is often 10–13 mm in length, as posterior medialization most often is used (in women this measurement is typically closer to mid aspect of the window, 6–8 mm) (Fig. 38.17). The other measurement is the depth of medialization, and is read off the depth gauge instrument. The measurement is taken off the inner table of the cartilage, not the outer table (Fig. 38.18). Typically, 5–7 mm of medialization is needed at the posterior aspect of the window. It is rare that any medialization is needed at the anterior aspect of the window, except in females. 16. Once the appropriate measurements are made, 3 × 0.5-inch Cottonoids soaked in 1:10,000 epinephrine are placed inside the window to aid in hemostasis while the implant is carved. 17. An implant is then carved out of medium-grade Silastic wedge on the back table to meet the specifications provided by the depth gauge measurements. a) Carving the Silastic implant The implant may be carved from a medium-grade Silastic block to meet the specifications provided by the depth gauge measurements. A preformed 20-mm wedge block

ner perichondrium) superiorly, posteriorly, and inferiorly

the inferior strut of the thyroid ala. This can be achieved by undermining from below the strut, using the long or a cottle elevator. The TA fascia in the window should be displaced medially to avoid perforation/penetration of the TA muscle fibers (Fig. 38.15). 14. The TA muscle is then displaced within the window while visualizing the effects on vocal fold displacement on the videomonitor. This helps establish the correct plane of medialization. Within the window, the inferior aspect generally is the most desirable for medialization, and corresponds to the free edge of the vocal fold. Displacement within the superior aspect of the window usually medializes the false vocal fold or ventricular mucosa, and results in suboptimal results in most cases. 15. A depth gauge is used to displace the paralyzed TA muscle medially, while the patient counts to “10” (Fig. 38.16). A combination of visual feedback from the videolaryngoscopy monitor and the patient’s vocal quality are used to judge the correct amount of medialization needed. Ideally, the paralytic vocal fold will assume a straight contour in the midline, allowing for complete glottic closure and significant voice improvement. Two principle measurements are obtained. The first is the distance from the anterior

release of cricothyroid fibers. This will allow space for the flanges of the implant to rest

 

Chapter 38

Fig. 38.16  Displacement of TA muscle with the depth gauge. Note

the displacement is generally at the posterior, inferior border of the window









(“silicone strip” by Medtronic ENT) simplifies this task and shortens surgical time. This section describes its proper preparation for implantation. The distance from the anterior edge of the window to the point of maximal medialization (typically 11–13 mm in males and 3–8 mm in females) is measured along the block (measurement “A” on the diagram), and a dot is placed with a marking pen (Fig. 38.19). From the dot, a line is extended into the substance of the block (measurement “B” in the diagram) which corresponds to the depth of medialization (Fig. 38.20). This measurement was obtained using the depth gauge and is typically 5–7 mm in most patients. Lines are then drawn connecting the tip of line B with both the anterior and posterior portions of the block (“C” and “D,” respectively) (Fig. 38.21). This creates a characteristic triangular shape of the implant, with the edge C corresponding to the portion of the implant that displaces the vocalis muscle medially, and segment D corresponding to the posterior extension of the implant that helps to hold it in place. A 10 blade is used to cut along lines C and D, removing the excess portion of the block (Fig. 38.22). One must be careful to make these cuts at 90° angles to maintain the integrity of the depth of the implant. The implant is placed in a customized implant holder for further shaping. The plane of medialization (lower, middle, or upper portion of the window) that corresponds to the plane of the true vocal fold is marked with a line along the implant border (Fig. 38.23). In general, this is the inferior or lower border of the window space. The line must be drawn along the medialization “zone” in the middle of the implant, not on the upper or lower “flange” portions

Fig. 38.17  Distance from the anterior window to the point of maximal

displacement of the depth gauge. This is generally 10–13 mm in males and 3–8 mm in females. This is referred to as the “A” length during implant carving

Fig. 38.18  Measuring the depth of medialization using the depth

gauge. This is typically 5–7 mm. The measurement should be taken of the inner (deep) aspect of the cartilage. This is referred to as the “B” measurement during implant carving

of the implant (Fig. 38.24). Using a 15-blade, the excess Silastic is removed superior and inferior to the plane of medialization, preserving an approximately 3-mm strip of material along the indicated line (Figs. 38.25, 38.26). The extreme upper and lower edges of the implant must be thinned considerably to make the flanges flexible. This

247

248

38

Silastic Medialization Laryngoplasty

 

Fig. 38.19  Carving a left-sided implant. A mark is made on the im-

plant corresponding to the point of maximal medialization (“A” length from Fig. 38.17)

Fig. 38.20  A line is drawn perpendicular, beginning from the “A”

mark, extending the distance determined by the depth of medialization (“B” length from Fig. 38.18)

Fig. 38.21  A triangular implant is then created

Fig. 38.22  Trimming excess Silastic, using a 10 blade

Fig. 38.23  Marking the plane of medialization (corresponding to the

inferior border in most implants)

 

Fig. 38.24  Medialization should only occur within the “medialization

zone” indicated. The implant material above and below this zone is strictly used as flanges to hold the implant in place

Fig. 38.26  Sculpting the final implant contour. Note the line of medi-

alization is at the inferior aspect of the medialization zone

Chapter 38

Fig. 38.25  Removal of Silastic, using a 15 blade

Fig. 38.27  Posterior 7-mm slot is removed from the implant to allow

placement

249

250

Silastic Medialization Laryngoplasty

38 Fig. 38.28  Trimming of excess implant

 

“pressed” or “strained,” then the anterior portion of the implant should be grasped and pulled out of the window slightly. If this improves the voice, then there is too much medialization anteriorly, and the implant should be removed and reduced by an appropriate amount. On the other hand, if the voice sounds breathy, then the implant can be displaced posteriorly. One must be patient to try a variety of maneuvers to insure the implant is ideally suited to improve the voice. This may take an extra 10–15 min, but pays dividends. 20. Trim the excess implant lateral to the thyroid ala to make it flush with the cartilage (Fig. 38.28). 21. Secure the implant to the thyroid cartilage with permanent sutures (4.0 Prolene) around the inferior “strut” of cartilage (Fig. 38.29). 22. Ensure the wound is dry, and close all layers including outer perichondrium, strap muscles, platysmal, and skin. In general, a drain is not necessary, but may be placed depending on the surgeon’s preference.

38.6

Postoperative Care and Complications

Postoperative care after medialization includes: ■ Overnight, 23-h observation ■ Pain management ■ Intravenous steroids at 8-hour intervals (Decadron, 8 mg, then 4 mg) ■ Elevation of the head of bed ■ A return to clinic is scheduled 2–4 weeks after surgery. ■ In general, the patient’s voice is poor within 6–8 h after surgery, due to edema.

Fig. 38.29  Securing the implant to the lower strut with two 4-0

Prolene sutures

will facilitate easier placement of a large implant through the window. The A and B measurements are rechecked for accuracy. Finally, the implant is removed from the holder, and the posterior 7 mm of the “slot” is removed from the implant (Fig. 38.27). The implant is now ready for placement. 18. Place the implant through the window using two Adson’s forceps with teeth. The posterior inferior part of the implant should be advanced into the paraglottic space first. 19. Once the implant is in place, the patient’s voice should be rechecked, and the laryngoscopic image should be observed to insure that the medialization recreates what was achieved with the depth gauge. If the voice sounds

Common mistakes include medialization too far superiorly within the window. In this instance, the indwelling laryngoscopic image will show a medialized false vocal fold or bulging of the ventricular mucosa—sometimes a subtle finding. Another common mistake is excess medialization of the anterior commissure. In this case, the voice has a distinctive “pressed” or “strained” quality. Implant extrusion or exposure is another potential complication. Implant extrusion probably arises due to unrecognized tear in the ventricular mucosa and soiling of the wound with respiratory secretions. The implant may extrude through the skin incision or into the airway, possibly precipitating an airway foreign body emergency. Securing the implant with sutures significantly reduces the risk of this complication. Yet another complication is undermedialization. This probably occurs when excessive edema of the vocal fold occurs prior placement of the implant. The patient is noted to have an excellent voice interoperative when the implant is placed, but the voice begins to fade 1–2 weeks post operatively, as the edema resolves. In cases where a prolonged period elapses between the opening of the window and final placement of the implant, one must anticipate the vocal fold will be slightly overmedialized, and the voice slightly strained to account for this edema.

 

Chapter 38

Key Points

Selected Bibliography

■ Silastic ML is a long-lasting treatment for symptomatic UVFP. ■ The procedure is performed under local anesthesia with an indwelling flexible laryngoscope so that vocal fold position and the patient’s voice can be used as feedback to optimize results. ■ The inferior muscular tubercle must be exposed to define the true lower border of the thyroid cartilage; this will aid in correctly identifying the horizontal plane of the true vocal fold. ■ The inner perichondrium of the thyroid cartilage must be divided to achieve unencumbered medialization. ■ The paraglottic space should not be undermined anteriorly so as to avoid violation of the ventricular mucosa.

1 2

3

Koufman JA (1986) Laryngoplasty for vocal cord medialization: an alternative to Teflon. Laryngoscope 96:726–731 Netterville JL. Stone RE. Luken ES. Civantos FJ (1993) Ossoff RH. Silastic medialization and arytenoid adduction: the Vanderbilt experience. A review of 116 phonosurgical procedures. Ann Otol Rhinol Laryngol 102:413–424 Wanamaker JR, Netterville JL, Ossoff RH (1993) Phonosurgery: Silastic medialization for unilateral vocal fold paralysis. Oper Tech Otolaryngol Head Neck Surg 4:207–217

251

Chapter 39

39

GORE-TEX® Medialization Laryngoplasty

39.1

Fundamental and Related Chapters

Please see Chaps. 5, 36, 37, 38, 40, for 41 further information.

39.2

Disease Characteristics and Differential Diagnosis

Gore-Tex® medialization laryngoplasty is an effective treatment option for many conditions that cause glottal imcompetence. This can be due to vocal fold atrophy, paresis or paralysis. Often patients will be found to have a “bowed” appearance of the vocal fold with these conditions. Vocal fold “bowing” is a term referring to a scalloped contour to the vocal fold. Bowing is a descriptive term, not a diagnostic one. Vocal fold bowing is most often due to age-related changes, or deinnervation of the vocal folds (complete paralysis, or partial paresis). A differential diagnosis of vocal fold bowing includes: ■ Deinnervation (vocal fold paralysis/paresis) ■ Age-related changes (presbylaryngis/vocal fold atrophy) ■ Tissue loss from ablative/destructive vocal fold procedures ■ Vocal fold scar ■ Sulcus vocalis deformity ■ Myopathic disease (rare)

Unilateral GORE-TEX ML can be used in cases of symptomatic glottal insufficiency due to: ■ Unilateral vocal fold immobility, paralysis paresis, or atrophy ■ Unilateral vocal fold scarring or soft tissue loss Bilaterally, GORE-TEX ML can be used to correct mild to severe degrees of glottal insufficiency in cases of: ■ Presbylaryngis (vocal fold atrophy) ■ Bilateral vocal fold paresis ■ Select cases of Parkinson’s disease with vocal fold atrophy Contraindications for GORE-TEX ML include: ■ Previous history of radiation therapy to the larynx (relative) ■ Malignant disease overlying the laryngotracheal complex ■ Poor abduction of the contralateral vocal fold (due to airway concerns) ■ Presence of lesion on the vocal folds

39.4

Surgical Equipment

Needed equipment comprises:

39.3

Surgical Indications and Contraindications

The use of GORE-TEX® as a medialization laryngoplasty (ML) implant material was first reported by McCulloch and Hoffman in 1998 and its ease of handling has made it use in this procedure increasingly common. Many surgeons prefer GORE-TEX for ML, especially in the bowed, mobile vocal fold. For some, it is faster than using Silastic, creates less edema, and therefore decreases the chance of overcorrecting the anterior commissure (particularly if performing a bilateral ML) and allows placement of the implants closer to the vocal process without limiting their abduction. GORE-TEX ML provides an excellent option for surgical treatment of symptomatic patients with moderate to severe vocal fold atrophy/bowing or paresis (glottal gap > 1 mm), as well as unilateral vocal fold paralysis.

■ ■ ■ ■ ■ ■ ■ ■

Drill with 2- to 3-mm cutting burr Kerrison rongeurs tray (1- to 3-mm-sized tips) Ruler Flexible laryngoscope C-mount camera with videocart/monitor Overdrape for laryngoscope (1010 drape) Local anesthetic (nasal and subcutaneous) GORE-TEX strip

The implant itself is a GORE-TEX cardiovascular patch (0.4 mm in thickness) cut in strips 3- to 4-mm wide (as described by McCullough) and soaked in 50,000 U of bacitracin in saline. Creating the GORE-TEX ribbon prior to patient contact allows the remainder of the patch to be reprocessed for future use. Preformed GORE-TEX ribbon for thyroplasty (0.6-mm thickness) is also available (Medtronic ENT, Jacksonville Fla.).

254

GORE-TEX® Medialization Laryngoplasty

 

39.5

Surgical Procedure

1. The surgical region is liberally infiltrated with 1% lido-

39

Fig. 39.1  Inferiorly based perichondrial flap is raised

Fig. 39.2  Axial view of 27-g needle penetrating thyroid ala as a “pilot

hole”

caine with1:100,000 epinephrine, from the hyoid down to the cricoid cartilage, on the side of the intended surgery. Typically, 15 ml is used. Preoperative intravenous Decadron (10 mg) is administered. 2. Four percent lidocaine and oxymetazoline nasal spray is applied to the most patent nasal cavity. An indwelling flexible laryngoscope with videomonitoring of the larynx is used during the entire surgical case. The visual feedback of the larynx is invaluable when performing this surgery. One-inch tape is used to secure the fiberoptic scope to a modified i.v. pole hanging above the patient’s head. The neck is then prepped and draped, including a clear overdrape to allow manipulation of the scope during the case (see Chap. 38, Fig. 38.1). 3. A horizontal incision is placed in a skin crease at the level of the midthyroid cartilage, typically 3–5 cm in length (see Chap. 38, Fig. 38.2). 4. Subplatysmal flaps are raised to the hyoid superiorly and the upper portion of the cricoid below; retention hooks are used to secure the flaps out of the way. 5. The midline raphae are divided between the strap muscles with cautery, exposing the laryngeal cartilage (see Chap., Fig. 38.3). 6. An inferiorly based cathedral arch–shaped outer perichondrial flap is elevated from the thyroid ala (Fig. 39.1). 7. The laryngoplasty window location is determined by needle localization under direct vision with the flexible laryngoscope. An 18-g needle is used to bore gently only through the cartilage, and then a 27-g needle or intravenous catheter is passed through the hole in the cartilage to precisely localize the level of the vocal fold (Fig. 39.2). This is easily observed on the monitor. 8. Using that as a guide, a small rectangular window is then marked on the thyroid cartilage approximately 4–6 mm posterior to the midline of the thyroid cartilage and usually 2–3 mm superior to the inferior border of the thyroid ala. The most common technical error is placing the window too high. The pilot-hole technique allows the surgeon to be certain of the height of the vocal fold and avoid this. A 2- to 3-mm cutting burr is used to initiate this window placement (Fig. 39.3). 9. These windows are usually 3 × 6–12 mm in size, placed parallel to the lower border of the thyroid ala, and are created using a scalpel or a drill. A small Kerrison rongeur is often helpful in removing residual cartilage (Fig. 39.4). 10. After creating the cartilage window, the inner perichondrium is incised along the inferior border with a scalpel. Incising the perichondrium allows a more precise control of medialization (particularly adjacent to the vocal process) with less chance for medialization of ventricular mucosa. A small pocket is formed using the Woodson elevator between the muscle and cartilage inferiorly, anteriorly, and posteriorly as needed, and the vocal fold is medialized with an elevator (note: there is no reason to elevate superiorly). The effect is observed on the video monitor

 

Chapter 39

and acoustically evaluated using vocal feedback from the patient. 11. The GORE-TEX implant is placed as a stacked strip using jeweler’s forceps (or middle ear alligator forceps), and its shape can be easily adjusted for optimal vocal fold medialization (Fig. 39.5). Care is taken to insert the ribbon into the window and when possible, medial to the edge of the anterior, inferior, and posterior edges of the cartilage. This helps maintain the implant’s position. Once the optimum voice is obtained, the vocal folds are slightly overcorrected to compensate for intraoperative edema and implant compression (Fig. 39.6). 12. The implant is stabilized by suturing the outer perichondrial flap back into place using 4-0 nylon sutures. The wound is closed in layers, and drains are rarely required.

39.6

Postoperative Care and Complications

Postoperative care after medialization includes: ■ ■ ■ ■

Overnight, 23-hr observation Pain management Oral antibiotics for 7 days Intravenous steroids at 8-hour intervals (Decadron, 8 mg, then 4 mg) ■ Elevation of the head of bed ■ A return to clinic is scheduled 2–4 weeks after surgery. ■ In general, the patient’s voice is poor within 6–8 h after surgery, due to edema. A common mistake includes medialization too far superiorly within the window. In this instance, the indwelling laryngoscopic image will show a medialized false vocal fold or bulging of the ventricular mucosa—sometimes a subtle finding. Another common mistake is excess medialization of the anterior commissure. In this case, the voice has a distinctive “pressed” or “strained” quality. It is important to note that the technique of bilateral GORE-TEX ML used for the treatment of bowed (but mobile) vocal folds is not the same as the standard ML for unilateral vocal fold paralysis. The technique differs in important ways. (1) Overcorrection anteriorly must be carefully avoided, since excessive anterior medialization will cause a harsh, strained voice. This error can easily occur during bilateral ML surgery. (2) The posterior extent of the implant must not contact the vocal process of the arytenoid cartilage. Since the vocal folds are mobile, an implant projecting too far posteriorly could impinge on the arytenoid, and thus restrict arytenoid motion. In active individuals, this can result in dyspnea with exertion. Implant extrusion or exposure is another potential complication. Implant extrusion probably arises due to unrecognized tear in the ventricular mucosa and soiling of the wound with respiratory secretions. The implant may extrude through the skin incision or into the airway, possibly precipitating an airway foreign body emergency. The implants should be fixed in place via replacement of the perichondrial flap.

