Otologic Surgery E-Book
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Otologic Surgery E-Book

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1438 pages
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Description

Otologic Surgery—the third edition of this invaluable surgical reference—has been thoroughly updated to reflect the latest advances in the field and covers all aspects of surgery of the ear and skull base. Derald E. Brackmann, MD, Clough Shelton, MD, and Moises A. Arriaga, MD bring you seven new chapters on the hot topics of Cartilage Tympanoplasty, Reversible Canal Wall Down Mastiodectomy, Superior Semicircular Canal Dehiscence Syndrome, Endoscopic Skull Base Surgery, Far Lateral Transcondylar Approach, Stereotactic Radiation Therapy, and Vascular Considerations in Neurotology. These extensive updates, along with the inclusion of new contributors and the elimination of redundant chapters, ensure that this book provides you with the essential information you need to choose and perform state-of-the-art surgical techniques. The companion web site at expertconsult.com features the fully searchable text, as well as a video library and question and answer section.
  • Discusses controversies and alternate approaches so you can make a well-informed decision from the full range of choices.
  • Presents the expertise and insights from more than 50 leading specialists to provide you with authoritative advice on surgical problems.
  • Provides detailed visual guidance on how to perform procedures through step-by-step illustrations.
  • Features the fully searchable text online at expertconsult.com, with references linked to Medline, a question and answer section ideal for board review, and a video library of procedures for convenient access and reference.
  • Includes seven new chapters—Cartilage Tympanoplasty, Reversible Canal Wall Down Mastiodectomy, Superior Semicircular Canal Dehiscence Syndrome, Endoscopic Skull Base Surgery, Far Lateral Transcondylar Approach, Stereotactic Radiation Therapy, and Vascular Considerations in Neurotology—for coverage of hot topics and the latest advances in technique.
  • Presents new contributors for 14 chapters to provide you with authoritative coverage and the dynamic perspectives of leaders in the field.
  • Streamlines the content by eliminating four redundant chapters of dated techniques so you only have the information you need.

Sujets

Ebooks
Savoirs
Medecine
Médecine
Surgical incision
Hearing
Meningitis
Cerebrospinal fluid rhinorrhoea
Surgical suture
Benignity
Rhizotomy
Dix?Hallpike test
Perforated eardrum
Office management
Superior semicircular canal
Internal auditory meatus
Perioperative
Encephalocele
Dehiscence
Neurofibromatosis type II
Atresia
Mastoiditis
Electronystagmography
Patulous Eustachian tube
Otology
Reconstructive surgery
Tympanoplasty
Otitis externa
Facial nerve paralysis
Neoplasm
Perichondrium
Craniotomy
Sensorineural hearing loss
Radiosurgery
Traumatic brain injury
Benign paroxysmal positional vertigo
Vestibular schwannoma
Electromyography
Hypereosinophilic syndrome
Labyrinthitis
Trauma (medicine)
Ear
Skin grafting
Dizziness
Stroke
Aminoglycoside
Unilateralism
Osteotomy
Hearing aid
Physician assistant
Stapedectomy
Anastomosis
Lesion
Congenital disorder
Cauterization
Trigeminal neuralgia
Tracheotomy
Otosclerosis
Facial nerve
Otitis media
Fistula
Streptomycin
Optometry
Pleasure
Atherosclerosis
Cholesteatoma
Hernia
Prosthesis
Headache
Ménière's disease
Middle ear
Bell's palsy
X-ray computed tomography
Hearing impairment
Cranial nerve
Temporomandibular joint disorder
Simplified molecular input line entry specification
Radiation therapy
Paranasal sinuses
Positron emission tomography
Paralysis
Otolaryngology
Neurologist
Neurology
Magnetism
Magnetic resonance imaging
Labyrinth
General surgery
Chemotherapy
Acoustics
Fractures
Perforation
Monitoring
Bypass
Neuraxis
Dissection
Drain
Maladie des exostoses multiples
Déglutition
Planning
Cartilage
Ablation
Fossa
Char
Vertigo
Surface
Son
Copyright
Photon

Informations

Publié par
Date de parution 26 novembre 2009
Nombre de lectures 0
EAN13 9781437719666
Langue English
Poids de l'ouvrage 10 Mo

Informations légales : prix de location à la page 0,0965€. Cette information est donnée uniquement à titre indicatif conformément à la législation en vigueur.