Fig. 39.3  Cutting burr is used to enlarge the pilot opening

Fig. 39.4  Further enlargement of the window using a Kerrison ron-

geur to a final size of 3 × 6–12 mm

255

256

GORE-TEX® Medialization Laryngoplasty

 

Key Points ■ GORE-TEX laryngoplasty is a long-lasting, but readily reversible treatment for symptomatic glottal insufficiency, and can be performed bilaterally. ■ The procedure is performed under local anesthesia, with an indwelling flexible laryngoscope so that vocal fold position and the patient’s voice can be used as feedback to optimize results. ■ Overcorrection anteriorly must be carefully avoided (especially when bilateral ML is performed) to avoid a harsh, pressed voice. ■ The posterior extent of the GORE-TEX implant must not contact the vocal process of the arytenoid cartilage, as this may restrict arytenoid motion and lead to airway difficulties.

39 Fig. 39.5  Folding in GORE-TEX ribbon through the thyroid cartilage

window

Fig. 39.6  Final contour of vocal fold after GORE-TEX is layered into

the window (axial view)

Selected Bibliography 1

McCulloch TM, Hoffman HT (1998) Medialization laryngoplasty with expanded polytetrafluoroethylene. Surgical techniques and preliminary results. Ann Otol Rhinol Laryngol 107:427–432 2 Giovanni A, Gras R, Grini MN, Robert D, Vallicioni JM, Triglea JM (1997) Medialization of paralysed vocal cord by expansive polytetrafluoroethylene implant (GORE-TEX). Ann Otolaryngol Chir Cervicofac 114:158–164 3 Giovanni A, Vallicioni JM, Gras R, Zanaret M (1999) Clinical experience with GORE-TEX for vocal cord medialization. Laryngoscope 109:284–288 4 Zeitels SM (2000) New procedures for paralytic dysphonia: adduction arytenopexy, Goretex medialization laryngoplasty, and cricothyroid subluxation. Otolaryngol Clin North Am 33:841–854 5 McCulloch TM, Hoffman HT, Andrews BT, Karnell MP (2000) Arytenoid adduction combined with GORE-TEX medialization thyroplasty. Laryngoscope 110:1306–3111 6 Zeitels SM, Mauri M, Dailey SH (2003) Medialization laryngoplasty with GORE-TEX for voice restoration secondary to glottal incompetence: indications and observations. Ann Otol Rhinol Laryngol 112:180–184 7 Cohen JT, Bates DD, Postma GN (2004) Revision GORE-TEX medialization laryngoplasty. Otol Head Neck Surg 131:236–240 8 Koufman JA (1989) Surgical correction of dysphonia due to bowing of the vocal cords. Ann Otol Rhinol Laryngol 98:41–45 9 Postma GN, Blalock PD, Koufman JA (1998) Bilateral medialization laryngoplasty. Laryngoscope 108:1429–1434 10 Koufman JA, Postma GN (1999) Bilateral medialization laryngoplasty. Oper Tech Otolaryngol Head Neck Surg 10:321–324 11 Cashman S, Simpson CB, McGuff HS (2002) Soft tissue response of the rabbit larynx to GORE-TEX implants. Ann Otol Rhinol Laryngol 111:977–982

Chapter 40

40

Arytenoid Adduction

40.1

Fundamental and Related Chapters

Please see Chaps. 5, 36, 37, 38, 39, and 41 for further information.

40.2

Fundamentals of Arytenoid Adduction

Arytenoid adduction (AA) is used in the treatment of glottal insufficiency. Unlike medialization laryngoplasty, AA acts through direct traction on the arytenoid cartilage at the muscular process, mimicking the action of the lateral cricoarytenoid muscle. AA is an important adjunct in selected cases of vocal fold paralysis. The physiologic effects of AA include the following: ■ ■ ■ ■

Lowers the position of the vocal process Medializes and stabilizes the vocal process Lengthens the vocal fold Rotates the arytenoid cartilage

In patients with vocal fold paralysis who have a lack of vocal process contact during phonation (large posterior gap), shortened immobile vocal fold, and those with vocal folds at different levels, AA should be considered in addition to ML. Videostroboscopy often provides valuable information about vocal process contact, vocal fold height and length, and therefore is useful preoperatively in assessing whether a patient may need an AA. A maximal phonation time (MPT) of less than 5 seconds has also been identified as a predictor of the need for AA in cases of vocal fold paralysis.

40.3

Surgical Indications and Contraindications

Arytenoid adduction for unilateral vocal fold paralysis is indicated in the following cases: ■ Large posterior glottic gap ■ Lateralized vocal fold during phonation ■ Vertical height differences (generally the paralyzed vocal fold is superiorly located) ■ Severely foreshortened vocal fold

■ Inability to achieve good voice intraoperatively with ML alone Contraindications include: ■ Intact vocal fold mobility ■ Vocal fold paralysis with the chance of recovery of motion (“early” paralysis) ■ Limited abduction of contralateral vocal fold

40.4

Surgical Equipment

Surgical equipment needed comprises: ■ ■ ■ ■

Medialization instruments (see Chap. 39) Kerrison rongeurs Sewell retractors 4-0 monofilament permanent suture (Prolene or Tevdek) on a double-armed needle ■ Straight drill bit (e. g., 1-mm wire-passing drill bit) ■ Kitner dissector (peanut)

40.5

Surgical Procedure

Arytenoid adduction is usually performed in conjunction with the ML procedures (see Chaps. 38, “Silastic Medialization Laryngoplasty for Unilateral Vocal Fold Paralysis” and 39, “GORE-TEX® Medialization Laryngoplasty”). The procedure is performed under local anesthesia, with an indwelling flexible laryngoscope. To prevent unnecessary duplication, the key portions of the ML up to the point of the AA are not illustrated in the chapter; however, certain additional steps that are needed to help achieve adequate exposure of the posterior laryngeal framework and arytenoid complex are included for clarity. 1. After the midline raphae are divided between the strap muscles, approximately 1 cm of the medial aspect of the sternohyoid muscle is sectioned below its insertion onto the hyoid. The step is necessary to improve posterior exposure of the laryngeal framework for AA (Fig. 40.1). 2. The outer perichondrium of the thyroid cartilage is then incised with a 15 blade, and a posteriorly based flap is raised with a cottle or freer elevator, including the inferior border of the thyroid ala.

258

Arytenoid Adduction

3. A window is outlined in the thyroid cartilage, and opened

as previously indicated in Chap. 38. A surgical plane is then developed in the paraglottic space (just superficial to the TA fascia) in all directions around the window except anteriorly. In general, preliminary measurements are taken for the ML portion of the case, before proceeding to the arytenoid exposure (see Chap. 38, Figs. 38.7–38.15 for details). 4. The outer perichondrial flap is then extended all the way to the posterior border of the thyroid ala. The outer peri-

40

Fig. 40.1  Partial division of sternohyoid muscle 1 cm below its inser-

tion

 

chondrium is incised with a 15 blade along the posterior border of the cartilage to prevent elevation of the inner perichondrium. The incision is continued to the level of the superior cornu above and the inferior cornu below (Fig. 40.2). 5. The surgical plane of the medialization window (paraglottic space) should then be connected to the posterior laryngeal dissection, so that there is one continuous surgical plane. A cottle or freer elevator is used to achieve this (Fig. 40.3). 6. A skin hook is placed on the posterior border of the cartilage to aid in retraction. Access to the arytenoid can then be achieved with one of two methods: a) Creation of a window in the posterior thyroid ala A window of cartilage is removed from the posterior border of the thyroid cartilage, using a 2-mm Kerrison rongeur. The cartilage is removed until the muscular process of the arytenoid is palpable and the anterior extension of the pyriform sinus can be visualized (Fig. 40.4). The size of the window ranges from 10 to 15 mm in height and extends approximately 10 mm anteriorly, although the dimensions vary. The posterior aspect of this window should be located on the same level of the ML window. It is important not to allow the anterior and posterior windows to “connect,” as this will likely lead to framework instability. b) Separation of the cricothyroid joint Another way to gain exposure is by separation of the cricothyroid joint along with lateral thyroid ala retraction. A small dissection scissor (tenotomy) is used to separate the cricothyroid joint. Skin hook retractors are placed, and the thyroid ala is gently retracted laterally. Often, additional muscular or perichondrial attachments along the inferior and superior cornu must be divided to facilitate lateral alar retraction (Fig. 40.5). 7. The pyriform sinus mucosa must be identified and retracted posteriorly before the muscular process of the arytenoid is identified. Great care must be taken with this step

Fig. 40.2  A posteriorly based flap is separating the mus-

cle away from the posterior cartilaginous border.

 

Chapter 40

Fig. 40.3  The paraglottic space is connected between the posterior

cartilage border and the ML window

to avoid perforation of this delicate mucosa. The pyriform mucosa can be seen extending anteriorly onto the posterior cricoarytenoid (PCA) muscle. To aid in its identification, the patient is asked to blow against pursed lips (“blow out the birthday candles”), which results in distension and easy identification of the pyriform mucosa. The mucosa is grasped and dissected posteriorly, using blunt dissection with a Kitner (Fig. 40.6). The pyriform can then be shielded under a Sewell retractor (Fig. 40.7). 8. The muscular process can then be identified using a number of landmarks. The muscular process is usually at the same vertical height of the vocal fold and found by tracing the fibers of the PCA muscle anterior/superiorly to its tendinous insertion (Fig. 40.8). The muscular process is small (about the size of a grain of rice), but can be palpated. In addition, if the cricothyroid joint is separated as in step 6b, then this can be used as a nearby landmark, as the muscular process can be reliably found within 1 cm above this point. By grasping the muscular process with a toothed forceps, and rotating the arytenoid (anteriorly), one should be able to easily rotate the arytenoid into a medial position while confirming this with the endolaryngeal image on the monitor (Fig. 40.9). 9. In order to obtain a secure purchase on the muscular process, a 4-0 monofilament suture (double armed) is passed through the lateral edge of the muscular process in a figure of eight fashion (Fig. 40.10). 10. Both needles are brought through the dissected paraglottic space into the medialization window, taking great care not to inadvertently catch any tissue with the needle tips, which could adversely affect the vector of pull for the AA stitch. Generally, the needles are passes with the dull end as the leading edge (Fig. 40.11). 11. One of the needles is passed through the cartilage anterior to the medialization window, using a 1-mm wire-passing drill bit if the cartilage is calcified (Fig. 40.12). The other needle is passed underneath the inferior strut and is secured anteriorly through the anterior cricothyroid membrane (Fig. 40.13). 12. The two ends of the suture are then clamped with hemostats. The sutures are gently pulled anteriorly to adduct the

Fig. 40.4  Posterior “cookie-bite” window is created with a Kerrison

rongeur

Fig. 40.5  Alternately, the cricothyroid joint can be divided for poste-

rior exposure

arytenoid, and the effect on the voice is tested by having the patient count from 1 to 10. In addition, at this time the effects of medialization, using the previously mentioned depth gauge instrument are tested both in isolation, and with the addition of tension of the AA suture. 13. Once the implant is created, it is placed through the window, taking care to keep the AA suture lines deep to the implant (Fig. 40.14).

259

260

Arytenoid Adduction

 

Fig. 40.6  The pyriform mucosa is dissected posteriorly using a Kitner

40

Fig. 40.7  Axial representation of larynx after posterior pyriform mu-

cosa dissection/protection with Sewell retractor

Fig. 40.8  Muscular process of the arytenoid is identified

Fig. 40.10  A 4-0 double-armed Prolene suture is passed through the

muscular process in a figure of eight fashion

Fig. 40.9  Axial representation of manual traction on the muscular

process to demonstrate adduction of the vocal fold

 

Fig. 40.11  Passage of the suture through the ML window

Chapter 40

Fig. 40.12  A 1-mm wire-passing drill bit is used to create an anterior

passage for one arm of the AA suture near the midline

Fig. 40.13  After successful passage of both arms of the AA suture

through the midline

Fig. 40.15  Final tying of a surgeon’s knot over the thyroid ala

Fig. 40.14  Axial representation of AA sutures deep to ML implant

261

262

Arytenoid Adduction

 

14. Finally, the AA suture tension is adjusted and the knot is

secured over the anterior thyroid cartilage, again assessing the voice. In general, only a small amount of tension is required for this (Fig. 40.15). 15. Sternohyoid muscle is re-attached. Wound is closed in layers. Drain is placed at the surgeons discretion.

40.6

■

Postoperative Care and Complications

Postoperatively, care should encompass:

40

■ Overnight, 23-hours observation ■ Pain management ■ Intravenous corticosteroids at 8-hour intervals (Decadron, 8 mg, then 4 mg) ■ Elevation of the head of bed ■ A return to clinic is scheduled 2–4 weeks after surgery ■ In general, the patient’s voice is poor within 6–8 hours after surgery, due to edema. ■ An additional corticosteroid taper may be warranted on discharge from the hospital. Complications and common surgical errors include laryngeal edema with airway compromise, which is more common with framework surgery that involves AA. The additional retraction and dissection necessary for exposure and manipulation of the arytenoid complex results in increased paraglottic and arytenoid edema post operatively. Additional corticosteroids may be warranted in patients undergoing ML and AA. Pharyngocutaneous fistula is a possible complication with AA, although it is quite uncommon. Careful handling of the pyriform mucosa and protection of the mucosa with a retractor should prevent this complication. If an injury to the mucosa is suspected, then the field can be irrigated and the patient instructed to perform the Valsalva maneuver. If air bubbles occur during this maneuver, then the pyriform mucosa should be repaired with absorbable suture, and the patient should be retested for air leakage. One should consider whether it is prodent to proceed with the ML and/or AA at this point. Excessive tension on the AA suture can create over-rotation of the arytenoid and worsening of the voice. The tension needed on this suture is actually minimal in most cases; therefore, the surgeon should err on the side of light tension on the AA suture.

Key Points ■ Arytenoid adduction (AA) is a framework surgery where the pull of the LCA muscle is recreated to achieve vocal fold repositioning. The physiologic effects of AA include the following: ■ Lowers the position of the vocal process ■ Medializes and stabilizes the vocal process

■

■ ■

■

■

■ Lengthens the vocal fold ■ Rotates the arytenoid cartilage AA is used as an adjuvant surgical treatment along with ML in cases of vocal fold paralysis where one of the following occurs: ■ Posterior glottic gap/lateralized vocal fold during phonation ■ Vertical height differences between vocal folds (generally the paralyzed vocal fold is superiorly located) ■ Severely foreshortened vocal fold ■ Inability to achieve good voice intraoperatively with ML alone AA requires a posterior dissection technique separate from ML, where either a posterior window in created in the thyroid ala, or the cricothyroid joint is divided to allow outward retraction of the posterior thyroid ala. The pyriform mucosa must be dissected off the muscular process of the arytenoid to allow proper exposure of this structure. A double-armed needle is secured at the muscular process of the arytenoid and passed anteriorly near the midline of the thyroid ala to recreate the pull of the LCA muscle. The sutures lie deep to the medialization implant. The needles from the AA sutures should be passed through the paraglottic space carefully (dull end as the leading edge) to avoid picking up soft tissue, which may change the vector of pull. Only mild–moderate tension is required on the AA suture to achieve desirable arytenoid positioning.

Selected Bibliography 1

2 3

4

5 6

McCulloch TM, Hoffman HT, Andrews BT et al (2000) Arytenoid adduction combined with Gore-Tex medialization thyroplasty. Laryngoscope 110:1306–1311 Woo P. Arytenoid adduction and medialization laryngoplasty (2000) Otolaryngol Clin N Am 33:817–839 Noordzij JP, Perrault DF, Woo P (1998) Biomechanics of combined arytenoids adduction and medialization laryngoplasty in an ex vivo canine model. Otol Head Neck Surg 119:634–642 Woodson GE, Picerno R, Yeung D et al (2000) Arytenoid adduction: controlling vertical position. Ann Otol Rhinol Laryngol 109:360–364 Isshiki G (1978) Arytenoid adduction for unilateral vocal cord paralysis. Arch Otolaryngol 104:555–558 Miller FR, Bryant GL, Netterville JL (1999) Arytenoid adduction in vocal fold paralysis. Oper Tech Otolaryngol Head Neck Surg 10:36–41

Chapter 41

41

Cricothyroid Subluxation

41.1

Fundamental and Related Chapters

Please see Chaps. 5, 36, 37, 38, 39, and 40 for further information.

41.2

Disease Characteristics and Differential Diagnosis

Cricothyroid subluxation was developed by Steve Zeitels to address the problems of a shortened vocal fold frequently seen in unilateral vocal fold paralysis. The concept of the procedure is to lengthen the vocal fold by increasing the distance from the cricoarytenoid joint (cricoid) to the anterior commissure (thyroid cartilage) by subluxating the cricothyroid joint on the side of the unilateral vocal fold paralysis. This results in a rotation of the anterior commissure away from the midline in a direction contralateral to the side of the unilateral vocal fold paralysis. Cricothyroid subluxation is an adjunct procedure to medialization laryngoplasty. This can be done with arytenoid adduction also, but is typically used with medialization laryngoplasty. Cricothyroid subluxation addresses the commonly seen problem of a shortened vocal fold associated with unilateral vocal fold paralysis. The only other procedure that can lengthen a paralyzed vocal fold is arytenoid adduction (see Chap. 40, “Arytenoid Adduction”).

41.3

Surgical Indications and Contraindications

Indications for cricothyroid subluxation involve: ■ Unilateral vocal fold paralysis associated with vocal fold shortening with resultant glottal insufficiency and reduced pitch range (preoperative assessment) ■ Poor pitch range and/or significantly shortened vocal fold, as seen on endoscopy during medialization laryngoplasty after adequate implant positioning (intraoperative) Contraindications include present or impending laryngeal fracture of thyroid ala from the associated medialization laryngoplasty procedure.