Exrait

OTOLOGIC SURGERY
Edition: 3

Derald E. Brackmann, MD, FACS
Clinical Professor of Otolaryngology-Head and Neck Surgery and Neurological Surgery, University of Southern California School of Medicine
President, House Ear Clinic, Board of Directors, House Ear Institute, Los Angeles, California

Clough Shelton, MD, FACS
C. Charles Hetzel Jr., MD and Alice Barker Hetzel Presidential Endowed Chair in Otolaryngology, Professor of Otology, Neuro-Otology, and Skull Base Surgery, Chief, Otolaryngology-Head and Neck Surgery, University of Utah
Medical Director, Otolaryngology-Head and Neck Surgery, Otology/Neuro-Otology Surgeon, Otolaryngology-Head and Neck Surgery, University of Utah Hospital and Clinics, Salt Lake City, Utah

Moisés A. Arriaga, MD, MBA, FACS
Clinical Professor of Otolaryngology and Neurosurgery, Director of Otology and Neurotology, Department of Otorhinolaryngology-Head and Neck Surgery, Louisiana State University Health Science Center, New Orleans
Medical Director, Hearing and Balance Center, Our Lady of the Lake Regional Medical Center, Baton Rouge, Louisiana
SAUNDERS
Copyright
1600 John F. Kennedy Blvd.
Ste 1800
Philadelphia, PA 19103-2899
OTOLOGIC SURGERY ISBN: 978-1-4160-4665-3
Copyright © 2010, 2001, 1994 by Saunders, an imprint of Elsevier Inc.
All rights reserved. No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopying, recording, or any information storage and retrieval system, without permission in writing from the publisher. Permissions may be sought directly from Elsevier's Health Sciences Rights Department in Philadelphia, PA, USA: phone: (+1) 215 239 3804, fax: (+1) 215 239 3805, e-mail: healthpermissions@elsevier.com . You may also complete your request on-line via the Elsevier homepage ( http://www.elsevier.com ), by selecting “Customer Support” and then “Obtaining Permissions”.

Notice
Knowledge and best practice in this field are constantly changing. As new research and experience broaden our knowledge, changes in practice, treatment and drug therapy may become necessary or appropriate. Readers are advised to check the most current information provided (i) on procedures featured or (ii) by the manufacturer of each product to be administered, to verify the recommended dose or formula, the method and duration of administration, and contraindications. It is the responsibility of the practitioner, relying on his or her own experience and knowledge of the patient, to make diagnoses, to determine dosages and the best treatment for each individual patient, and to take all appropriate safety precautions. To the fullest extent of the law, neither the Publisher nor the Editors assume any liability for any injury and/or damage to persons or property arising out of or related to any use of the material contained in this book.
The Publisher
Library of Congress Cataloging-in-Publication Data
Otologic surgery / [edited by] Derald E. Brackmann, Clough Shelton, Moisés A. Arriaga. — 3rd ed.
p. ; cm.
Includes bibliographical references and index.
ISBN 978-1-4160-4665-3
1. Ear—Surgery. I. Brackmann, Derald E. II. Shelton, Clough. III. Arriaga, Moises A.
[DNLM: 1. Ear—surgery. 2. Otologic Surgical Procedures. WV 200 O878 2010]
RF126.O87 2010
617.8’059—dc22 2009032119
Acquisitions Editor: Stefanie Jewell-Thomas
Developmental Editor: Rachel Yard
Project Manager: Jagannathan Varadarajan
Design Direction: Ellen Zanolle
Publishing Services Manager: Hemamalini Rajendrababu
Printed in the United States of America
Last digit is the print number: 9 8 7 6 5 4 3 2 1
Dedication
This book is dedicated to our mentors and teachers, Drs. Howard P. House, William F. House, and James L. Sheehy. Each of these outstanding physicians has special talents and characteristics that, when melded together, resulted in an outstanding clinical, research, and educational facility, The House Ear Clinic and Institute. Regrettably, Drs. Howard House and James Sheehy have passed away since the publication of the previous edition of this book.
Howard House, the founder of our institution, was among the first to concentrate his activities in the field of otology. He devoted his career to the treatment of otosclerosis. In addition to his surgical genius, Howard was recognized as an outstanding statesman and fundraiser. Without him the House Ear Institute, which has provided so many opportunities for all of us, would not exist. He died in 2003 at the age of 95. At the time of his death, he was still coming to the office regularly and was active in development work for the Institute.

William F. House joined his brother in practice after completing his residency. A creative genius, Bill recognized that the future of otology lay in the diagnosis and treatment of diseases of the inner ear. He introduced the operating microscope and microsurgical techniques to the field of neurosurgery and revolutionized the treatment of acoustic tumors and other neurotologic problems. Bill is also recognized as instrumental in bringing the cochlear implant to the state of a practical clinical device that is now widely applied. Bill is now retired from clinical practice but, at the age of 86, remains extremely creative and is currently pursuing a number of new innovations in otology and audiology.

The final link in the chain that resulted in the success of the House Ear Clinic and Institute was Dr. James L. Sheehy. His special interest was in the field of chronic otitis media. In addition to his outstanding surgical ability, Jim possessed exceptional talent in organizational ability and teaching. Jim was responsible for developing all the patient educational materials as well as serving as the editor for all of the many publications produced by members of the House Ear Clinic. His course development, panel discussions, and slide preparation techniques became standards for our specialty. Jim had been a member of the House Ear Clinic for 48 years and died in 2006.
It was our great privilege to be under the personal tutelage of each of these outstanding men. In addition to all the attributes enumerated above, first and foremost each was an outstanding physician. They practiced the art and science of surgery in the finest fashion, making it most appropriate that this book on surgical technique be dedicated to them.

Derald E. Brackmann, MD

Clough Shelton, MD

Moisés A. Arriaga, MD
In Memoriam
On October 19, 1996, the field of otology lost one of its most influential leaders of modern times. Harold Frederick Schuknecht, MD, Professor Emeritus of the Department of Otology and Laryngology at the Harvard Medical School and Chief Emeritus of the Department of Otolarynology at the Massachusetts Eye and Ear Infirmary, was a world-renowned clinical otologist, otopathologist, teacher, and scholar. His contribution to human otopathology is unparalleled. His book, Pathology of the Ear, which he solely authored, is without question the most complete and comprehensive thesis on the subject. His clinical approach and technical innovations were based on scientific principle, and he unabashedly held others to the same standard. His influence as a teacher and role model is evidenced by the unprecedented number of his students who have followed in his footsteps and have risen as leaders in our specialty. Through his life's work and through the lives of those he has touched, his influence lives on.

Harold Frederick Schuknecht
Mendell Robinson, MD, known for his eponymous stapes prosthesis, passed away on September 29, 2007. A sketch on a napkin during an air flight in 1960 led to the development of this popular and successful prosthesis. Dr. Robinson was an internationally renowned otosclerosis surgeon and had a successful otologic practice in Providence, Rhode Island, for almost 50 years. He was so appreciated that the mayor of Providence officially declared “Mendell Robinson Day” on two separate occasions. We have chosen to leave his chapter unchanged from the previous edition.

Mendell Robinson
As this edition of Otologic Surgery was going to press, we were saddened by the sudden death of our dear colleague Antonio De la Cruz. He succumbed to a malignant lymphoma after a very brief illness.
Antonio was a member of the House Ear Clinic and Institute for 34 years and director of the Institute's Department of Education. He directed hundreds of temporal bone dissection courses at the Institute and was responsible for teaching otologic surgery to thousands of physicians. His colleagues recognized him by election to the presidency of the American Academy of Otolaryngology– Head and Neck Surgery and the American Otologic Society.
Antonio participated in more national and international courses than any physician in the history of our specialty. All of us marveled at his tireless energy, which allowed him to travel at least on a monthly basis to courses around the world. In addition to his teaching activities, Antonio maintained an active otologic and neurotologic practice, benefiting many patients with his expertise. He contributed greatly in many areas, particularly in the surgical correction of congenital atresia of the external auditory canal. His techniques are described in the chapter that he contributed to this volume.
A former House Fellow wrote the following: “I am saddened to hear of Antonio's passing. He had a unique ability to encourage others to perceive the skills of the expert to be achievable by them. His humble style, though, belied a high level of skill and savvy. His focused energy, his keen intellect, and his eagerness to teach all made him a great mentor and colleague, roles that touched so many of us over the last 30+ years. I am sure many, many will miss him but will forever cherish the perspective, skills, and tips he gave so freely. His contributions will live on.”

Antonio De la Cruz
Contributors

Oliver F. Adunka, MD, Assistant Professor, Department of Otolaryngology−Head and Neck Surgery, University of North Carolina School of Medicine, Chapel Hill, North Carolina
Translabyrinthine Vestibular Neurectomy

Moisés A. Arriaga, MD, MBA, FACS, Clinical Professor of Otolaryngology and Neurosurgery, and Director of Otology and Neurotology, Department of Otorhinolaryngology−Head and Neck Surgery, Louisiana State University Health Science Center, New Orleans; , Medical Director, Hearing and Balance Center, Our Lady of the Lake Regional Medical Center, Baton Rouge, Louisiana
Malignancies of the Temporal Bone—Limited Temporal Bone Resection ; Mastoidectomy—Canal Wall Down Procedure ; Overview of Transtemporal Skull Base Surgery ; Surgery for Glomus Tumors and Other Lesions of the Jugular Foramen ; Anterior and Subtemporal Approaches to the Infratemporal Fossa