41.4

Surgical Equipment

Surgical equipment needed for cricothyroid subluxation comprises: ■ See “Surgical Equipment” sections in Chaps. 38, “Silastic Medialization Laryngoplasty for ® Unilateral Vocal Fold Paralysis” and 39, “GORE-TEX Medialization Laryngoplasty.” ■ Right-angle clamp (vascular clamp) ■ 2-0 Prolene suture with narrow diameter, semicircle needle ■ Surgical headlight

41.5

Surgical Procedure

1. Cricothyroid subluxation is done as a planned procedure

in conjunction with medialization laryngoplasty, or done immediately after a medialization laryngoplasty due to a restricted pitch range despite a well-positioned medialization laryngoplasty implant. 2. Further dissection than what is typically performed for a medialization laryngoplasty approach alone is required. Complete skeletonization of the inferior cornu of the thyroid cartilage should be performed using electric cautery or cold steel instrumentation. This will involve removal of the cricothyroid muscle immediately anterior and inferior to the inferior cornu and release of the inferior constrictor muscle off the posterior aspect of the inferior cornu. The recurrent laryngeal nerve is at risk in this region; thus, it is wise to keep dissection close to the inferior cornu of the thyroid cartilage to avoid deinnervation of the immobile but partially reinnervated vocal fold. 3. Soft tissue overlying the superior and inferior aspect of the cricoid cartilage at the midline should be removed. 4. Separation of the cricothyroid joint This can be done using a scissors or a cottle elevator. Care should be taken during this step not to fracture the inferior cornu. The use of scissors to separate the cricothyroid joint is most likely less traumatic to the inferior cornu. The blades of the scissors are placed up against the posterior, lateral aspect of the cricoid cartilage to allow the tips of the scissors to be positioned on either side of the cricothyroid joint (Fig. 41.1). 5. After separation of the cricothyroid joint, care should be taken to insure the inferior cornu of the thyroid cartilage is completely free of any soft tissue attachments.

264

Cricothyroid Subluxation

 

41

Fig. 41.1  Separation of cricothyroid joint with scissors

6. A 2-0 Prolene suture is then passed around the neck of the

inferior cornu. This can be done with a relatively narrow diameter, semicircle needle, or by using a right-angled clamp (vascular clamp) to pass the free end of the suture around the neck of the inferior cornu. The suture should be positioned as superior as possible on the neck of the inferior cornu and then tied with relatively equal lengths of the suture on both sides of the knot. 7. The arm of the suture with the needle is then passed underneath the cricoid cartilage anteriorly at the midline. Care should be taken not to fracture the cricoid cartilage and to pass the needle in a submucosal plane under the anterior aspect of the cricoid ring (Fig. 41.2). 8. The free end of the suture tied at the inferior cornu is then tied to the end of the suture passed underneath the anterior cricoid cartilage. The voice and vocal fold length (endoscopically) should be evaluated as tension is applied to the knot (Fig. 41.3). Typically, only moderate tension is required to position the inferior cornu into an anterior, subluxated position. This anterior subluxation of the inferior, cornu of the thyroid cartilage results in vocal fold lengthening and an expanded pitch range (Fig. 41.4). Once an optimal tension is found (predominantly by perceptual voice assessment), the suture is secured with several surgical knots.

Fig. 41.2  Placement of cricothyroid subluxation suture submucosally

at the midline of the anterior cricoid cartilage

41.6

Postoperative Care and Complications

Postoperative care is identical to that of medialization laryngoplasty. The reader is referred to Chaps. 38, “Silastic Medialization Laryngoplasty for Unilateral Vocal Fold Paralysis” and 39, “GORE-TEX® Medialization Laryngoplasty” for details. Complications involve: ■ Fracture of the inferior cornu ■ To remedy this complication, a suture can be placed through the thyroid cartilage near the fracture line and then be used in a similar fashion as described above to complete the cricothyroid subluxation. ■ Fracture of the main aspect of the thyroid cartilage ala ■ If fractures of the thyroid cartilage ala occur, then all fractures should be reduced and secured with either suture or plating and the cricothyroid subluxation procedure should be aborted (see Chap. 44, “Repair of Laryngeal Fracture”).

 

Chapter 41

265

Key Points ■ Cricothyroid subluxation is an adjunctive procedure to medialization laryngoplasty which lengthens the shortened vocal fold associated with unilateral vocal fold paralysis. ■ Cricothyroid subluxation rotates the anterior commissure attachment of the vocal fold away from the cricoarytenoid joint, thus lengthening the vocal fold. ■ Care should be taken not to fracture the inferior cornu of the thyroid cartilage during the procedure. ■ Excessive tension applied to the suture securing the cricothyroid subluxation position may worsen voice quality.

Bibliography 1

2

Zeitels SM (2000) New procedures for paralytic dysphonia: adduction arytenopexy, Goretex medialization laryngoplasty, and cricothyroid subluxation. Otolaryngol Clin North Am 33:841–854 Zeitels SM, Hillman RE, Desloge RB, Bunting GA (1999) Cricothyroid subluxation: a new innovation for enhancing the voice with laryngoplastic phonosurgery. Ann Otol Rhinol Laryngol 108:1126–1131

Fig. 41.3  Suture fixation of cricothyroid subluxation

Fig. 41.4  Axial view of vocal fold position

before and after cricothyroid subluxation

Chapter 42

42

Translaryngeal Removal of Teflon Granuloma

42.1

Fundamental and Related Chapters

Please see Chaps. 24, 36, 37, 38, and 40 for further information.

42.2

Disease Characteristics and Differential Diagnosis

In every Teflon injection, an inflammatory response to the Teflon occurs. In most cases, the inflammatory response remains localized, and no significant clinical complications are noted. However, there is a risk of clinically evident expansile granuloma formation in these patients if long-term follow up (10 years or more) is used. Often this occurs years after the initial injection, after a prolonged period of good voice. Anecdotal

evidence suggests that subsequent laryngeal trauma (i. e., intubation) may contribute to growth of the granuloma. Teflon granuloma is typically a submucosal smooth mass that presents as a bulge in the false vocal cord, ventricular mucosa, and/or the true vocal fold. The granuloma may grow inferiorly resulting in a subglottic bulge as well. Videostroboscopy is quite consistent in these patients, revealing a stiff, nonvibratory vocal fold mass. This is due to either a mass effect (stretching of vocal fold mucosa with dampening of wave) or, more commonly, the infiltration of the granuloma into the lamina propria and/or mucosa. Glottic incompetence is commonly present, secondary to the mass lesion. Occasionally, the patient’s airway is compromised, especially if the granuloma is subglottic. It is helpful to obtain a CT scan of the neck with contrast to assess the location of the Teflon and extent of granuloma formation. In this way, superficial Teflon granulomas can be distinguished from more extensive granulomas, which guides the surgeon in choosing the appropriate approach (endoscopic, see Chap. 24 “Endoscopic Management of Teflon Granuloma”) versus the external approach described in this chapter). Typical CT appearance is a brightly enhancing, fairly well-circumscribed mass in the paraglottic space.

42.3

Surgical Indications and Contraindications

Indications include: ■ Symptomatic Teflon granuloma in a patient with UVFP in which there is sparing of the free edge of the vocal fold (vocal ligament/mucosa appear uninvolved with granuloma) (Fig. 42.1) ■ Desire for complete removal of granuloma Relative contraindications although these are not absolute contraindications to this approach, include the following: ■ Extensive granuloma infiltration along the medial edge of the vocal fold (vocal ligament involvement) (Fig. 42.2) ■ Minimally symptomatic patient ■ These clinical settings may be better suited for endoscopic treatment (see Chap. 24) Fig. 42.1  Coronal section of larynx with Teflon granuloma sparing

the vocal fold mucosa and vocal ligament (arrow)

268

Translaryngeal Removal of Teflon Granuloma

 

1. The surgical region is liberally infiltrated with 1% lido-

2.

3.

4. 5.

42

Fig. 42.2  Coronal section of the larynx with Teflon granuloma involv-

ing the free edge of the vocal fold (arrow). This is a relative contraindication for translaryngeal removal

42.4

Surgical Equipment

Equipment includes: ■ Netterville medialization tray (Medtronic ENT, Jacksonville, Fla.) ■ Drill with 2- or 3-mm cutting burr ■ Kerrison rongeurs tray (1- to 3-mm-sized tips) ■ Medium-grade Silastic block (Medtronic ENT) ■ 4-0 monofilament suture, double-armed needle ■ Ruler (15-mm section of plastic ruler at tip of hemostat) ■ Flexible laryngoscope ■ C-mount camera with videocart/monitor ■ Overdrape for laryngoscope (1010) ■ Local anesthetic (nasal and subcutaneous) ■ High-power surgical loops (optional) ■ Middle ear instrument tray (especially a no. 2 House knife; optional)

42.5

Surgical Procedure

This advanced framework technique requires experience with the techniques of ML and AA. The surgeon should be well versed in the techniques of Chaps. 38, “Silastic Medialization Laryngoplasty for Unilateral Vocal Fold Paralysis” and 40, “Arytenoid Adduction” before attempting this technique.

6. 7. 8. 9.

caine with1:100,000 epinephrine, from the hyoid down to the cricoid cartilage, on the side of the intended surgery. Typically, 20–25 ml is used. Four percent lidocaine and oxymetazoline nasal spray is applied to the most patent nasal cavity. Placement of an indwelling flexible laryngoscope, allows videomonitoring of the larynx during the entire surgical case. The visual feedback of the larynx is invaluable when performing this surgery. After sterile prep of the neck and flexible laryngoscope placement, a horizontal incision is placed in a skin crease at the level of the cricothyroid membrane extending past the midline, in a cervical skin crease, typically 7–8 cm in length. Subplatysmal flaps are raised to the hyoid superiorly and the upper portion of the cricoid below; retention hooks are used to secure the flaps out of the way. A randomly pedicled flap is raised that is composed of the superficial layer of the deep cervical fascia covering the strap muscles, with its overlying fat. This flap is posteriorly based and has a wide base lateral to the omohyoid muscle (Fig. 42.3). The flap should be raised with cold dissection and bipolar cautery to avoid thermal damage. Once reflected, the flap is covered with moist gauze. The midline raphae is divided between the strap muscles with cautery, exposing the thyroid lamina on the involved side. A single-prong hook is placed under the thyroid notch, and the larynx is retracted to the side opposite the paralysis, bringing the entire hemilaryngeal cartilage into view. A vertical parasagittal laryngotomy is performed 5–7 mm posterior to the midline on the ipsilateral side, using a 15 blade or a powered sagittal saw (Fig. 42.4). The thyroid lamina is retracted laterally with hooks allowing for wide exposure of the paraglottic space (Fig. 42.5). Dissection of the granuloma can now proceed (Fig. 42.6). Identification of the correct plane of dissection between the granuloma and normal paraglottic tissue is frequently difficult; surgical loops may be helpful during this portion of the case. A variety of dissection tools may be employed; Jamison scissors, Freer, and Woodson elevators are useful for the gross dissection, while middle ear instruments (no. 2 House knife) can be used for dissection with surgical loops. The mucosa of the ventricle should be avoid anteriorly where is may be adherent to the granuloma. Care is taken to preserve the vocal ligament/conus elasticus and lamina propria, as their integrity has proven an important prognostic indicator of postoperative voice quality. The granuloma often encases most of the paraglottic laryngeal musculature (thyroarytenoid/vocalis, lateral cricoarytenoid), such that complete removal may result in an “empty” paraglottic space. Not infrequently, defects in the ventricular or subglottic mucosa may be created during dissection. These mucosal defects should not compromise the end result. In contrast, removal of the vocal fold mucosa and/or vocal ligament should be avoided as this has a detrimental effect on the voice result.

 

Chapter 42

Fig. 42.3  Posteriorly based fat flap is raised

Fig. 42.6  Dissection of granuloma from the paraglottic space

Fig. 42.4  Vertical laryngotomy is performed 5–7 mm off the midline

for exposure of the paraglottic space

Fig. 42.7  After removal of the granuloma, the laryngotomy is repaired Fig. 42.5  Axial view of parasagittal laryngofissure

with 2-0 Prolene sutures, and windows are made for medialization laryngoplasty and arytenoid adduction

269

270

42

Translaryngeal Removal of Teflon Granuloma

 

Fig. 42.8  The patient’s voice is tested while simultaneously putting

traction on the arytenoid adduction suture and depressing the depth gauge within the thyroplasty window. A Cottonoid is placed in the paraglottic space for cushioning

Fig. 42.9  Axial view of fat flap advanced into the paraglottic space

10. The lateral laryngotomy is reduced and secured with two

Fig. 42.10  Final configuration of the fat flap within the paraglottic

space. Note sutures securing the flap both anteriorly and inferiorly

to three 2-0 Prolene sutures. Windows are made for medialization and arytenoid adduction (both posterior and anteriorly) as described in Chaps. 38 and 40 (Fig. 42.7). 11. An arytenoid adduction suture (4-0 Prolene, doublearmed) is placed through the muscular process, secured, and the two ends are passed through separate holes in the anterior (midline) of the thyroid lamina, similar to the technique of arytenoid adduction described in (Chap. 40). 12. A Cottonoid is then placed within the thyroplasty window to provide cushioning to the paraglottic space (approximating the effect that the fat flap will provide), while a depth gauge is used to medialize the vocal fold. The effects of medialization and tension on the arytenoid adduction suture should be used to gauge the best vocal outcome (Fig. 42.8). 13. The fat flap is tucked deep to the strap muscles and advanced into paraglottic space via the posterior thyroid cartilage window (Fig. 42.9). The flap’s apex should be brought as anteriorly as possible to reconstitute the true vocal fold at the anterior commissure. The voice should be tested as the flap is manipulated within the paraglottic space in a variety of configurations. The flap serves the important function of providing bulk to the paraglottic tissues, which is vital to the success of the primary surgery and any additional augmentative procedures attempted in

 

Chapter 42

the future. The flap is secured to the thyroid and cricoid cartilages using 3- or 4-0 Prolene sutures through 1-mm drill bit holes as needed (Fig. 42.10). 14. The patient is asked to phonate, while tension on the arytenoid adduction suture is adjusted, until optimal voice result (or vocal fold positioning in the midline position) is obtained. The suture is secured over the thyroid lamina near the midline. 15. Medialization should be deferred until a later date if there is a mucosal tear, to avoid complications of foreign body contamination. However, if no mucosal defect is present, then a Silastic implant may be placed at this time. Medialization measurements are obtained by displacing the posterior/mid aspect of the window using a depth gauge. The vocal fold should be slightly overmedialized to account for inevitable fat flap atrophy. It is important to emphasize that a number of possible combinations using one or all of the three techniques (fat flap, ML, AA) can be employed at the same time to achieve the best vocal result. This takes a fair amount of trial and error to optimize the vocal results. Wound irrigation, layered closure over a closed suction drain is then performed.

42.6

Postoperative Care and Complications

complication is encountered months after surgery. The fat flap may slowly atrophy over several month-years, resulting in glottic insufficiency eventually. Additional procedures can be attempted when this happens, including lipoinjection and/or revision Silastic medialization. In addition, implant exposure, infection, and/or extrusion are more likely in the setting of Teflon granuloma removal due to the higher risk of mucosal violation within the endolarynx.

Key Points ■ Laryngotomy is the only surgical approach that allows for complete removal of granuloma in most cases. ■ The ideal case for laryngotomy/fat flap reconstruction is symptomatic Teflon granuloma in a patient with UVFP in which there is sparing of the free edge of the vocal fold (vocal ligament/mucosa appear uninvolved with granuloma). ■ The surgeon should master the techniques of ML and AA before attempting this procedure. ■ The pedicled fat flap may atrophy over time, necessitating additional procedures to restore glottal competence, such as lipoinjection or revision Silastic ML.

Postoperative care comprises: ■ Overnight, 23-hour observation ■ Pain management ■ Intravenous steroids at 8-hour intervals (Decadron, 8 mg, then 4 mg) ■ Elevation of the head of bed ■ A return to clinic is scheduled 2–4 weeks after surgery. Complications include those seen in medialization laryngoplasty and arytenoid adduction (Chaps. 38 “Silastic Medialization Laryngoplasty for Unilateral Vocal Fold Paralysis” and 40, “Arytenoid Adduction”); however, the most common

Selected Bibliography 1

2

Netterville JL, Coleman JR, Chang S et al (1998) Lateral laryngotomy for the removal of Teflon granuloma. Ann Otol Rhinol Laryngol 107:735–744 Conoyer MJ, Netterville, Chen A et al (2006) Pedicled fat flap reconstruction of the atrophic or “empty” paraglottic space after resection of Teflon granuloma or oversized implant. Ann Otol Rhinol Laryngol 115:837–845

271

Chapter 43

Excision of Combined Laryngocele

43.1

Fundamental and Related Chapters

Please see Chaps. 25, 36, and 37 for further information.

43.2

Disease Characteristics and Differential Diagnosis

43.2.1 Anatomy and Classification

43

2. Combined (external and internal) laryngoceles originate

in the endolarynx as with internal laryngoceles, but extend through the thyrohyoid (TH) membrane, into the neck (Fig. 43.2). A foramen in the TH membrane where the superior laryngeal nerve (internal branch) and vessels enter provides the pathway for extension of the laryngocele into the neck. This constriction at the TH membrane gives combined laryngoceles their characteristic “dumbbell” appearance (Fig. 43.3). These lesions are usually removed externally through a transthyroid approach, as described in this chapter.

The normal saccule arises as a diverticulum originating at the anterior portion of the ventricle, and extending upward into the supraglottis. It is sandwiched between the false vocal fold medially and the aryepiglotticus muscle and thyroid cartilage laterally. The saccule contains numerous mucus-secreting glands, and acts as a reservoir, expressing secretions onto the vocal folds due to the squeezing action of the surrounding supraglottic musculature. A laryngocele represents an abnormal dilation or herniation of the saccule. In contrast to a saccular cyst (Chap. 25, “Endoscopic Excision of Saccular Cyst”), a laryngocele communicates with the lumen of the larynx and is distended with air. Any factor that increases intralaryngeal pressure can lead to development of a laryngocele: ■ ■ ■ ■

Coughing Straining Playing wind instruments Glass blowing

Another etiology in the development of laryngoceles may be air trapping due to ball-valve closure of the neck of the saccule, allowing for entry of air into the saccule, but preventing its egress. This “valve-like” effect can occur from inflammatory or neoplastic processes in the ventricle or false vocal fold. For this reason, neoplastic causes should be ruled out, especially in high-risk patients (tobacco/alcohol users). Laryngoceles occur predominantly in males, most often in the fifth or sixth decade of life. Laryngoceles are categorized based on anatomic extension of the lesion: 1. Internal laryngoceles are contained entirely within the endolarynx. They originate in the anterior ventricular membrane, and extend posteriorly–superiorly into the paraglottic space (Fig. 43.1). This creates are characteristic bulge in the false vocal fold and aryepiglottic fold. The lesions can usually be managed endoscopically, similar to the treatment of a saccular cyst (see Chap. 25).

Fig. 43.1  Coronal representation of internal laryngocele

274

Excision of Combined Laryngocele

 

Fig. 43.3  CT scan depicting combined laryngocele, with characteris-

tic dumbbell appearance

43

Fig. 43.2  Coronal representation of combined laryngocele

43.2.2 Clinical Presentation and Differential Diagnosis Most laryngoceles are asymptomatic and may be incidental findings on radiographic studies of the neck. When symptoms arise, hoarseness is the most common clinical presentation, although cough or globus sensation are also seen. Patients with combined laryngoceles may present with a neck mass. The neck mass often appears only intermittently, and may be reproduced by asking the patient to valsalva. Office laryngoscopy will typically reveal a submucosal fullness or bulge in the false vocal fold/ aryepiglottic fold region. If a neck mass is present it is typically located at the superior/lateral aspect of the thyroid cartilage, and is soft and easily compressible. Differential diagnosis of a laryngocele includes: ■ ■ ■ ■

Saccular cyst Mucous retention cyst Hemangioma Laryngeal neoplasm (e. g., squamous cell carcinoma, neuroendocrine/neural tumors)

A CT scan should be obtained to define the extent of the lesion (internal versus combined), and to delineate the internal content of the mass. Laryngoceles will contain air (black), while saccular cysts will contain mucous (gray/soft tissue signal). A biopsy is rarely indicated due to the unique nature of the lesion. However, a ductal lavage/biopsy may be indicated in the anterior ventricular region, if malignancy is suspected.

43.3

Surgical Indications and Contraindications

Absolute indications are symptomatic combined laryngocele (hoarseness/airway compromise) and suspicion of malig­ nancy. A relative indication is cosmetic concerns (especially in large combined laryngoceles in horn players). Contraindications include asymptomatic lesions found incidentally/radiographically Caution should be exercised in the rare case of bilateral combined laryngoceles. Bilateral injury to the internal branch of the superior laryngeal nerve can lead to aspiration. The surgeon may wish to “stage” their resections, insuring intact sensation (via functional endoscopic evaluation of swallowing and sensory testing) on the operated side before proceeding with the contralateral laryngocele.

 

Chapter 43

43.4

Surgical Equipment

■ Microlaryngoscopy equipment ■ Neck dissection tray ■ Blunt dissection instruments (Kitner/peanut)

43.5

Surgical Procedure

1. Perform a direct microlaryngoscopy, examining the ante-

2. 3. 4. 5.

6. 7.

rior false vocal fold, ventricular region, to rule out malignancy (note: 30 and 70° telescopes are well suited for this). A horizontal incision (5–7 cm) is made at the superior aspect of the thyroid cartilage, in a skin crease. Subplatysmal flaps are raised from the upper aspect of the cricoid to just superior to the hyoid. Skin retraction hooks are placed. The midline raphae are identified, and divided from the hyoid down to the cricoid, exposing the thyroid ala. The infrahyoid strap muscles (sternohyoid, omohyoid, and thyrohyoid) are identified on the side of the lesion, and divided superiorly near their origin. A small cuff of fascially encased muscle should be preserved at its attachment to the hyoid, to aid in reapproximation of each muscle near the end of the case (Fig. 43.4). The ipsilateral hemilarynx is rotated into the field by retraction at the thyroid notch, using a single-prong hook. The external component of the laryngocele is identified within the thyrohyoid region. The lateral aspect of the laryngocele is defined by carefully excising the soft tissue covering on its surface, until the glistening capsule of the laryngocele is clearly identified. A small amount of soft tissue covering is left in place at the superior aspect of the

capsule; this area is grasped with a Babcock retractor (Fig. 43.5). 8. The laryngocele is retracted gently as blunt dissection is used to define the external (extralarnygeal) portion of the laryngocele capsule (Fig. 43.6). Some sharp dissection with hemostat/15 blade is usually necessary as well. It is important to “hug” the laryngocele capsule closely during dissection. This is especially important posteriorly within the TH membrane region, where the SLN branch is immediately adjacent to the laryngocele. 9. The “back wall” of the laryngocele should be well defined before proceeding with dissection of the intralaryngeal portion of the dissection. 10. An inferiorly based flap is created from the outer perichondrium of the thyroid ala by incising at the superior

Fig. 43.4  Sectioning of strap muscles to allow exposure

of the TH space

Fig. 43.5  Identification of laryngocele capsule within the TH mem-

brane

Fig. 43.6  Blunt dissection of the external component of the laryngo-

cele

275

276

Excision of Combined Laryngocele

 

border of the thyroid lamina and using a freer elevator for dissection. 11. A triangular section of the thyroid ala is marked out, with its base superiorly, and its apex at a point half way along the vertical distance of the thyroid lamina. This segment of cartilage is removed with a 15 blade and/or Kerrison rongeurs. The inner perichondrium is then incised and removed from the triangular region, exposing the paraglottic space (Fig. 43.7). The cartilage can be discarded after removal.

12. Dissection continues inferiorly, defining the internal com-

Fig. 43.7  Inferiorly based outer perichondrial flap is

Fig. 43.8  Sharp dissection of muscular/fibrous tissue off

Fig. 43.9  The termination of the laryngocele is identified at the base

Fig. 43.10  A figure-eight suture is used to close the mucosal defect

ponent of the laryngocele. Sharp dissection through the ventricularis and aryepiglotticus muscles facilitates the identification of the capsule in the paraglottic space (Fig. 43.8). 13. The termination of the laryngocele is identified at the base of the saccule. This is typically located at the anterior ventricular mucosa. This corresponds with a point 3–5 mm posterior to the midline of the thyroid lamina at the midway point along its vertical height (Fig. 43.9).

43

raised and triangular portion of the thyroid ala is removed for exposure of the internal component of the lesion

of the saccule. The airway is entered, excising a cuff of ventricular mucosa around its entry into the endolarynx.

the internal (paraglottic) portion of the lesion

(4.0 chromic)

 

Chapter 43

14. The airway is entered, excising a cuff of ventricular muco-

sa around its entry into the endolarynx. A figure-eight suture is used to close the mucosal defect (4.0 chromic) (Fig. 43.10.) If the saccular base cannot be clearly identified, then a clamp may be placed at the base of the laryngocele, and a silk ligature placed prior to removing the specimen. 15. The wound is thorough irrigated and closed in layers, along with placement of a closed suction drain: a) Outer perichondrium to superior thyroid lamina b) Sternohyoid, omohyoid, thyrohyoid reanastamosed c) Skin closed 16. A close suction drain is placed. 17. A tracheostomy is rarely indicated, but may be performed at the end of the case if there are airway concerns.

43.6

Postoperative Care and Complications

Postoperative care includes: ■ Overnight, 23-h observation (consider pulse oximetry monitoring) ■ Pain management ■ Intravenous steroids at 8-hour intervals (Decadron, 8 mg, then 4 mg) ■ Elevation of the head of bed ■ Diet can be advanced as tolerated. Complications can include: ■ Laryngeal edema or hemorrhage with respiratory compromise ■ Recurrence of the laryngocele ■ Incomplete removal of the base of the saccule can lead to recurrence. Therefore, one must enter the airway, removing a cuff of ventricular mucosa surrounding the base of the saccule if possible. ■ Damage to the internal branch of the SLN with dysphagia or aspiration ■ Elderly patients are more susceptible to the effects of sensory deficits in the larynx, and may be more likely to have dysphagia as a result of SLN injury.

Key Points ■ A laryngocele is an air-filled dilation or herniation of the saccule. Any factor that increases intralaryngeal pressure such as coughing, straining, playing wind instruments, or glass blowing can lead to development of a laryngocele. ■ Neoplasm in the ventricle or false cord should be ruled out with microlaryngoscopy in high-risk patients (tobacco/alcohol users). ■ Laryngoceles are categorized as: ■ Internal: confined to the endolarynx; usually removed endoscopically (see Chap. 25, “Endoscopic Excision of Saccular Cyst”) ■ Combined: extension of internal laryngocele into the neck through the TH membrane. These are usually removed through an external approach. ■ During dissection of the external component of a combined laryngocele, care should be taken to avoid trauma to the SLN as it enters the TH membrane posteriorly. ■ The internal dissection of the laryngocele is facilitated by removing a triangular wedge of thyroid lamina. This provides wide exposure to the paraglottic space. ■ The saccular opening into the airway is located in the anterior ventricular mucosa. The saccular opening into the airway should be included in the laryngocele resection to insure complete excision of the lesion.

Selected Bibliography 1 2

Holinger LD, Barnes DR, Smid LJ et al (1978) Laryngocele and saccular cysts. Ann Otol Laryngol Rhinol 87:675–685 Thome R, Thome DC, De La Cortina RAC (2000) Lateral thyrotomy approach on the paraglottic space for laryngocele resection. Laryngoscope 110:447–450

277

Chapter 44

Repair of Laryngeal Fracture

44.1

Fundamental and Related Chapters

Please see Chaps. 6, 10, 36, 37, and 45 for further information.

44.2

Disease Characteristics

Laryngeal fractures (Fig. 44.1) are most commonly associated with external blunt trauma, often caused by a severe or violent body trauma such as a motor vehicle accident. Laryngeal fractures can also occur from isolated or direct injuries to the larynx such as falls, gunshot or knife wounds, or traumatic emergency airway procedures (i. e., cricothyrotomy). Laryngeal fractures incorporating either the thyroid cartilage and/or the cricoid cartilage can range from minimal, (nondisplaced fractures) to severe disruption of the integrity of the larynx with avulsion of portions of the thyroid and/or cricoid cartilage. The ABC’s of emergency care must be first attended to for patients with a suspected laryngeal fracture. After the airway, circulatory, cervical spine and neurologic systems have been stabilized, the laryngeal fracture(s) can be evaluated. The mechanism of injury and patient’s initial and present airway status are extremely important historical data to obtain when evaluating a patient with a suspected laryngeal fracture.

44

A “close-line” injury can suggest laryngotracheal separation; a strangulation injury can cause delayed edema in an otherwise benign appearing clinical setting. Furthermore, specific history should be found regarding intubation indications, who performed the intubation, where the intubation was performed, why it was performed, and what was seen on initial intubation. Also, initial airway and voice quality symptoms are helpful in the assessment process. The overriding key principal to laryngeal fracture evaluation and treatment is assessment and protection of the airway, followed by assessment and preservation of voice quality and function. The former is crucial given that proper evaluation and treatment of laryngeal fractures in the acute and possibly subacute setting can prevent severe laryngeal stenosis, which is extremely difficult to treat. The key variables of assessment for a thyroid cartilage fracture are the exact location and degree of displacement of the fractures. Furthermore, laryngeal palpation should identify if the thyroid and cricoid cartilages are stable to gentle palpation. Other key variables when assessing patients with a laryngeal fracture include vocal fold mobility, tension, and length, and if there is any exposed cartilage or mucosal lacerations within the larynx. If the patient is not initially evaluated prior to intubation, then many of the endo­ laryngeal key variables mentioned above are difficult to assess until direct laryngoscopy can be performed. Essential components of a complete assessment for laryngeal fracture include: ■ Flexible laryngoscopy (if possible) to assess vocal fold mobility and airway potency ■ Fine cut CT imaging of the larynx/cervical trachea ■ Microlaryngoscopy, tracheoscopy and esophagoscopy

44.3

Surgical Indications and Contraindications

Indications include:

Fig. 44.1  Laryngeal trauma (fracture on left ala)

■ Thyroid cartilage fracture involving: ■ Displaced thyroid cartilage with airway lumen compromise and/or negative voice implications ■ Exposed intralaryngeal cartilage (anterior two thirds of cartilage) ■ Shortened or avulsed vocal fold(s) ■ Cricoid fracture ■ Displaced fracture with lumen encroachment

280

Repair of Laryngeal Fracture

Contraindications comprise: ■ Unstable vital systems (sepsis, head injury, etc.) or cervical spine injury ■ Nondisplaced thyroid cartilage fracture ■ Fracture limited to posterior third of thyroid cartilage ■ Nondisplaced cricoid fracture, no encroachment of the subglottic airway

44.4

Surgical Equipment

Surgical equipment needed includes: ■ Standard microlaryngoscopy set up and equipment (see Chap. 10) ■ Laryngeal/bronchial telescopes (0, 30, and 70°) ■ Soft tissue neck surgical instrument tray ■ Maxillofacial fracture plating system (microplates with emergency screws) ■ Internal laryngeal stent devices ■ Montgomery internal laryngeal stent (Boston Medical, Boston, Mass.) ■ Rolled Silastic sheeting ■ Aboulker stent ■ Sterile glove and surgical foam ■ T-tube stenting devices

44 44.5

Surgical Procedure

1. Initial assessment of laryngeal fracture The most important initial surgical assessment technique for patients with suspected laryngeal fracture include gentle palpation of the thyroid and cricoid cartilage. This palpation should assess the overall integrity and strength of the three-dimensional configuration of the thyroid and cricoid cartilage. This assessment is crucial for decision making regarding the need for internal laryngeal stenting of the larynx. Microlaryngoscopy and bronchoscopy are also essential features of the initial assessment. This assessment should include any mucosal injury, specifically avulsion injuries, looking for exposed thyroid and cricoid cartilage. In addition, the anterior commissure tendon and the arytenoid position should be carefully evaluated and documented. Finally, the overall length and tension of the vocal folds should be carefully assessed with flexible laryngoscopy and/ or direct laryngoscopy (see Chap. 10, “Principles of Phonomicrosurgery”). Tracheoscopy and esophagoscopy may also need to be considered. 2. Thyroid fracture exploration and repair a) Isolated thyroid cartilage fracture i. Secure airway with tracheotomy or endotracheal intubation. ii. Horizontal incision is placed in the closest deep rhytid to the inferior border of the thyroid cartilage or

 

through any preexisting neck wound in the laryngeal area. iii. Dissection down through the soft tissues of the neck to preserve strap muscles and expose the thyroid cartilage (strap muscles that are avulsed or dislocated should be reattached into their anatomic position as much as possible). Exploration of the thyroid cartilage fracture with minimal disruption of the surrounding tissue is then performed with the goal of reducing the fractures, if possible. With this exposure, palpation directly of the thyroid cartilage as a whole from externally can be performed to assess the three dimensional integrity of the structure, and to determine if the patient will require internal laryngeal stenting. iv. As the thyroid cartilage fractures are explored and reduced, minimal tissue should be removed from the area. This will help reduce and stabilize the fractures. v. 0 Prolene sutures or small mini-reconstruction plates can be used across the fracture to secure the reduced laryngeal fracture into a stable position (Fig. 44.2). When noncalcified thyroid ala occurs (seen commonly in younger patients), the larger diameter “emergency” screws should be employed to improve purchase to the cartilage. vi. A small drain is placed in the dependent portion of the wound and removed within 24 hours. b) Displaced thyroid fracture with internal mucosal lacerations, exposed cartilage or arytenoid displacement i. Same approach to the thyroid cartilage as described above.

Fig. 44.2  Laryngeal fracture repaired with a miniplate, inferiorly and

superiorly

 

Chapter 44

ii. If there is a preexisting laryngotomy from the pen-

etrating neck wound, then the internal laryngeal structures can be explored through this wound (it can be expanded if absolutely required). It is important to limit the size of the laryngotomy to as small as possible. iii. A midline laryngofissure can be performed if no laryngotomy is present from the injury itself. Great care must be obtained to stay in the midline protecting the right and left anterior commissure and the vocal fold attachments to the thyroid cartilage (Figs. 44.3, 44.4). iv. Exploration of mucosal injury is then performed. v. Absorbable sutures (5.0 or smaller) are used to replace avulsed or lacerated mucosal flaps to obtain as

much cartilaginous covering as possible (Fig. 44.5). Free mucosal grafts or perichondrium can be used to resurface the internal larynx. vi. External palpation of the thyroid cartilage can be used to determine the strength/support of the thyroid cartilage to determine if the patient will require internal laryngeal stenting. If laryngeal stenting is required, then a stent size should be selected or created that will allow adequate internal laryngeal stenting without placing excessive pressure on the internal laryngeal mucosa. vii. The internal laryngeal stent options in order of preference are the following: 1. Montgomery laryngeal stent (Fig. 44.6) 2. Aboulker stent

Fig. 44.4  Completed laryngofissure with exposed vertical transglottic Fig. 44.3  Planned laryngofissure incision. Note lateral extension of

laceration

incision superior to the thyroid ala

Fig. 44.5  Repaired laceration

Fig. 44.6  Placement of Montgomery internal laryngeal stent

281

282

Repair of Laryngeal Fracture

 

d) Microlaryngoscopy and telescopic examination of the

larynx and upper trachea should then be performed to evaluate the structural integrity and mucosal integrity of the larynx. e) Mitomycin C can be applied (as need; see Chap. 29, “Subglottic/Tracheal Stenosis: Laser/Endoscopic Management”). Endoscopic replacement of the stent can be done on an as-needed basis (see Chap. 26, “Anterior Glottic Web”).