Gregory A. Ator, MD, Associate Professor, Department of Otolaryngology−Head and Neck Surgery; Director, Division of Otology/Neurotology, University of Kansas Medical Center, Kansas City, Kansas
Traumatic Facial Paralysis

James E. Benecke, Jr., MD, Clinical Professor, Otolaryngology−Head and Neck Surgery, St. Louis University School of Medicine; , Section Chief, Otolaryngology, Missouri Baptist Medical Center; Director, Otology Associates, Inc. St. Louis, Missouri
Otologic Instrumentation

Leonard P. Berenholz, MD, Trumbull Memorial Hospital, Department of Otolaryngology, Warren, Ohio
Special Problems of Otosclerosis Surgery

K. Paul Boyev, MD, Assistant Professor, Department of Otolaryngology-Head and Neck Surgery; Director, Division of Otology/Neurotology, and Director, Hearing and Balance Center, University of South Florida College of Medicine, Tampa, Florida
Cochleosacculotomy

Derald E. Brackmann, MD, FACS, Clinical Professor, Otolaryngology-Head and Neck Surgery and Neurological Surgery, University of Southern California School of Medicine; President, House Ear Clinic, and Board of Directors, House Ear Institute, Los Angeles, California
Drainage Procedures for Petrous Apex Lesions ; Surgery for Glomus Tumors and Other Lesions of the Jugular Foramen ; Middle Fossa Approach ; Auditory Implants for the Central Nervous System ; Management of Postoperative Cerebrospinal Fluid Leaks

Craig A. Buchman, MD, FACS, Professor and Chief, Division of Otology, Neurotology, and Skull Base Surgery, Department of Otolaryngology-Head and Neck Surgery, University of North Carolina School of Medicine, Chapel Hill, North Carolina
Translabyrinthine Vestibular Neurectomy

John P. Carey, MD, Associate Professor, Otolaryngology-Head and Neck Surgery, Johns Hopkins University School of Medicine; Attending, The Johns Hopkins Hospital, Baltimore, Maryland
Superior Semicircular Canal Dehiscence Syndrome

Ricardo L. Carrau, MD, Professor, Departments of Neurological Surgery and Otolaryngology, University of Pittsburgh School of Medicine; Minimally Invasive EndoNeurosurgery Center and Center for Skull Base Surgery, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania
Anterior and Subtemporal Approaches to the Infratemporal Fossa ; Endoscopic Endonasal Approaches to the Skull Base and Paranasal Sinuses

Stephen P. Cass, MD, Associate Professor, Department of Otolaryngology, University of Colorado, Denver, Colorado
Chemical Treatment of the Labyrinth

Ray C. Chang, MD, Department of Otolaryngology, University of Miami; Department of Otolaryngology, Jackson Memorial Hospital/University of Miami, Miami, Florida
Intraoperative Neurophysiologic Monitoring

Douglas A. Chen, MD, Adjunct Associate Professor of Surgery, Allegheny University of the Health Sciences; Director, Division of Neurology, Hearing and Balance Center, Allegheny General Hospital, Pittsburgh, Pennsylvania
Dural Herniation and Cerebrospinal Fluid Leak

Henry H. Chen, MD, MBA, Resident Physician, Department of Otolaryngology, University of Colorado Health Sciences Center, Denver, Colorado
Traumatic Facial Paralysis

Joseph M. Chen, MD, FRCS(C), Associate Professor, Department of Otolaryngology, University of Toronto; Staff Surgeon, Sunnybrook and Women's College Health Science Center, Toronto, Ontario, Canada
Middle Cranial Fossa—Vestibular Neurectomy ; Transotic Approach

Sarah S. Connell, MD, Neuro-otology Fellow, Department of Otolaryngology, University of Miami Ear Institute, Miami, Florida; Physician, Otolaryngology, Kaiser Permanente, Walnut Creek, California
Intraoperative Neurophysiologic Monitoring

Benjamin T. Crane, MD, PhD, Assistant Professor, Department of Otolaryngology, University of Rochester; Assistant Professor, Otolaryngology, Strong Memorial Hospital, Rochester, New York
Superior Semicircular Canal Dehiscence Syndrome

Antonio De la Cruz, MD † , Formerly Clinical Professor, Otolaryngology-Head and Neck Surgery, University of Southern California, Los Angeles, California
Congenital Malformation of the External Auditory Canal and Middle Ear ; Transcochlear Approach to Cerebellopontine Angle Lesions

Robert D. Cullen, MD, Otologic Center, Inc., and Midwest Ear Institute, Kansas City, Missouri
Surgery for Cochlear Implantation ; Translabyrinthine Approach