44.6

Postoperative Care and Complications

Postoperative care comprises: ■ ■ ■ ■ Fig. 44.7  External fixation of Montgomery stent

44

3. Rolled Silastic sheeting 4. Sterile glove finger packed with foam viii. Suture or miniplates can be used to repair the laryngofissure/fracture sites at the laryngotomy. ix. After the stent has been placed, supporting sutures that go through the stent should be drawn out through the thyroid cartilage and to the outside of the neck and secured over buttons to hold the internal laryngeal stent in place (Fig. 44.7). 3. Cricoid fracture exploration and repair a) Same exposure as described above b) Exposure and reduction of the cricoid fracture(s) c) After reduction of the cricoid fracture(s), cricoid ring stability should be assessed with external palpation. d) Suture or miniplate fracture repair can then be performed (with 0 Prolene), after the reduction and repair of the cricoid fracture. The internal stability of cricoid ring should be once again assessed with external palpation. e) If the cricoid ring is unstable, then placement of an internal stent endoscopically or through an injury-induced laryngofissure can be performed. The best and preferred laryngeal stent options are listed above. 4. Internal laryngeal stent removal (Two-three weeks post-operatively) a) General anesthesia is induced via the preexisting tracheotomy. b) Direct laryngoscopy is performed to visualize the internal laryngeal stent. c) A large cup forceps is used to grasp the stent and then the securing sutures of the stent can be released from the neck and the stent removed.

Tracheotomy care and education (as needed) Intravenous antibiotics for 24 hours Removal of drain within 24 hours Maintain internal laryngeal stent for approximately 14–30 days ■ Microlaryngoscopy/bronchoscopy and stent removal (see above) Complications can include: ■ Laryngeal infection ■ Stent migration (superior–inferior dimension) ■ Stenotic laryngeal airway (anterior–posterior dimension and/or lateral dimension) ■ Anterior commissure blunting/webbing ■ Granuloma formation

Key Points ■ All evaluation and treatment of laryngeal fractures should focus on: ■ Airway lumen protection ■ Voice quality and function ■ Mucosal coverage is crucial for obtaining the best possible results after laryngeal fracture and injury. ■ Internal laryngeal stenting should be performed if the lumen integrity of the laryngeal airway is compromised due to laryngeal fractures.

Selected Bibliography 1

Thor A, Linder A (2007) Repair of a laryngeal fracture using miniplates. Int J Oral Maxillofac Surg 36:748–750

Chapter 45

Glottic and Subglottic Stenosis: Laryngotracheal Reconstruction with Grafting

45.1

Fundamental and Related Chapters

Please see Chaps. 6, 29, 46, and 47 for further information.

45.2

Disease Characteristics and Differential Diagnosis

Subglottic stenosis is a narrowing of the subglottic airway, seen as both a congenital and an acquired lesion. The subglottis is the narrowest section of the airway, and it is contained entirely within a nonflexible cartilaginous ring. In contrast, the trachea has C-shaped cartilage anteriorly with an intervening posterior membranous section. Narrowing in this segment of the airway is termed tracheal stenosis. Subglottic stenosis may be caused by a multitude of factors, depending on the age of occurrence and the presence of inciting factors. Congenital stenosis is caused by a failure of recanalization of the laryngeal lumen during embryogenesis. This type of stenosis is divided into membranous or cartilaginous types. The membranous type is marked by circumferential fibrous tissue, sometimes extending upwards to include the true vocal folds. The cartilaginous type is comprised of a sheet of cartilage extending posteriorly from the inner surface of the anterior cricoid ring, with a small posterior airway. Acquired subglottic stenosis accounts for 95% of cases subglottic stenosis, of which 90% is intubation related. Subglottic stenosis after prolonged or repeated intubations occurs in 3–8% of children and adults. While intubation is the leading cause of stenosis, other potential internal and external disease processes may lead to the development of stenosis. A more comprehensive list of these etiologies is included in Chap. 6, “Glottic and Subglottic Stenosis: Evaluation and Surgical Planning.” Although endoscopic methods are often employed in the treatment of subglottic and tracheal stenosis, there are clearly cases where these methods will fail. In these instances, external techniques such as laryngotracheal reconstruction with grafting (described in this chapter) or cricotracheal/tracheal resection with primary anastomosis (Chaps. 46, “Glottic and Subglottic Stenosis: Cricotracheal Resection with Primary Anastomosis” and 47, “Tracheal Stenosis: Tracheal Resection with Primary Anastomosis”) are commonly used.

45.3

45

Surgical Indications and Contraindications

Indications include: ■ Failed endoscopic treatment of laryngotracheal stenosis ■ Cartilage collapse/tracheomalacia with obstruction ■ Laryngotracheal stenosis> 2–3 cm in length Contraindications (relative) comprise: ■ Diabetes ■ Steroid dependency (especially in autoimmune patients) ■ Moderate–severe lung disease (COPD/restrictive disease) ■ Moderate–severe heart disease ■ Obstructive sleep apnea ■ Renal failure ■ Untreated autoimmune disease (e. g., Wegener’s granulomatosis) ■ Untreated LPR

45.4

Surgical Equipment

Equipment needed for surgery includes: ■ ■ ■ ■ ■ ■ ■ ■

Standard neck dissection tray Cottle and freer elevators Drill with cutting burr (optional) Nonabsorbable, monofilament suture with taper needle (such as Prolene or nylon) Malleable retractors Montgomery laryngeal stent of appropriate size (Boston Medical, Boston, Mass.) Sterile buttons and 0 or 2-0 permanent suture to secure stent Tracheotomy tube of appropriate size

284

Laryngotracheal Reconstruction

45.5

Surgical Procedure

1. The airway is obtained preferably by endotracheal intubation

using a small-bore tube (4.0 ETT).

2. The neck and chest are prepped and draped. 3. A 5- to 6-cm horizontal incision is made over the seventh or

eighth rib as indicated (Fig. 45.1). a) Both of these ribs have adequate bulk for fashioning grafts. In addition, they are located in a region where the diaphragm is thicker, so there is less risk of pneumothorax. Dissection should be carried out until an appropri-

 

ately sized cartilage piece is exposed. In this region, the surgeon will encounter fibers from the rectus abdominus muscle, which must be dissected off the rib to expose the cartilage. Care should be taken to preserve the overlying perichondrium. The perichondrium is then incised along the superior, inferior, and lateral borders of the proposed graft. 4. Using a cottle or Freer elevator, the perichondrium is elevated along the periphery of the proposed graft (Fig. 45.2). a) Elevation should continue around the undersurface of the rib, until the rib is freed circumferentially. It is crucial in this dissection to remain in the subperichondrial plane to avoid injury to the nerves and vessels running on the inferior surface of the rib and to avoid pneumothorax. 5. Malleable retractors are placed below the exposed rib to protect the underlying pleura. a) Using a no. 10 blade, the rib graft is incised laterally and medially to free it from the rest of the rib (Fig. 45.3). The inner perichondrium should remain intact deep to

45

Fig. 45.1  Diagram demonstrating the site of costal cartilage harvest,

typically the medial aspect of the seventh or eighth rib

Fig. 45.2  The rib is freed circumferentially, staying in a subperichon-

drial plane on the undersurface of the rib

Fig. 45.3  Malleable retractors are placed below the exposed rib to pro-

tect the underlying pleura while sharp dissection is used to free the rib graft

Fig. 45.4  The inner perichondrium should remain intact deep to the

rib, after graft removal

 

Chapter 45

the rib, after graft removal (Fig. 45.4). The graft is then soaked in a saline solution. 6. The wound is closed in layers over a suction drain. 7. An incision is made in the skin of the neck horizontally overlying the cricoid and trachea. a) If there is a previous tracheostomy, then one should incorporate the superior aspect of tracheostoma into the incision (Fig. 45.5). The incision should be wide enough to allow exposure of the lower portion of the thyroid cartilage and the first few tracheal rings. 8. Elevation of subplatysmal flaps is carried out, the midline raphae are divided, and the strap muscles are separated and retracted laterally to expose the laryngotracheal complex (Fig. 45.6). 9. Using a 15 blade, a midline cricoidotomy is performed and extended into the upper two to three tracheal rings (Fig. 45.7). a) The extent of the incision is dependent on the length of stenosis. The cricothyroid membrane is divided horizontally to facilitate retraction of the cricoid segments laterally. Using this method, the entire length of stenosis is exposed, with extension of the incision above and below the stenotic site as well. The superior aspect of the incision may be extended into the inferior thyroid cartilage as depicted in Fig. 45.7. If not already present, a tracheostomy is then performed two or more rings below the inferior-most incision through the affected airway (Fig. 45.8). Ideally, the tracheostomy site is separate from the stented region, but this is not always possible. Having a tracheostomy site adjacent to the rib graft can lead to graft infection, granulation tissue formation, and restenosis.

10. The previously harvested costal cartilage graft is now pre-

Fig. 45.5  A horizontal incision is made at approximately the second

Fig. 45.6  Exposure of the laryngotracheal complex and proposed

tracheal ring

pared. a) The cartilage is modified to the appropriate size and shape using a scalpel and/or drill with cutting bur. The ideal shape is either a modified boat shape or hexagon (Fig. 45.9). The beveled design prevents the graft from falling into the airway. Care should be taken to preserve the perichondrium; since this will serve as the internal lining of the reconstructed airway and a scaffold for epithelialization. 11. A Montgomery stent (appropriate for size/gender) is placed in the wound to help keep the lumen patent (Fig. 45.10). 12. The graft is inserted such that the perichondrium is oriented toward the lumen, and the graft is sutured into place. a) Suture material is typically non-absorbable and monofilament (3-0 or 4-0 Vicryl). Sutures should be placed submucosally to reduce the incidence of granulation tissue formation. The sutures are not tied until the graft placement and position are confirmed (Fig. 45.11). The perichondrial surface of the graft should sit flush with the edges of the cricoidotomy. 13. The Montgomery stent is secured in place by passing two permanent sutures (0 or 2-0 Prolene) through the skin on one side, piercing the stent, and coming out on the skin of the opposite side. a) These two suture ends are then tied over a button on the skin, taking care not to tie the ends too tightly, allowing for some postoperative edema (Fig. 45.12).

midline incision through the stenotic region

285

286

Laryngotracheal Reconstruction

 

Fig. 45.7  The stenotic region

has been exposed prior to graft placement

Fig. 45.8  Location of tracheostomy. This should be separate from the

graft site to lessen the chance of infection

45

Fig. 45.9  Proposed configuration of the costal cartilage graft after

shaping. The perichondrium should be left intact at the diamond shaped portion of the graft

Fig. 45.10  Montgomery stent is placed prior to suturing the graft

 

Chapter 45

Fig. 45.11  Securing of the graft with multiple sutures extraluminally

45.6

Postoperative Care and Complications

Postoperative care involves: ■ Broad-spectrum antibiotics (first-generation cephalosporin, possibly clindamycin for coverage of anaerobes) ■ A nasogastric tube is often placed during the initial postoperative period. This permits suctioning of the gastric contents to diminish the possibility of nausea and vomiting that put the surgical site at risk. It later serves as a vehicle for feeding. ■ Acid-suppression medication (PPIs) ■ Routine tracheostomy care ■ Pain management ■ Return to OR in 3–4 weeks for stent removal endoscopically Complications can include: ■ ■ ■ ■

Voice alteration Pneumothorax or pneumomediastinum Loss of airway Graft failure

Voice alterations can occur if a laryngofissure is performed as a part of the surgery. Even small displacements of the anterior cartilage can disrupt voice quality. Pulmonary complications

Fig. 45.12  The stent is stabilized with percutaneous sutures tied over

buttons

are also seen, including pneumothorax, pneumomediastinum, emphysema, and chest or neck wound infections. Infection is also of concern, particularly in its role in the development of a laryngocutaneous fistula. The most feared complication after any such surgery is loss of control of the airway. Emergent airway compromise may develop, in a patient with a tracheotomy by plugging or accidental decannulation. Finally, failure of the reconstruction with the need for a revision surgery is always a possibility of which patients and their families must be aware. The most common complication is failure to correct the stenosis. This is attributable to several aspects of the initial surgery, including inappropriate choice of graft or stent, inappropriate stent length, insufficient duration of stenting, inadequate endoscopic follow-up, slipped stent, persistent LPR or keloid formation.

Key Points ■ Laryngotracheal reconstruction with costal cartilage rib graft is indicated in the following cases: ■ Failed endoscopic treatment of laryngotracheal stenosis ■ Cartilage collapse /tracheomalacia with airway obstruction ■ Laryngotracheal stenosis > 2–3 cm in length

287

288

Laryngotracheal Reconstruction

■ Patients with significant co-morbid medical conditions are generally poor candidates for open laryngotracheal treatment of airway stenosis. This is due to a high failure rate and tendency toward restenosis, as well as higher morbidity/mortality. ■ Costal cartilage is an ideal graft material for laryngotracheal reconstruction. ■ The ideal shape for the costal cartilage graft is a modified boat shape or hexagon. The beveled design prevents the graft from falling into the airway. The preserved perichondrium on the graft serves as the internal lining of the reconstructed airway and a scaffold for epithelia­ lization. ■ A Montgomery stent is used to maintain the airway lumen during the healing process, and is removed endoscopically 3–4 weeks later in the operating room.

45

 

Selected Bibliography 1

2 3

4

5 6

Pena J, Cicero R, Marin J, Ramirez M, Cruz S, Navarro F (2001) Laryngotracheal reconstruction in subglottic stenosis: an ancient problem still present. Otolaryngol Head Neck Surg 125:397–400 Cotton RT (2000) Management of subglottic stenosis. Otolaryngol Clin N Am 33:111–130 Gray S, Miller R, Myer CM, Cotton RT (1987) Adjunctive measures for successful laryngotracheal reconstruction. Ann Otol Rhinol Laryngol 96:509–513 Little FB, Koufman JA, Kohut RI, Marshall RB (1985) Effect of gastric acid on the pathogenesis of subglottic stenosis. Ann Otol Rhinol Laryngol 94:516–519 Simoni P, Wiatrak BJ. Microbiology of stents in laryngotracheal reconstruction. Laryngoscope 114:364–367 Zalzal GH, Cotton RT (1986) A new way of carving cartilage grafts to avoid prolapse into the tracheal lumen when used in subglottic reconstruction. Laryngoscope 96(Pt. 1):1039

Chapter 46

Glottic and Subglottic Stenosis: Cricotracheal Resection with Primary Anastomosis

46.1

Fundamental and Related Chapters

46

reserve, prior radiation to the larynx or trachea and patients taking immunosuppressive agents, i. e., high-dose steroids.

Please see Chaps. 6, 29, 45, and 47 for further information.

46.4 46.2

Diagnostic Characteristics for Open Treatment of Subglottic Stenosis

Numerous surgical procedures have been described to improve airway function in patients with benign acquired subglottic/tracheal stenosis, and the reported outcomes of these techniques vary, with no consensus on the optimal treatment. In patients with cricotracheal stenosis, a one-stage procedure that includes circumferential resection of the subglottis and tracheal region with primary thyrotracheal anastomosis has resulted in excellent outcomes. As outlined in Chaps. 6, “Glottic and Subglottic Stenosis: Evaluation and Surgical Planning” and 29, “Subglottic/Tracheal Stenosis: Laser/Endoscopic Management,” endoscopic treatments are often used as a first-line treatment of glottic and subglottic stenosis. In cases where this approach fails, or conditions in which endoscopic treatment is not possible (e. g., cartilaginous collapse of the airway), open treatment with either laryngotracheal reconstruction (Chap. 45, “Glottic and Subglottic Stenosis: Laryngotracheal Reconstruction with Grafting”) or cricotracheal resection with primary anastomosis is indicated.

46.3

Surgical Indications and Contraindications

Equipment needed for this procedure includes: ■ ■ ■ ■ ■ ■

Relative contraindications can comprise associated comorbidities including severe vascular dysfunction, poor pulmonary

Standard head and neck surgery set Kerrison rongeurs Drill with 3-mm cutting burr T-tube (sizes 11–14, Hood) 2 endotracheal tubes 35 gauge wire, 4-0 Vicryl

46.5

Surgical Procedure

1. The airway is generally secured with endotracheal intuba-

2. 3.

4.

The primary indication for the procedure is laryngotracheal stenosis contained within the cervical region, which fails endoscopic management. Contraindications include: ■ Stenosis at the glottic level (within 5 mm of free edge of the vocal folds) ■ “Active” autoimmune or inflammatory process (e. g. Wegener’s granulomatosis) ■ Stenosis that includes > 6.5 cm of the trachea

Surgical Equipment

5.

tion using a small-caliber endotracheal tube (ETT), such as a 4.0 microlaryngeal tube (MLT). If this is not possible, then an ETT can be placed though a tracheostomy during the resection portion of the case, and replaced by a oral endotracheal tube just prior to the re-anastomosis. Under general anesthesia, the patient is placed in a supine position, and a shoulder roll is placed to extend the neck. A standard, low-collar incision is utilized and the flaps are developed in the subplatysmal plane, exposing the airway from the hyoid bone superiorly to the manubrium inferiorly (Fig. 46.1). The strap muscles are then retracted and the thyroid isthmus divided in the midline. The distal end of the stenosis is then identified, and the trachea is circumferentially mobilized to the inferior border of the cricoid cartilage (Fig. 46.2). Blunt dissection is used along the anterior wall of the trachea to the level of the aortic arch/carina, which then permits further mobilization of the trachea and a reduction of tension on the anastomosis. To maintain the vascular supply to the trachea, minimum lateral dissection is performed. The cricothyroid muscle is then identified and reflected superiorly. The perichondrium on the upper and lower border of the cricoid cartilage is then incised, and the anterior segment is excised (Fig. 46.3). Dissection then continues on the inner aspect of the cricoid cartilage to protect the recurrent laryngeal nerves, which are located posteriorly and inferiorly. A Kerrison rongeur is used to excise further

290

Cricotracheal Resection

 

the thickened area of stenosis (Fig. 46.4). The dissection is within the lumen of the cricoid, preserving the outer perichondrium of the cricoid plate. The cricoid plate is thinned posteriorly using a sharp burr with preservation of 50% of the posterior aspect (Fig. 46.5). 6. The distal and proximal margins of the stenosis are identified, and the stenotic segment is resected en bloc as described in Chap. 47. When the site of stenosis extends superiorly close to the vocal folds, a laryngofissure is

Fig. 46.1  Wide exposure of the laryngotracheal complex

Fig. 46.3  Diagrammatic representation of the amount of cricoid ring

Fig. 46.2  The distal end of the stenosis is identified and the trachea is

Fig. 46.4  Further intraluminal removal of the stenotic region with a

46

circumferentially mobilized to the inferior border of the cricoid cartilage

that is excised, sparing the posterior third of the ring and protecting the recurrent laryngeal nerves (arrow)

Kerrison rongeur, sparing the outer perichondrium and underlying recurrent laryngeal nerves

 

Chapter 46

Fig. 46.5  A cutting burr is used to thin the posterior cricoid plate

Fig. 46.7  Cricotracheal anastomosis into the posterior glottic region

Fig. 46.6  Prior to cricotracheal anastomosis. Dashed lines in-

dicate the incision of posterior glottic scar (if present) and the corresponding posterior tracheal mucosa that is to be advanced into this region

Fig. 46.8  Completed cricotracheal anastomosis. Note how the trache-

al rings are completely contained within the cricoid shell

291

292

Cricotracheal Resection

performed to provide greater visualization and to permit resection closer to the vocal folds and enables the surgeon to complete the anastomosis. Posterior glottic stenosis can be treated by division of interarytenoid adhesions and advancement of posterior tracheal mucosa into the interarytenoid region (Figs. 46.6, 46.7). 7. Once proximal and distal clearance has been achieved, an anastomosis is performed approximating the proximal margin of the trachea to the immediate subglottic area, using no. 35 gauge wires posteriorly and 4-0 Vicryl laterally and anteriorly (Fig. 46.8). 8. During the completion of the anastomosis, a T-tube is inserted and placed at least 6–7 mm cephalic to the vocal folds, through a tracheostomy that is located inferior to the anastomotic site (Fig. 46.9). 9. The proximal end of the T-tube is occluded to permit ventilation distally through its horizontal arm. This can be accomplished with a bronchial block or a Fogarty catheter placed into the proximal end of the T-tube (Chap. 29, “Subglottic/Tracheal Stenosis: Laser/Endoscopic Management”). Occasionally, a no. 4 distal tracheostomy tube is used rather than a T-tube. 10. At the end of the procedure, a heavy suture is placed from the submental area to the anterior chest wall to maintain the patient’s cervical spine in a flexed position and to eliminate tension on the tracheal anastomosis, thereby minimizing the risk of dehiscence.