Calhoun D. Cunningham, III, MD, Consultant Clinical Professor of Otolaryngology−Head and Neck Surgery, Duke University School of Medicine; Vice-President of Carolina Ear and Hearing Clinic, and Co-Director of Carolina Research Institute, Raleigh, North Carolina
Ossicular Reconstruction

Shervin R. Dashti, MD, PhD, Neurosurgical Institute of Kentucky, Norton Neuroscience Institute, Louisville, Kentucky
Vascular Considerations in Neurotologic Surgery

M. Jennifer Derebery, MD, Clinical Professor of Otolaryngology, University of Southern California School of Medicine; Staff, St. Vincent's Medical Center, and Associate, House Ear Clinic, Los Angeles, California
Surgery of Ventilation and Mucosal Disease

Shaun C. Desai, MD, The George Washington University Medical Center, Washington, DC
Vascular Considerations in Neurotologic Surgery

Vivek R. Deshmukh, MD, Director, Cerebrovascular and Endovascular Neurosurgery, Department of Neurosurgery, George Washington University, Washington, DC
Vascular Considerations in Neurotologic Surgery

John L. Dornhoffer, MD, FACS, Professor and Director, Division of Neurotology, Department of Otolaryngology−Head and Neck Surgery; Professor, Department of Neurobiology and Developmental Sciences; and Medical Director, ENT Clinic and Audiology Services, University of Arkansas for Medical Sciences, Little Rock, Arkansas
Cartilage Tympanoplasty

Adrien A. Eshraghi, MD, Associate Professor, Department of Otolaryngology, University of Miami, Miller School of Medicine, Miami, Florida
Intraoperative Neurophysiologic Monitoring

Jose N. Fayad, MD, Associate Professor, Clinical Otolaryngology, University of Southern California; Associate, Otology/Neurotology, House Ear Clinic, Los Angeles, California
Otologic Instrumentation ; Tympanoplasty—Outer Surface Grafting Technique ; Auditory Implants for the Central Nervous System

Ugo Fisch, MD, Professor Emeritus of Otolaryngology, University of Zurich; Head of ENT and Skull Base Surgery, University Hospital, Zurich, Switzerland
Middle Cranial Fossa—Vestibular Neurectomy ; Transotic Approach

David R. Friedland, MD, PhD, Associate Professor and Chief, Division of Otology and Neuro-otologic Skull Base Surgery, Department of Otolaryngology and Communication Sciences, Medical College of Wisconsin; Attending Physician, Division of Pediatric Otolaryngology, Children's Hospital of Wisconsin; Attending Physician, Department of Otolaryngology-Head and Neck Surgery, Froedtert and The Medical College of Wisconsin Hospital, Milwaukee, Wisconsin
Stereotactic Radiosurgery of Skull Base Tumors

Rick A. Friedman, MD, PhD, Associate Professor, Otolaryngology, University of Southern California; Chief, Division of Skull Base Surgery, Cedars-Sinai Medical Center; Chief, Section on Hereditary Disorders, Cell and Biology Genetics Division, House Ear Clinic/House Ear Institute, Los Angeles, California
Surgery of Ventilation and Mucosal Disease ; Translabyrinthine Approach ; Extended Middle Cranial Fossa Approach

Takanori Fukushima, MD, MMSc, Consulting Professor, Department of Neurosurgery, Duke University Medical Center, Durham, North Carolina; Professor, Department of Neurosurgery, West Virigina University, Morgantown, West Virginia
Extreme Lateral Infrajugular Transcondylar Approach for Resection of Skull Base Tumors

Bruce J. Gantz, MD, FACS, Professor and Department Head, Otolaryngology-Head and Neck Surgery, University of Iowa; Professor and Department Head, Otolaryngology-Head and Neck Surgery, University of Iowa Hospitals and Clinics, Iowa City, Iowa
Canal Wall Reconstruction Tympanomastoidectomy ; Management of Bell's Palsy and Ramsay Hunt Syndrome

Gale Gardner, MD, Clinical Professor, Otolaryngology/Head and Neck Surgery, Louisiana State University Health Science Center-Shreveport; Active Staff, Otolaryngology-Head and Neck Surgery, Louisiana State University Medical Center, Shreveport, Louisiana
Tympanoplasty—Undersurface Graft Technique: Transcanal Approach

Paul A. Gardner, MD, Department of Neurological Surgery, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania
Tympanoplasty—Undersurface Graft Technique: Transcanal Approach ; Endoscopic Endonasal Approaches to the Skull Base and Paranasal Sinuses

Neil A. Giddings, MD, Sacred Heart Medical Center and Deaconess Medical Center, Spokane, Washington
Drainage Procedures for Petrous Apex Lesions

Michael E. Glasscock, III, MD, FACS, Adjunct Professor, Otolaryngology−Otology, Vanderbilt University Medical Center, Nashville, Tennessee
Tympanoplasty—Undersurface Graft Technique: Postauricular Approach

Samuel P. Gubbels, MD, Assistant Professor, Surgery, Division of Otolaryngology, University of Wisconsin–Madison, Madison, Wisconsin
Canal Wall Reconstruction Tympanomastoidectomy ; Management of Bell's Palsy and Ramsay Hunt Syndrome

Ophir Handzel, MD, LLB, Department of Otology and Laryngology, Harvard Medical School; Fellow, Otology/Neurotology, Otolaryngology, Massachusetts Eye and Ear Infirmary, Boston, Massachusetts
Diagnosis and Management of the Patulous Eustachian Tube

Steven A. Harvey, MD, Clinical Assistant Professor, Department of Otolaryngology, Medical College of Wisconsin, Milwaukee, Wisconsin
Complications of Surgery for Chronic Otitis Media

Todd A. Hillman, MD, Adjunct Clinical Faculty, Otolaryngology, Louisiana State University, New Orleans, Louisiana; , Associate, Pittsburgh Ear Associates, and Staff, Division of Neurotology, Allegheny General Hospital, Pittsburgh, Pennsylvania
Petrosal Approach

William E. Hitselberger, MD, Neurosurgery, St. Vincent's Hospital, Los Angeles, California
Auditory Implants for the Central Nervous System

Barbara Stahl Hoskins, RN, BSN, Allied Health Practitioner, Doheny Surgery, St. Vincent's Medical Center, Los Angeles; Allied Health Practitioner, Surgery, Kaiser Sunset, Hollywood; Private Scrub Nurse, Neurosurgical Department, St. Vincent's Medical Center, Los Angeles, California
Otologic Instrumentation

Howard P. House, MD † , Formerly Professor Emeritus, University of Southern California; Founder and Chairman Emeritus, House Ear Institute, St. Vincent's Medical Center, Los Angeles, California
Total Stapedectomy

John W. House, MD, Clinical Professor, Department of Otolaryngology, University of Southern California School of Medicine; President, House Ear Institute, Los Angeles, California
Translabyrinthine Approach

William F. House, MD, Formerly at Hoog Hospital, Newport Beach, California
Middle Fossa Approach

Brandon B. Isaacson, MD, Assistant Professor, Otolaryngology-Head and Neck Surgery, University of Texas Southwestern Medical Center at Dallas; Attending, Otolaryngology-Head and Neck Surgery, Zale Lipshy University Hospital, Dallas, Texas
Office Management of Tympanic Membrane Perforation and the Draining Ear

Robert K. Jackler, MD, Sewall Professor and Chair and Associate Dean (CME), Otolaryngology-Head and Neck Surgery, Stanford University School of Medicine, Stanford, California
Retrosigmoid Approach to Tumors of the Cerebellopontine Angle

C. Gary Jackson, MD, FACS, Clinical Professor, Department of Surgery, University of North Carolina School of Medicine, Chapel Hill, North Carolina
Tympanoplasty—Undersurface Graft Technique: Postauricular Approach

Ivo P. Janecka, MD, FACS, Professor, Harvard Medical School; Director, Skull Base International; Staff, Children's Hospital, Brigham and Women's Hospital, Boston, Massachusetts
Malignancies of the Temporal Bone-Radical Temporal Bone Resection

Peter J. Jannetta, MD, Professor of Neurosurgery, Department of Neurosurgery, Drexel University College of Medicine, Philadelphia; , Vice Chairman, Department of Neurosurgery, Allegheny General Hospital, Pittsburgh, Pennslyvania
Operations for Vascular Compressive Syndromes

Herman A. Jenkins, MD, Professor and Chairman, Department of Otolaryngology, University of Colorado Health Sciences Center; Chief, Otolaryngology Service, University of Colorado Hospital, Denver, Colorado
Traumatic Facial Paralysis

Amin B. Kassam, MD, FRCS(C), Associate Professor, Department of Neurological Surgery, University of Pittsburgh School of Medicine; Director, Minimally Invasive EndoNeurosurgery Center, and Co-Director, Center for Skull Base Surgery, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania
Anterior and Subtemporal Approaches to the Infratemporal Fossa ; Endoscopic Endonasal Approaches to the Skull Base and Paranasal Sinuses

David M. Kaylie, MD, Associate Professor, Department of Surgery, Division of Otolaryngology, Duke University Medical Center, Durham, North Carolina
Tympanoplasty—Undersurface Graft Technique: Postauricular Approach