46

 

11. The closure includes reapproximation of the strap muscles,

the platysma, and the soft tissue in the subcutaneous plane using 4-0 Vicryl. The skin is closed in standard fashion.

46.6

Postoperative Management

Postoperative care involves the following: ■ Airway patency is maintained and the suture line protected by a soft Silastic T-tube. The T-tube must be kept capped to prevent drying of secretions and obstruction of the tube. ■ To protect the anastomosis, the chin suture is removed 4–5 days after surgery. ■ Dietary intake is initiated 48 hours postoperatively, beginning with carbonated fluids and progressed gradually as tolerated. ■ The T-tube is removed 3–6 weeks postoperatively, depending on the extent and complexity of the resection. Complications can comprise: ■ Patients with significant comorbidities (i. e., diabetes mellitus) are at an increased risk of complications, and these comorbidities should be treated and/or considered preoperatively to minimize this risk. ■ Dehiscence of the anastomotic suture line ■ Restenosis of the airway ■ Recurrent laryngeal nerve injury ■ Granulation tissue from the T-tube ■ Post-operative decrease in pitch (speech) can occur and is related to cricothyroid muscle division. ■ Dysphagia ■ A moderate number of patients develop dysphagia for up to 2 weeks postoperatively, especially when the tracheal resection exceeds 4 cm.

Key Points

Fig. 46.9  Indwelling T-tube.

Note that the proximal end of the tube extends beyond the true vocal folds into the supraglottis

■ In the authors’ experience, definitive decannulation of 92% of patients with no evidence of recurrence, and excellent airway and vocal function supports the efficacy of cricotracheal resection with primary thyrotracheal anastomosis. A successful outcome depends on the following factors: ■ Patient selection is critical and must include the consideration of the level, site, and extent of the lesion and the known patient comorbidities. ■ This procedure should be performed only in patients with mature cricotracheal stenosis in which the acute inflammatory stage has subsided. ■ A complete segmental cricotracheal resection of the stenotic tissue is essential.

 

Chapter 46

■ The addition of a laryngofissure provides excellent exposure for patients with a cricotracheal stenosis that is located close to the vocal folds. This therefore permits excision of all pathologic tissue and meticulous anastomosis of the trachea to the immediate subglottic region in close proximity to the vocal folds. Another advantage of a laryngofissure includes the accurate placement of the T-tube, which decreases the risk of postoperative complications associated with T-tube misplacement. Correct placement of the T-tube is imperative to maintain a patent airway and provide support to the anastomosis in the early postoperative period. ■ Release of the suprahyoid or infrahyoid muscles is not routinely performed, as it appears to exacerbate dysphagia postoperatively. ■ To avoid injury to the recurrent laryngeal nerves, it is imperative to perform the dissection on the inner aspect of the remaining cricoid cartilage after excision of its anterior arch. ■ In general, the use of a T-tube is superior to a tracheostomy because is provides a physiologic airway stent and is less traumatic to the airway.

Selected Bibliography 1

Ashiku SK, Kuzucu A, Grillo HC, Wright CD, Wain JC, Lo B, Mathisen DJ (2004) Idiopathic laryngotracheal stenosis: Effective definitive treatment with laryngotracheal resection. J Thorac Cardiovasc Surg 127:99–107 2 Couraud L, Brichon PY, Velly JF (1988) The surgical treatment of inflammatory and fibrous laryngotracheal stenosis. Eur J Cardiothorac Surg 2:410–415 3 Delaere PR, Blondeel PN, Hermans R, Guelinckx PJ, Feenstra L (1997) Use of a composite fascial carrier for laryngotracheal reconstruction. Laryngoscope 106:175–181 4 Gerwat J, Bryce DP (1974) The management of subglottic laryngotracheal stenosis by resection and direct anastomosis. Laryngoscope 84:940–947 5 Grillo HC (1982) Primary reconstruction of airway after resection of subglottic laryngeal and upper tracheal stenosis. Ann Thorac Surg 33:3–18 6 Grillo HC, Mark EJ, Mathisen DJ, Wain JC (1993) Idiopathic laryngotracheal stenosis and its management. Ann Thorac Surg 56:80–87 7 Grillo HC, Mathisen DJ, Ashiku SK, Wright CD, Wain JC (2003) Successful treatment of idiopathic laryngotracheal stenosis by resection and primary anastomosis. Ann Otol Rhinol Laryngol 112:798–800 8 Maddaus MA, Toth JL, Gullane PJ, Pearson FG (1992) Subglottic tracheal resection and synchronous laryngeal reconstruction. J Thorac Cardiovasc Surg 104:1443–1450 9 Pearson FG, Cooper JD, Nelems JM, Van Nostrand AW (1975) Primary tracheal anastomosis after resection of the cricoid cartilage with preservation of recurrent laryngeal nerves. J Thorac Cardiovasc Surg 70:806–816 10 Pearson FG, Gullane PJ (1996) Subglottic resection with primary tracheal anastomosis: including synchronous laryngotracheal reconstructions. Semin Thorac Cardiovasc Surg 8:381–391

293

Chapter 47

Tracheal Stenosis: Tracheal Resection with Primary Anastomosis

47.1

Fundamental and Related Chapters

Please see Chaps. 6, 29, 45, and 46 for further information.

47.2

Background Information and Diagnosis of Tracheal Stenosis

Tracheal stenosis is a complex and difficult problem to manage. Patient health and comorbidities, degree and length of stenosis, and propensity for restenosis need to be considered when determining the best treatment option for tracheal stenosis. Most cases of benign tracheal stenosis are caused by prolonged tracheal intubation or tracheotomy. Patients will typically present with reports of exertional dyspnea or progressive shortness of breath along with a history of previous intubation(s) or tracheotomy. Diagnostic information can be obtained from CT scans to determine the length, site, and degree of tracheal involvement. This information should be used in conjunction with tracheobronchoscopy to identify the extent and length of stenosis, and the number of tracheal rings or length proximal and distal to the site of stenosis. It is also important to determine if multilevel obstruction exists. Flexible laryngoscopy should be performed to determine the status of vocal fold mobility. This allows for surgical planning to determine the manner and extent of the surgical resection.

47.3

Surgical Indications and Contraindications

Indications for tracheal resection with primary anastomosis include: ■ Symptomatic tracheal stenosis after failure of endoscopic management ■ Focal (short-segment) tracheomalacia/cartilage collapse ■ Primary tracheal neoplasm Contraindications can comprise: ■ Stenotic tracheal segment > 5 cm (without the use of additional laryngeal releasing maneuvers)

47

■ Subglottic stenosis with involvement of vocal cords (see Chaps. 45, “Glottic and Subglottic Stenosis: Laryngotracheal Reconstruction with Grafting” and 46, “Glottic and Subglottic Stenosis: Cricotracheal Resection with Primary Anastomosis” for the treatment of this condition) ■ Multiple levels of tracheal stenosis or configuration not amenable to primary anastomosis ■ Uncontrolled mucosal inflammation secondary to LPR, Wegener’s disease, or infection

47.4

Surgical Equipment

Surgical equipment needed includes: ■ Monopolar and bipolar electrocautery ■ Standard soft tissue or neck dissection tray ■ A no. 15 scalpel (occasionally no. 10 or 20 for severely scarred, calcified tracheal wall, particularly during tracheotomy under local anesthesia)

47.5

Surgical Procedure

1. Intubation a) Patients without tracheotomy are orotracheally or naso-

tracheally intubated with appropriately sized endotracheal tubes (4.0 MLT) if possible. b) Some patients with severe stenosis must be managed with bronchoscopic dilation, jet ventilation, or tracheotomy under local anesthesia until safe intubation of the distal trachea is achieved. 2. Positioning of patient Patients are placed in a supine position with shoulder roll for full neck extension. 3. Incision a) A low collar or U-shaped incision is made that extends from the anterior borders of the sternocleidomastoid muscles. b) If the stenotic segment involves the tracheotomy site, then the incision should include the tracheotomy tract and will be removed with the stenotic tracheal segment. c) Preserve the tracheotomy in patients that have an unrelated stenotic tracheal segment.

296

Tracheal Resection with Primary Anastomosis

4. Exposure of stenosis a) Subplatysmal flaps are elevated and the strap muscles are

identified. b) Strap muscles are separated in the midline and retracted laterally to expose the trachea (Fig. 47.1).

47

 

c) In patients without tracheotomy, the stenotic segment is

easily identifiable by external changes.

d) The trachea is isolated by careful sharp dissection directly

on the cartilage (Fig. 47.2). Bipolar cautery is used if necessary. The recurrent laryngeal nerves are not identified. It is not necessary to dissect the membranous trachea at this time. e) A vertical incision is then made in the midline of the stenotic segment and extended inferiorly and superiorly until normal mucosa and an acceptable lumen caliber is achieved (Fig. 47.3). f) In patients with tracheotomy site involvement, the trachea can be incised vertically through the stoma site inferiorly and superiorly until normal mucosa and tracheal caliber is identified; most of the stenotic segment in these cases, however, is at the tracheostomy site itself. 5. Excision of stenosis a) Horizontal incisions are then made superiorly and inferiorly at the margins of the stenotic segment (Fig. 47.4). b) An endotracheal tube is then used to intubate the distal trachea through the neck. c) If present, the orotracheal endotracheal tube is then withdrawn until the tip is above the proximal or superior resection line. It is not removed completely, as it is useful later in the procedure. d) The superior and inferior circumferential resection incisions are then completed. e) Dissection is then completed around the stenotic segment to be resected.

Fig. 47.1  Wide exposure of stenotic region of trachea

Fig. 47.3  Vertical incision through stenotic region to define its bound-

aries

Fig. 47.2  Dissection of stenotic segment

Fig. 47.4  Proximal and distal division of stenotic segment

 

Chapter 47

f) The posterior aspect of the stenotic segment is separated

from the esophagus using blunt and sharp dissection. This is done from the endotracheal side (Fig. 47.5). g) If the posterior trachea in uninvolved and the stenotic segment does not involve more than two or three tracheal rings, then a wedge resection, leaving the posterior tracheal wall intact can be performed. It is important to perform the dissection close to the tracheal wall to avoid injury to the recurrent laryngeal nerves. It is also important not to dissect more than 1 or 2 cm of normal trachea above and below the resected stenotic segment. This will allow for a successful the anastomotic closure and will minimize the risk for devascularization of the healthy tracheal tissue. 6. Anastomosis a) The shoulder roll is then removed to allow the neck to move to a more flexed position. This “crowds” the closure and may be saved for the last few sutures. b) The posterior membranous trachea is closed first, using 3-0 Vicryl sutures on an RB-1 needle. Submucosal sutures are placed in the posterior midline and laterally on both sides. Three sutures are all that is typically required. Sutures should be placed so that the knots will be outside of the trachea lumen both for the posterior membranous and cartilaginous closure (Fig. 47.6). c) Once all of the posterior sutures are placed, the lateral most sutures in this area are tied simultaneously by the surgeon and assistant to reduce tearing. d) The cartilaginous trachea is closed using 2-0 Prolene sutures on an SH needle (taper) in a similar fashion (Fig. 47.7). e) Additional methods for gaining extra length for a primary anastomosis include mobilization of the distal trachea from the thorax, suprahyoid laryngeal release, and infrahyoid laryngeal release. These techniques are

Fig. 47.5  Blunt dissection of posterior tracheoesophageal party wall,

with complete removal of stenotic region. Note placement of an endotracheal tube into the distal trachea

Fig. 47.6  Posterior re-anastomosis. Note tying of the knots extralu-

minally

Fig. 47.7  Completed anastomosis with additional sutures externally

spanning two tracheal rings for additional support

297

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Tracheal Resection with Primary Anastomosis

typically not required for tracheal stenosis segments less than 5 cm and are not included in this chapter. f) Prior to closing the anterior and lateral portion of the anastomosis, the distal endotracheal tube is withdrawn and the oral or nasotracheal tube is passed distally to bridge the anastomosis and eventual primary closure. g) The anastomotic closure is then leak tested by flooding the field with saline solution and deflating the cuff on the endotracheal tube while ventilating the patient. 7. Closure a) A Penrose drain is used and positioned at the anastomosis. b) The wound is then closed in three layers. The strap muscles are reapproximated, followed by platysma and dermis, and finally skin closure. c) A 2-0 Prolene suture is placed between the submentum and anterior chest wall to keep the neck in a flexed position. 8. Extubation a) Patients are extubated the following day in the operating room or monitored intensive care unit. Many surgeons prefer immediate extubation. One theoretical advantage to overnight intubation is to reduce air leak at the closure site in case of cough or need for ventilatory support.

47.6

Postoperative Care and Complications

 

Complications can comprise: ■ Wound dehiscence/infection. This is minimized by the use of perioperative antibiotics and by maintaining cervical flexion. ■ Stenosis at site of anastomotic closure ■ Tracheobronchoscopy may be used to identify and treat. Granulation tissue can be removed, and stenotic sites can be dilated.

Key Points ■ Cervical flexion is necessary to decrease anastomotic tension during the initial phases of wound healing. ■ Minimize the amount of tracheal dissection that is performed superior and inferior to the anastomotic site. This will decrease the amount of devascularization and improve healing. ■ All sutures for closure are placed with the knots extraluminally. ■ For select patients with sites of stenosis < 5 cm, tracheal resection with primary anastomosis can be performed without the need for additional laryngeal releasing maneuvers. The need for laryngeal release needs to be made intraoperatively and depends on the degree of anastomotic tension.

Postoperative management includes:

47

■ Postoperative chest radiograph to evaluate for pneumothorax and to confirm that the endotracheal tube (if present) is below the anastomosis ■ Keep neck in flexed position. ■ Voice rest for 3–5 days to minimize glottic pressure and subsequent airflow at the site of the anastomosis. ■ Empiric antibiotic coverage for 5–7 days ■ If inflammation or infection is suspected at the time of surgery, then antibiotic coverage can be determined by culture of these organisms. ■ PPIs ■ Antiemetics ■ Pain medication ■ Soft diet may begin after extubation, usually postoperative day 1. Feeding tubes are rarely required unless extensive releasing maneuvers are performed. Diet is advanced as tolerated. ■ Penrose drain removal on day 3 if no complications or evidence or air leak/crepitus. ■ Skin sutures are removed at 1 week. ■ Chin flexion suture is removed at 2 weeks.

Selected Bibliography 1

2

3

4

5

Grillo HC, Mark EJ, Mathisen DJ, Wain JC (1993) Idiopathic laryngotracheal stenosis and its management. Ann Thorac Surg 56:80–87 Grillo HC, Mathisen DJ, Ashiku SK, Wright CD, Wain JC (2003) Successful treatment of idiopathic laryngotracheal stenosis by resection and primary anastomosis. Ann Otol Rhinol Laryngol 112:798–800 Laccourreye O, Brasnu D, Cauchois R et al (1996) Tracheal resection with end-to-end anastomosis for isolated postintubation cervical trachea stenosis: long-term results. Ann Otol Rhinol Laryngol 105:944–948 Har-El G, Chaudry R, Shaha A et al (1993) Resection of tracheal stenosis with end-to-end anastomosis. Ann Otol Rhinol Laryngol 102:670–674 Merati AL, Rieder AA, Patel N, Park DL, Girod D (2005) Does successful segmental tracheal resection require releasing maneuvers? Otolaryngol Head Neck Surg 133:372–376

Chapter 48

The Gray Minithyrotomy for Vocal Fold Scar/Sulcus Vocalis

48.1

Fundamental and Related Chapters

Please see Chaps. 1, 3, 4, 8, 23, and 36 for further information.