Bradley W. Kesser, MD, Assistant Professor, Department of Otolaryngology-Head and Neck Surgery, University of Virginia Health System, Charlottesville, Virginia
Surgery of Ventilation and Mucosal Disease

Joe W. Kutz, MD, Assistant Professor, Otolaryngology-Head and Neck Surgery, University of Texas Southwestern Medical Center at Dallas; Attending, Otolaryngology-Head and Neck Surgery, Zale Lipshy University Hospital, Dallas, Texas
Office Management of Tympanic Membrane Perforation and the Draining Ear

Jed A. Kwartler, MD, MBA, Clinical Associate Professor, Division of Otolaryngology, University of Medicine and Dentistry of New Jersey, Newark, New Jersey
Total Stapedectomy

John P. Leonetti, MD, Otolaryngology-Head and Neck Surgery, Loyola University Medical Center, Maywood, Illinois
Malignancies of the Temporal Bone-Radical Temporal Bone Resection

Robert E. Levine, MD, Clinical Professor, Ophthalmology, University of Southern California Keck School of Medicine; Co-Founder and Co-Director, Facial Nerve Clinic, House Ear Clinic, Los Angeles, California,
Care of the Eye in Facial Paralysis

James Lin, MD, Assistant Professor, Department of Otolaryngology, Louisiana State University Health Sciences Center, New Orleans, Louisiana
Translabyrinthine Approach

William H. Lippy, MD, FACS, Chief Physician/Surgeon, Otolaryngology, The Lippy Group for Ear, Nose, and Throat; Physician, Otolaryngology, Trumbell Memorial Hospital, Warren, Ohio
Special Problems of Otosclerosis Surgery

Philip D. Littlefield, MD, Otology and Neurotology, Department of Otolaryngology, Walter Reed Army Medical Center, Washington, DC
Complications of Surgery for Chronic Otitis Media

Teresa M. Lo, MD, Department of Otolaryngology, The Southeast Permanente Medical Group, Atlanta, Georgia
Perilymphatic Fistula

Larry B. Lundy, MD, Associate Professor, Otolaryngology-Head and Neck Surgery, Mayo Clinic, Jacksonville, Florida,
Laser Revision Stapedectomy

William M. Luxford, MD, Clinical Professor, Otolaryngology, University of Southern California Keck School of Medicine; Associate, House Clinic, Los Angeles, California
Hypoglossal Facial Anastomosis ; Surgery for Cochlear Implantation

John T. McElveen, Jr., MD, Consultant Clinical Professor of Otolaryngology–Head and Neck Surgery, Duke University School of Medicine; President of Carolina Ear and Hearing Clinic, and Director of Carolina Research Institute, Raleigh, North Carolina
Ossicular Reconstruction

Michael J. McKenna, MD, Professor of Otology and Laryngology, Department of Otology and Laryngology, Harvard Medical School; Surgeon in Otolaryngology, Department of Otolaryngology, Massachusetts Eye and Ear Infirmary, Boston, Massachusetts
Cochleosacculotomy ; Transcanal Labyrinthectomy

Lloyd B. Minor, MD, Andelot Professor and Director, Department of Otolaryngology-Head and Neck Surgery, The Johns Hopkins University School of Medicine, Baltimore, Maryland
Superior Semicircular Canal Dehiscence Syndrome

Edwin M. Monsell, MD, PhD, Professor, Otolaryngology-Head and Neck Surgery, Wayne State University, Detroit, Michigan
Chemical Treatment of the Labyrinth

Joseph B. Nadol, Jr., MD, Walter Augustus Lecompte Professor and Chair, Department of Otology and Laryngology, Harvard Medical School; Chief of Otolaryngology, Department of Otolaryngology, Massachusetts Eye and Ear Infirmary, Boston, Massachusetts
Transcanal Labyrinthectomy

Julian M. Nedzelski, MD, FRCS, Professor Emeritus, Department of Otolaryngology-Head and Neck Surgery, University of Toronto; Consultant, Department of Otolaryngology-Head and Neck Surgery, Sunnybrook Health Sciences Centre, Toronto, Ontario, Canada
Chemical Treatment of the Labyrinth

J. Gail Neely, MD, FACS, Professor and Director, Otology/Neurotology/Base of Skull Surgery; Director of Research, Department of Otolaryngology-Head and Neck Surgery, Washington University School of Medicine; , Attending, Otolaryngology-Head and Neck Surgery, Barnes-Jewish Hospital and St. Louis Children's Hospital, St. Louis, Missouri
Surgery of Acute Infections and Their Complications