48.2

General Considerations

The Gray minithyrotomy offers: ■ Access to physiologically important subepithelial vocal fold tissue without epithelial incision ■ The ability to carry out delicate dissection of areas of adhesion/fibrosis under excellent visualization ■ A means of introducing shorter dissecting instruments into the vocal fold mucosa that may be easier to handle than the usual microlaryngoscopic tools ■ Dissection orientation in a practical direction along the long axis of the vocal fold The Gray minithyrotomy is designed for access to subepithelial tissue planes of the membranous vocal fold. The integrity of the layered structure of the membranous vocal fold, essential for normal phonation, is compromised in sulcus vocalis, vocal fold scar, and other clinical conditions. Surgical repair is challenging because of the possibility of additional tissue injury and the technical difficulty of placing and stabilizing appropriate replacement tissue or grafts via a mucosal incision using microlaryngoscopic instrumentation. The Gray minithyrotomy requires a skin incision, and does not correct epithelial abnormalities, such as changes associated with the sulcus vergeture deformity. The procedure does not permit substantial medialization of the vibratory margin, as the implant space is limited in volume. It has also not been used to remove subepithelial lesions; its principal utility has been to divide epithelial-deep tissue adhesion and implant appropriate replacement tissue or grafts. The Gray minithyrotomy is named for Steven Gray, M.D., who, together with his colleagues, developed the operation in anticipation of the availability of bioengineered superficial lamina propria replacement material.

48.3

48

Surgical Indications and Contraindications

The patient with a loss of pliability of the mucosal cover of the vocal fold, but with normal gross vocal fold motion is an ideal candidate for this procedure. Conditions meeting these criteria include: ■ Vocal fold scar ■ Sulcus vocalis ■ Mild vocal fold bowing, especially when associated with age-related alterations in lamina propria thickness and pliability The Gray minithyrotomy is not intended to provide substantial medialization, as required to correct typical cases of glottic insufficiency related to vocal fold paralysis and vocal fold atrophy for example.

48.4

Surgical Equipment

Equipment for the Gray minithyrotomy need is: ■ Suspension microlaryngology equipment (see Chap. 10) ■ Zero degree endoscope (30 and 70° are also useful), camera, and video monitor (Chap. 10) ■ C-mount camera and video monitor ■ Standard neck surgery instrument set, including small self-retaining retractor ■ 22-g needle ■ Powered drill with 3-mm cutting burr ■ Mastoid curette ■ Tympanoplasty instrument tray, especially: ■ Duckbill and Gimmick elevators ■ Blunt probes ■ Bellucci scissors, straight and angled ■ Alligator forceps

48.5

Surgical Procedure

1. Preoperative measures and anesthesia a) Anesthesia

The procedure is performed under a general anesthetic, as the delicate and precise nature of the dissection places

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The Gray Minithyrotomy

a premium on patient immobility and optimal visualization via rigid rod-lens endoscope or surgical microscope. b) Intubation The patient should be intubated with a 5.0 (female) or 5.5 (male) cuffed endotracheal tube so as not to obstruct visualization of the membranous vocal fold from the anterior commissure to the vocal process of the arytenoid cartilage. c) Intravenous steroids d) Because the minithyrotomy usually involves dissection of the lamina propria along the entire length of the vocal fold, edema begins early and accumulates quickly, rendering the effects of surgery difficult to assess by the end of the typical case. To minimize this, 10–12 mg of intravenous Decadron is administered intravenously before the case begins.

 

2. Patient positioning and surgical exposure a) Laryngoscopy

A laryngoscope which offers exposure of the full length of the membranous vocal folds is introduced and stabilized using a Lewy-type arm on a table-mounted Mayo stand or suspended using a Boston gallows, in the same manner as if performing laryngeal phonomicrosurgery (see Chap. 10, “Principles of Phonomicrosurgery”). b) Prep and drape. The neck is prepped and draped, anticipating a 2-3cm horizontal incision overlying the thyroid cartilage. The arm of the laryngoscope suspension/stabilization device overlies the surgical field and must be draped, as inadvertent contact with it is almost inevitable during the procedure. The primary surgeon will be most comfortable working from the patient’s right if right-handed, and from the left if left-handed. Fig. 48.1  The patient is placed

under suspension laryngoscopy and a horizontal incision is made overlying the thyroid cartilage

48 Fig. 48.2  Harvest of 8- to 15-mm

strips of fat from the incisional site

 

c) Visualization The assistant introduces a 0° endoscope connected to a camera into the laryngoscope and performs a preliminary inspection to: i. Correlate the appearance of the vocal folds with that noted on preoperative stroboscopy and confirm preoperative diagnosis ii. Check laryngoscope position. The leading tip of the laryngoscope must not interfere with the anatomy of the anterior commissure. If positioned too distally, then the tip can slightly evert the vocal folds and give a false impression of the location of their vibratory margin. The video monitor must be positioned so that it may be seen by both surgeon and assistant. The video tower is best placed on the side of the patient contralateral to the surgeon, at the level of the thorax, rotated slightly cephalad. iii. Video monitoring of internal view of the anterior commissure and the vocal folds can be done throughout the procedure via microlaryngoscopy with a camera attached to the microscope or try an assistant using a zero or thirty degree telescope with a camera. 3. Extralaryngeal dissection a) Incision A 2- to 3-cm horizontal incision is centered over the prow of the thyroid cartilage at the anticipated level of the vocal folds (Fig. 48.1). b) Dissection Gentle dissection proceeds through subcutaneous tissues and fat until the strap muscles are encountered. These are divided along the midline and retracted laterally. A Kitner dissector (peanut) can be used to sweep remaining connective tissue off of the underlying thyroid cartilage. Needle tip cautery may be used cautiously for hemostasis, taking care not to excessively cauterize adjacent fat. c) Fat harvest and preparation Adequate fat for implantation may be harvested from the area of the incision and approach to the thyroid cartilage in most cases. No more than 1 to 2 ml of fat is necessary per vocal fold. Every effort should be made to minimize mechanical and thermal trauma to the graft, as this likely decreases graft survival. Ideally, the fat is harvested as strips the length of the vocal fold (8–15 mm, or area to be augmented), which are as homogenous as possible (Fig. 48.2). Fascial fibers or bands are trimmed from the grafts, and the graft is placed into saline to await implantation. 4. Making the minithyrotomy a) Perichondrial elevation The external perichondrium of the thyroid cartilage is incised in the midline and elevated superiolaterally to expose an area about 1 cm2 on each side of the prow of the cartilage. b) Needle localization of vocal fold level Using gentle pressure, a 22-g needle is passed through the anterior midline of the thyroid cartilage at the anticipat-

Chapter 48

Fig. 48.3  A 22-g needle is passed through thyroid cartilage to localize

the level of the vocal folds

Fig. 48.4  Endoscopic view of correct orientation of the 22-g needle

at the anterior commissure (at the level of the free edge of the vocal folds)

ed level of the vocal folds. Using a zero degree endoscope the assistant visualizes the needle as it enters the larynx near the anterior commissure. The needle is reinserted as necessary under endoscopic guidance to definitively establish the level of the glottis, and the surgeon marks this on the thyroid cartilage (Figs. 48.3, 48.4). As greater experience is gained with placement of the minithyrotomy, the needle localization angle can be done to simulate/ identify the optimal path of the minithyrotomy. Thus,

301

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The Gray Minithyrotomy

  Fig. 48.5  A cutting burr is used to gain

access to the subepithelial space of the vocal fold. Note the special angle of the minithyrotomy to allow longitudinal access to the vocal fold

48

Fig. 48.6  Subepithelial dissection of the vocal fold through the

minithyrotomy (endoscopic view)

instead of placing the localizing needle perpendicular to the thyroid cartilage in the midline, the needle is passed at the suspected angle and level of the anterior commissure while visual inspection is performed to provide feedback on the needle placement. c) The minithyrotomy The minithyrotomy is centered some 3–5mm off the midline at the level of the vocal fold (Fig. 48.5). A powered drill with a 3-mm cutting burr is used to create a tunnel through the thyroid cartilage. Once the “give” of penetra-

tion through the internal cartilaginous cortex is felt, the drill is promptly withdrawn. A mastoid curette may be used to finish the inside margin of the minithyrotomy to avoid a “saucerized configuration.” It is important that the minithyrotomy be oriented to the long axis of the vocal fold (and thus somewhat obliquely—not perpendicular—to the plane of the thyroid lamina) so as not to restrict the mobility of the dissecting instruments. 5. Endolaryngeal dissection a) Entering the correct tissue plane Initial entry into the subepithelium is best made gently with a blunt instrument such as a probe. The tip of the dissecting instrument should be visible endoscopically underneath the epithelium of the vocal fold. b) Subepithelial dissection A tympanoplasty set contains a variety of instruments of the right size and length for efficient dissection via the minithyrotomy. It is usually possible to do most of the dissection with blunt instrumentation of varying thickness, like a Gimmick elevator. Bellucci scissors are used in only the most severe cases of adhesion. Surgeons who do not routinely use the tympanoplasty set should note that the duckbill is usually kept quite sharp, and may easily tear the mucosa if used in a cavalier manner (Fig. 48.6). c) Creating the implant pocket The surgeon should have a good idea of the size and shape of the implant pocket preoperatively from careful study of the patient’s stroboscopic examination. The extent of defects in mucosal pliability may be very difficult to assess during surgery, when the vocal fold mucosa is not engaged in phonatory oscillation. The implant pocket should be limited as much as possible to the area of pathology. This takes considerable lightness of touch, as normal superficial lamina propria offers little resistance to dissecting instruments. It is not difficult to elevate too widely, and this creates areas into which a fat graft may migrate under phonatory forces, away from where it is needed. This is a particular problem if dissection proceeds too far laterally along the superior surface of the vocal fold.

 

Fig. 48.7  Placement of fat graft into pocket (endoscopic view)

d) Inserting the fat graft The fat graft is inserted via the minithyrotomy to lie evenly in the area to be augmented. Ideally, only one fat graft per side is used. This is a technically troublesome step, as the fat tends to bunch in the subepithelial plane and adhere to the instruments used to insert it. An alligator is useful to pull the leading edge of the graft (which lies posteriorly on the vocal fold) into place, and a blunt probe is used where necessary to push it into place (Fig. 48.7). The assistant may also use the shaft of a microlaryngoscopic instrument to smooth the medial margin of the vocal fold and help position the graft (Fig. 48.8). An alternative method of graft placement is to use the outside, plastic sheath of an angiocatheter (~ 16 gauge) the fat graft(s) can be placed into a 3rc luer lock syringe and attached to the angiocatheter sheath. The sheath is then passed through the mini thyrotomy and into the pocket previously dissected along the free edge of the vocal fold. After visual confirmation of the angiocatheter position, the fat can be gently “injected” into the vocal fold. e) Because of the edema that accumulates during dissection, it is difficult to assess the effect of the graft on vocal fold contour, but this should in no way discourage the surgeon into using less fat. Most unsatisfactory outcomes have resulted from using too little fat. 6. Closure a) The minithyrotomy may be sealed with fibrin glue or bone wax. The perichondrial flap is replaced if possible.

Chapter 48

Fig. 48.8  Assistant smoothing medial margin of the vocal fold after fat

graft implantation (endoscopic view)

The area is irrigated and checked for hemostasis. If this seems satisfactory, then the wound may be closed without a drain; if not, a rubber band drain may be placed, to be removed the next morning.

48.6

Postoperative Care and Complications

Postoperative care entails: ■ Overnight, 23-hour observation ■ Pain management ■ Intravenous steroids at 8-hour intervals (Decadron, 8 mg, then 4 mg) ■ Elevation of the head of bed ■ A week of voice rest ■ A return to clinic is scheduled 2–4 weeks after surgery. ■ Prolonged phonatory recovery times are typical (around 1 month). As this is a relatively new procedure, there are limited data on long-term (>6 months) voice results. Clearly, any improvement in voice quality post-operatively may deteriorate in certain cases after several months, and these late changes have been attributed to poor fat graft survival.

303

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The Gray Minithyrotomy

Complications can include: ■ Vocal fold epithelial perforation ■ In cases of severe scar, it is not difficult to perforate the vocal fold epithelium. Pinhole perforations do not require that the procedure be terminated. Careful fat implantation may proceed, although if the defect is enlarged, it may result in graft extrusion. Small perforations may be patched using a piece of perichondrium from the outside of the thyroid cartilage. In the presence of a large tear, the procedure is probably best abandoned, to be reattempted after healing of the defect. ■ Suboptimal results ■ Fat implantation via the Gray minithyrotomy does not restore normal voice in most cases. In part, this is because fat is not a perfect rheologic replacement for absent or altered lamina propria tissues. Alternatives and substitutes currently under development may offer superior results via this same surgical approach. Furthermore, as in all clinical applications of autologous fat, graft survival is somewhat unpredictable. This may account for some deterioration over the long term in certain cases. Finally, scar, sulcus, and similar conditions may involve more than just alterations in the superficial lamina propria, and may involve epithelial and deep tissue changes as well, neither of which the Gray minithyrotomy addresses.

48

 

Key Points ■ The Gray minithyrotomy offers access to subepithelial tissues of the vocal folds, without the need for mucosal incision. ■ Dissection and fat implantation are performed via a neck incision under endoscopic guidance, which offers advantages over microlaryngoscopic techniques. ■ The angle and approach of the minithyrotomy must allow dissection along the longitudinal axis of the vocal fold and not be perpendicular to the thyroid cartilage. ■ The Gray minithyrotomy has been especially well suited to rehabilitation of sulcus vocalis and scar, conditions associated with superficial lamina propria disturbance.

Selected Bibliography 1

2

Gray SD, Bielamowicz SA, Titze IR, Dove H, Ludlow C (1999) Experimental approaches to vocal fold alteration: Introduction to the minithyrotomy. Ann Otol Rhinol Laryngol 108:1–9 Paniello RC, Sulica L, Khosla SM, Smith ME (2008) Clinical experience with Gray’s minithyrotomy procedure. Ann Otol Rhinol Laryngol 117:437–442

Subject Index

A abductor spasmodic dysphonia  221 Abraham cannula  210, 226 acetylcholine  221 adductor spasmodic dysphonia  221, 225 adenopathy  31 Adson’s forcep  250 air trapping  54 airway – edema  235 – foreign body  236 – obstruction  235 – vocal fold injection  202 airway anatomy  38 airway management – equipment  53 airway protection  7 airway stenosis  37, 38 allergic rhinitis  46 amyloidosis  44 anastomosis  297 ANCA. see antinuclear cytoplasmic antibody angiocatheter  162 anterior commissure  133, 161 – microweb  106 anterior glottic web  113, 116, 124, 159 – endoscopic flap  160 – endoscopic keel placement  161 – keel removal  163 antinuclear cytoplasmic antibody (ANCA)  44 aryepiglottic fold  155 aryepiglotticus muscle  155 arytenoid  4 – cartilage  3, 25 – dislocation  31 – edema  262 – perichondrium  25 – prolapsed  236 arytenoid adduction  231, 235, 237, 257, 263 – suture  270 arytenoid cartilage  169, 175 – perichondritis  119 arytenoidectomy  88, 167, 170, 176 arytenopexy  231 aspiration of liquid  241 autoimmune disorder  44 autologous fat  93

B Babcock retractor  275 beclomethasone dipropionate  44 Bell’s palsy  30 Bellucci scissor  302 bilateral vocal fold paralysis (BVFP)  167 Björk flap  37 Boston gallow  300 Botox  215, 221 – injection  121 botulinum toxin (BTX)  43, 45, 221 – dilution  223 – injection approach  222 – laryngoscopic guidance  225 – percutaneous EMG-guided injektion  223 – reconstitution  223 – retrolaryngeal approach  225 – supraglottic injection  225 – translaryngeal approach  225 botulinum toxin injection – laryngeal injection  226 – topical anesthesia  226 – videomonitoring  226 Bouchayer forcep  65 breathiness  9, 12 breathy dysphonia  45 bronchiogenic carcinoma  30 bronchoscopic dilation  184 Broyles’ ligament  5 budesonide  44 BVFP. see bilateral vocal fold paralysis C calcium hydroxylapatite (Radiesse)  94, 213 candidiasis  123 carcinoma – vocal fold  191 carcinoma in situ – of the vocal fold  22 cardiopulmomary resuscitation (CPR)  22 cartilage collapse  39 cartilage graft  285 cartilaginous collapse  55 cartilaginous trachea  297 Cetacaine spray  210, 226 chemical laryngitis  44 chemodenervation  221

306

Subject Index

chondrosarcoma of the cricoid  181 christmas tree adaptor  114 chromophore  85 chronic obstructive pulmonary disease (COPD)  10 Cidofovir  130, 133, 215 CO₂ laser  67, 85, 86, 133, 136, 152, 153, 169, 192 – thermal injury  137 – vascular lesion  137 – vocal fold carcinoma  191 collagen  92, 198 conazole  44 consensus auditory-perceptual evaluation of voice (CAPEV)  13 conus elasticus  5 COPD. see chronic obstructive pulmonary disease cordotomy  101, 111, 153, 167, 202 – extension  169 corniculate  3 corticosteroid  47 Cosmoderm  92 Cosmoplast  92, 205 Cottonoid  89, 100, 137, 138, 156, 169, 246, 270 – epinephrine-soaked  236 – mitomycin c-saturated  184 Coumadin  77, 139 CPR. see cardiopulmomary resuscitation cranial neuritis  30 cricoarytenoid  7 cricoarytenoid (CA) arthritis  44 cricoarytenoid (CA) joint  4, 167 – ankylosis  175 – palpation  168 cricoarytenoid (CA) joint arthritis  32 cricoarytenoid muscle  225 cricoid – cartilage  3, 4, 264, 268, 289 cricoid fracture  279 – exploration  282 – repair  282 cricoidotomy  285 cricothyroid  7 cricothyroid joint  4 cricothyroid membrane  215, 216, 224 cricothyroid muscle  5, 263, 289 cricothyroid space  217 cricothyroid subluxation  232, 263 cricotracheal anastomosis  291 cricotracheal stenosis  289 cuneiform cartilage  3 cup forcep  70 curved alligator  106, 120, 192 Cymetra  92, 205 cyst – of left vocal fold  24 D Danazol  47 Decadron  189, 235, 236, 242, 300 deep brain stimulation  45 deep vocal fold augmentation. see vocal fold augementation

 

difficult airway exposure  56 diplophonia  141 drip catheter  211 dynamic voice assessment  19 – base of tongue  19 – larynx (global)  19 – nasopharynx  19 – vocal fold (focal)  19 dysarthria  45 dysgeusia  81 dysphagia  45, 292 dysphonia  9, 10, 30, 34, 109, 119 – breathy  241 – glottal insufficiency  29 – inhaler-related  44 – postoperative  81, 112, 235 – psychogenic  46 – spasmodic  12, 45, 221, 222 – vocal fold polyp  99 dysplasia  21 – carcinoma in situ  22 dyspnea  222 – with exertion  255 E ee-sniff maneuver  31, 33 electroglottography  18 electromyography  30 EMG – interpretation  222 – machine  222 endo-extralarnygeal suture lateralization  170 endo-extralaryngeal needle carrier  171 endolaryngeal bleeding  233 endolaryngeal dissection  302 endolarynx  47, 66, 68, 69, 103 – telescope for visualization  71 endoscopic flap  160 endotracheal intubation  182 endotracheal tube (ETT)  37, 53, 67, 69, 133, 176 – laser protected  54 epiglottis  4, 68, 69 epinephrine  66, 130, 206, 242, 254 epinephrine-soaked pledget  120, 130 epithelial hypertrophy  21 epithelium  6 essential tremor  45 essential voice tremor  223 ETT. see endotracheal tube (ETT) extra-esophageal reflux disease  175 extralaryngeal dissection  301 extrathoracic airway obstruction  40 F false vocal fold (FVF)  157 fat flap  270 fat graft  303 – harvest  147 – implantation  145 fat harvest  200

 

FEESST  274 fiber optic airway examination  39 fibrous mass – ligamentous  24 – subepithelial  24 flap elevation  124 flexible endoscope  216 flexible laryngoscope  31, 211, 223, 234, 257 flexible laryngoscopy  18, 39, 210 Fogarty catheter  188 framework surgery – monitored anesthesia  58 Freer elevator  268, 284 functional aphonia  46 functional dysphonia  46 fungal laryngitis  44 G gallows suspension device  70 gastroesophageal reflux disease (GERD)  10, 43 Gelfoam  92 GERD. see gastroesophageal reflux disease (GERD) Gimmick elevator  302 globus sensation  119 glottal – hyperfunction  9 – incompetence  198 – insufficiency  91, 142, 209, 215 glottic – enlargement procedure  51 – insufficiency  29, 33, 94, 231 – stenosis  38, 289 GORE-TEX  253 – implant  255 granuloma  172 Gray minithyrotomy  142, 143, 299 – Pinhole perforation  304 GRBAS scale  12 Guaifenesin  47 H hematoma  219 hemilarynx  275 hemostasis  73 herbal remedy  47 histamine type 2 receptor antagonist  43 hoarseness  9, 10, 12, 13 holmium:YAG (Ho:YAG) laser  86 Hopkins rod telescope  67 horizontal belly  5 human papilloma virus  133 Hunsaker Mon–Jet catheter  55 Hyalaform  93 Hyaluronic acid  92 hyperkeratosis  123 hypernasality  12 hyponasality  12 hypopharynx  226 hypophonia  45 hypothyroidism  10

Subject Index

I IA. see interarytenoid muscle iatrogenic nerve injury  29 inferior cornu  263 informed consent  51 infrahyoid strap muscle  275 injection augmentation  197 interarytenoid muscle (IA)  5 interarytenoid synchiae  176 intubation granulomas  43 J Jamison scissor  268 jet ventilation  54, 67, 171, 183 K keratosis  22 Kerrison rongeur  244, 254, 258, 259, 276, 289 Kitner  259 Kitner dissector  301 KTP laser  130 L lamina propria  6, 17, 24, 27, 63 – benign lesion  50 laryngeal – amyloidosis  44 – cancer  43 – edema  235 – electromyography (LEMG)  32, 175 – examination  19 – fracture  279 – initial assessment  280 – framework stenosis  159 – framework surgery  91, 197, 231 – function  7 – gargle  210 – inflammation  10 – injection  221 – nerve  297 – stenosis  279 – stent  281 – stent removal  282 – trauma  38, 267, 279 – vestibule  4 laryngitis  44 laryngocele  273 – combined  273 – internal  273 – recurrence  277 – termination  276 – transthyroid excision  274 laryngocutaneous fistula  287 laryngofissure  281, 287, 290 – parasagittal  269 laryngopathia premenstrualis  10 laryngopharyngeal reflux (LPR)  10, 43, 119 laryngopharyngeal reflux disease  25, 49, 75 laryngoplasty  231 – window  254

307

308

Subject Index

laryngoscope – flexible  210 – optimal position  70 – placement  81 – positioning  81 laryngoscopic guidance  223 laryngoscopy – flexible  19, 216 – placement  68 laryngospasm  7, 224 laryngotomy  281 – vertical parasagittal  268 laryngotracheal reconstruction with grafting  283 laryngotracheal stenosis  289 laryngovideostroboscopy  50 larynx – age-related change  34 – allergic disease  46 – difficult exposure  56 – extrinsic muscle  5 – innervation  6 – intrinsic muscle  4 – squamous cell carcinoma  155 – thyrohyoid approach  218 – vasculature  6 – videocart system  210 – videomonitoring  210 – visualization  17 laser – CO₂  86 – contraindication  86 – damage  88 – equipment  87 – fire  89 – indication  86 – nonspecific thermal damage  85 – safety  88 – setting  88 – smoke evacuation  88 – surgery  85 – tissue interaction  85 – type  85, 86 – vaporization  88 – wavelength  85 lateral cricoarytenoid muscle (LCA)  4 LCA. see lateral cricoarytenoid muscle Lee Silverman voice treatment (LSVT)  45 LEMG. see laryngeal electromyography (LEMG) leukoplakia  21, 43, 123 – multiple patch  124 – recurrence  126 Lichtenberger endo-extralaryngeal needle passer  162, 170 lidocaine  38, 199, 218, 242, 254, 268 – nebulization  211 Lindholm laryngoscope  156 lipoinjection  200 – liposuction fat harvest  201 – preparation of fat  201

 

liposuction  200 – cannula  201 LPR. see laryngopharyngeal reflux (LPR) lung capacity  7 M malleable retractor  284 mask ventilation  185, 187 maximal phonation time (MPT)  31, 257 Mayo stand  72, 300 medial arytenoidectomy (MA)  167, 169 medialization – depth  247 – implant extrusion  255 – postoperative care  250 – window  258 – zone  249 medialization laryngoplasty (ML)  32, 231, 263, 264 – airway obstruction  235 – complications  235 – edema  236 – GORE-TEX  253 – implant material  232 – patient selection  232 – revision surgery  237 – Silastic  241 – undercorrection  236 medical laser  85 micro-ovoid cup forcep  65, 121 microalligator  111 microalligator forcep  147 microcup forcep  65, 75, 106, 192 microcurved scissor  74 microdebrider  66, 130, 132 microelevator  65, 75 microflap  24, 73, 109, 114, 143, 146 – injury  73 – vocal fold polyp  101 microforcep  133 microlaryngeal instrumentation  64 microlaryngoscopy  41, 53, 131, 142, 143, 145 – vocal fold cancer  192 microscissor  66, 106, 111, 130 microsuture  147 microtrap-door flap  177 Midazolam  58 midmembranous vocal fold lesion  23 mitomycin C  161, 170, 176, 179, 184, 282 monitored anesthesia care  58 Montgomery stent  281, 282, 285, 286 MPT. see maximal phonation time MTD. see muscle-tension dysphonia mucosa – perforation  236 mucosal cordotomy  110, 143 mucosal flap elevation  176 mucosal wave  8, 17, 33 muscle-tension dysphonia (MTD)  45

 

N nasogastric (NG) tube  185 nasolaryngoscopy  38 neck mass  274 neodymium-coupled YAG (Nd:YAG) laser  86 neurological disorder  10 neurotoxin  221 nonlaryngeal malignancy  30 nucleus ambiguus  6 O odynophonia  119 oropharynx  211, 226 Ossoff-Pilling laryngoscope  56, 65 otolaryngology  9 oxyhemoglobin absorption band  86 oxymetazoline  210, 218, 226, 242, 254, 268 P palatal paralysis  31 papillary ectasia  135 papilloma virus infection  21 paradoxical vocal fold motion disorder (PVFMD)  46 paraffin  197 paralytic dysphonia  4 paralytic falsetto  31 paraplegia  30 Parkinson’s disease (PD)  34, 45 patient – history  9 – occupational history  11 – social history  11 – speaking voice  11 PCA. see posterior cricoarytenoid muscle Penrose drain  298 percutaneous vocal fold augmentation  215 perichondrial flap  258, 303 perichondrial inflammation  120 perichondritis of the arytenoid cartilage  119 perichondrium  233, 244, 254, 284, 301 periodicity  18 PGS. see posterior glottic stenosis (PGS) pharyngocutaneous fistula  262 phonation  7 phonatory glottal closure  231 phonomicrosurgery  49, 63 – anesthesia  67 – anterior glottic web  159 – apneic technique for anesthesia  67 – CO₂ laser  67 – cold-steel  141 – complication  75, 81 – equipment  65, 105 – informed consent  51 – laryngoscope  65 – laryngoscope placement  68 – leukoplakia of the vocal fold  123 – medical complication  82

Subject Index

– microflap approach  73 – microscope  67 – patient position  68 – physical complication  82 – polypoid corditis  113 – recurrent respiratory papilloma (RRP)  129 – sulcus vocalis  141 – surgical microscope  72 – timing  49, 77 – total voice rest  78 – vascular lesion  136 – vocal fold cyst  109 – vocal fold fibrous masses  109 – vocal fold granuloma  119 – vocal fold nodule  105 – vocal fold polyp  100 – vocal fold scar  141 – voice therapy  77 phonosurgery  49 – decision-making process  50 – elective  50 phonotrauma  25, 43, 47, 105, 113 photolysis  85 Pilling posterior-commissure laryngoscope  120 Plavix  77 pneumomediastinum  54 pneumothorax  54, 89 polypoid corditis. see also Reinke’s edema – phonomicrosurgery  113 – polypoid material removal  114 – redundant mucosa  115 – saddle-bag appearance  113 polytetrafluoroethylene (Teflon)  93 Pontocaine  210, 226 posterior commissure  133 posterior cricoarytenoid muscle (PCA)  5, 259 posterior glottic scar  179 posterior glottic stenosis (PGS)  37, 167, 175 posterior transverse cordotomy (PTC)  167, 168, 172 postviral vagal neuropathy  46 potassium–titanyl–phosphate (KTP) laser  86 PPI. see proton pump inhibitor presbylaryngis  34, 213 presbyphonia  91 primidone  45 propofol  55, 58 propranolol  45 proton pump inhibitor (PPI)  43 pseudosulcus  43 pulmonary function  40 pulsed-KTP laser  138 pulsed dye laser (PDL)  86, 138 – therapy  136 pyriform mucosa  259, 262 Q quadrangular membrane  5

309

310

Subject Index

R RA. see rheumatoid arthritis Radiesse Voice Gel  93 raspiness  9 re-anastomosis  297 rectus abdominus muscle  284 recurrent respiratory papilloma (RRP)  21, 82, 129 – Cidofovir laryngeal injection  133 – glottis  132 – laser surgery  131 – microdebrider removal  132 – microflap removal  130 – microforcep removal  131 – phonomicrosurgery  129 – posterior commissure  133 – supraglottis  132 – telescopic surgery  132 reflux symptom index (RSI)  10 Reinke’s edema  25, 43 Reinke’s space  6, 95, 115 residual arytenoid overhang  170 Restylane  93 rheumatoid arthritis (RA)  44 rheumatological disorder  26 rough voice  9 RRP. see recurrent respiratory papilloma (RRP) RSI. see reflux symptom index S saccular cyst – endoscopic excision  155 – recurrence  157 saline-infusion trial  205, 206 scant gelatinous-appearing material  111 sevoflurane  54 Sewell retractor  260 sickle knife  66, 73, 124, 130 Silastic  253 – block  241, 246 – catheter  211 – medialization  271 – medialization laryngoplasty  241 – T-tube  292 silent cough  78 silicone  197 silk tape  71 singing voice  12 singing voice therapy  78 sinonasal allergic disease  49 SLE. see systemic lupus erythematosus Sliding Jackson laryngoscope  57 SLN. see superior laryngeal nerve sound production  7 spasmodic dysphonia (SD)  45, 222 speech–language pathologist  78, 138 speech–language pathology  142 spider telangiectasia  135 squamous cell carcinoma of the glottis  191 stenosis – congenital  283

 

– excision  296 – rigid dilation  184 – subglottic  181, 283 – tracheal  181 sternocleidomastoid muscle  295 steroid inhaler  44 strain  12 stroboscopy  17, 18, 105 – after phonomicrosurgery  78 – preoperative  63 strobovideolaryngoscopy  135 subepithelial dissection  302 subglottic jet ventilation tube  54 subglottic stenosis  38, 54, 55, 181, 283, 289 subplatysmal flap  242, 254, 275, 285, 296 sulcus vocalis  27, 91, 231, 299 – excision with reapproximation  143 – phonomicrosurgery  141 – vocal fold slicing technique  143 superficial vocal fold injection  205 superior laryngeal nerve (SLN)  6 supraglottis stenosis  159 Surgifoam  92 suspension laryngoscope  114, 176 suspension laryngoscopy  136, 171, 185 suspension microlaryngoscopy  199 suture lateralization  178, 179 systemic lupus erythematosus (SLE)  44 T T-tube  187, 292 – Hood package  189 – occlusion  189 – placement  185 – stenting  185, 189 T-tube stent  42 T-tube stenting  41 TA. see thyroarytenoid muscle (TA) Teflon  93, 197 – granuloma  151, 267 – injection  151, 267 – mass – laser ablation  152 Teflon injection  32 testosterone  47 thalamotomy  45 throat clearing  78 throat pain  81 thyroarytenoid muscle (TA)  5, 135 thyrohyoid membrane  155, 273 thyroid – artery  6 – notch  3 thyroid ala  217, 233, 237, 250 thyroid cartilage  3, 4, 155, 160, 161, 242, 243, 250, 263, 275, 301 – fracture  279, 280 thyroid fracture – exploration  280 – repair  280

 

thyroid lamina  268 thyroid mass  31 thyroplasty  3 – GORE-TEX ribbon  253 – type I  231 – window  6 thyrotracheal anastomosis  289 total arytenoidectomy  170, 172 total voice rest  78 tracheal – intubation  295 – stenosis  295 – stoma  39 tracheal airway narrowing  182 tracheal stenosis  38, 54, 55, 181, 283 – intrathoracic  55 tracheal stoma  38 tracheobronchoscopy  41, 298 tracheomalacia  39, 40, 181 tracheostomy  37, 55, 185, 285 – placement  38 – T-tube placement  185 – tube  54, 182 tracheotomy  21, 129, 167, 175, 176, 295, 296 Tramadol  47 trans cricothyroid membrane – placement of injection needle  217 transnasal esophagoscope  86 transthyroid cartilage  215 – placement of injection needle  217 triangular forcep  65, 111, 192 tympanoplasty  299, 302 U unilateral vocal fold paralysis (UVFP)  29, 91, 241 – imaging study  32 – screening laboratory test  32 – treatment  32, 33 upper airway stenosis  183 upper respiratory infection (URI)  9 URI. see upper respiratory infection UVFP. see unilateral vocal fold paralysis V vagus nerve  29 – herpes simplex infection  30 Valsalva maneuver  236, 262 vascular knife  136 velcro strap  71 ventricular mucosa  250, 255 vertical belly  5 VFP. see vocal fold paralysis – treatment  32 VHI. see voice handicap index video examination  19 videolaryngoscopy  199 videostroboscopy  29, 109, 199 – leukoplakia  123 – VFP  31 – vocal fold paresis  33

Subject Index

visual analogue scale  12 visualization – stroboscopic  17 vocal – fatigue  9, 13, 33, 241 – hygiene  47 – ligament  6, 110 – pathology  9 – professional  11 – testing  12 – tickle  13 – tremor  45 vocal fold  6 – amplitude  18 – atrophy  142, 213 – augmentation  91, 92, 142, 198 – microlaryngoscopy  199 – bamboo lesion  26 – bilateral paralysis (BVFP)  167 – bowing  34, 253 – carcinoma  22, 191 – cookie cutter defect  107 – cyst  23, 74 – phonomicrosurgery  109 – recurrence  112 – edema  237 – endoscopic injection  199 – epithelial perforation  304 – ETT trauma  173 – fat graft reconstruction  145 – fibrous mass  74 – phonomicrosurgery  109 – granuloma  25, 43, 223 – phonomicrosurgery  119 – hemorrhage  47 – immobility  30, 31 – injection  197, 211 – material  92, 197 – keratosis  21 – phonomicrosurgery  123 – knot tying  147 – leukoplakia  21 – phonomicrosurgery  123 – lipoinjection  94, 198, 200, 201 – medialization  231 – midmembranous lesion  23 – mobility testing  39 – mucosa  6 – nodule  23 – phonomicrosurgery  105 – surgery  105 – overmedialization  237 – papillary ectasia  135 – paralysis  29, 211, 232, 241, 257, 263 – paresis  11, 31, 33, 213 – pathologic condition  21 – pathology  72, 73, 82 – percutaneous augmentation  216 – peroral augmentation – in the clinic setting  215

311

312

Subject Index

– – – – –

– – – – – – – – – – – – – – – –

phonotrauma  22 pinching  147 placement of sutures  146 pliability  18 polyp  24 – microflap approach  100 – phonomicrosurgery  99 – truncation  101 – truncation approach  100 prevention of scar formation  82 reactive lesion  25 scar  27, 159, 205, 299 – phonomicrosurgery  141 scarring  116, 139 spider telangiectasia  136 stiffness after phonomicrosurgery  78 subepithelial space  63 superficial injection  205 swelling  219 transoral augmentation  209 trauma  10 true hemangioma  135 undermedialization  250 vascular lesion  26 – phonomicrosurgery  135 vibration  17 vibration symmetry  18

 

vocalis muscle  5 voice – aesthenic  12 – alteration  287 – disorder  43 – evaluation  17 – quality  49 – rest  107, 138 – vocal fold polyp  103 – therapy  23, 33, 50 – preoperative  49, 63 – prior to phonomicrosurgery  77 – speech–language pathologist  47 – tremor  221, 223 – unloading  30 voice handicap index (VHI)  12 W Wegener’s granulomatosis  44 Woodson elevator  244, 254, 268 Y YAG laser  86 Z Zyplast  92, 205