James L. Netterville, MD, The Mark C. Smith Professor, and Director of Head and Neck Surgery, Vanderbilt Department of Otolaryngology-Head and Neck Surgery, Vanderbilt Medical Center, Nashville, Tennessee
Rehabilitation of Lower Cranial Nerve Deficits after Neurotologic Skull Base Surgery

Steven R. Otto, MA, Chief Audiologist and Coordinator, ABI Program, Department of Auditory Implants and Perception, House Ear Institute, Los Angeles, California
Auditory Implants for the Central Nervous System

Mark D. Packer, MD, Neurotology Fellow, Otolaryngology, The Ohio State University; Lieutenant Colonel, United States Air Force, Columbus, Ohio
Surgery of the Endolymphatic Sac

Lorne S. Parnes, MD, FRCS(C), Professor, Otolaryngology and Clinical Neurological Sciences, University of Western Ontario; Site Chief, Otolaryngology, University Hospital–London Health Sciences Centre, London, Ontario, Canada
Posterior Semicircular Canal Occlusion for Benign Paroxysmal Positional Vertigo

Rodney Perkins, MD, Clinical Professor of Surgery, Stanford University, Palo Alto, California
Canalplasty for Exostoses of the External Auditory Canal and Miscellaneous Auditory Canal Problems

Brian P. Perry, MD, FACS, Clinical Associate Professor, The University of Texas, Health Science Center–San Antonio, San Antonio, Texas
Management of Bell's Palsy and Ramsay Hunt Syndrome

Thomas M. Pilkington, MD, Resident Physician, Division of Otolaryngology-Head and Neck Surgery, Department of Surgery, Duke University Medical Center, Durham, North Carolina
Extreme Lateral Infrajugular Transcondylar Approach for Resection of Skull Base Tumors

Dennis S. Poe, MD, Associate Professor, Otology and Laryngology, Harvard Medical School; Associate Surgeon, Otolaryngology, Children's Hospital, Boston, Massachusetts
Diagnosis and Management of the Patulous Eustachian Tube

Sanjay Prasad, MD, Clinical Assistant Professor, Department of Otolaryngology-Head and Neck Surgery, Georgetown University Medical Center, Washington, DC; President and Founder, Metropolitan Ear Group, Besthesda, Mayland
Malignancies of the Temporal Bone-Radical Temporal Bone Resection

Daniel M. Prevedello, MD, Department of Neurological Surgery, University of Pittsburgh School of Medicine; Minimally Invasive EndoNeurosurgery Center and Center for Skull Base Surgery, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania
Endoscopic Endonasal Approaches to the Skull Base and Paranasal Sinuses

Miriam I. Redleaf, MD, Assistant Professor, Otolaryngology, University of Chicago and University of Chicago Medical Center, Chicago, Illinois
Management of Bell's Palsy and Ramsay Hunt Syndrome

Joseph B. Roberson, Jr., MD, Stanford University Hospital, Palo Alto, and San Ramon Regional Medical Center, San Ramon, California
Canalplasty for Exostoses of the External Auditory Canal and Miscellaneous Auditory Canal Problems ; Avoidance and Management of Complications of Otosclerosis Surgery

Michael A. Roberts, MD, Comprehensive Ophthalmologist, St. Vincent's Medical Center, Los Angeles, California
Care of the Eye in Facial Paralysis

Mendell Robinson, MD † , Formerly Clinical Associate Professor, Brown University School of Medicine; Senior Surgeon, Miriam Hospital, Rhode Island Hospital, Providence, Rhode Island
Partial Stapedectomy

Grayson K. Rodgers, MD, Birmingham Hearing and Balance Center, Birmingham, Alabama
Management of Postoperative Cerebrospinal Fluid Leaks

Peter S. Roland, MD, Professor and Chairman, Otolaryngology-Head and Neck Surgery, University of Texas Southwestern Medical Center at Dallas; Chief of Service, Otolaryngology-Head and Neck Surgery, Zale Lipshy University Hospital, Dallas, Texas
Office Management of Tympanic Membrane Perforation and the Draining Ear

Christina L. Runge-Samuelson, PhD, Associate Professor and Co-Director, Koss Cochlear Implant Program, Department of Otolaryngology and Communication Sciences, Medical College of Wisconsin; Division of Pediatric Otolaryngology, Children's Hospital of Wisconsin, and Department of Otolaryngology-Head and Neck Surgery, Froedtert and The Medical College of Wisconsin Hospital, Milwaukee, Wisconsin
Stereotactic Radiosurgery of Skull Base Tumors

Leonard P. Rybak, MD, PhD, Professor of Surgery, Southern Illinois University; Memorial Medical Center and St. John's Hospital, Springfield, Illinois
Chemical Treatment of the Labyrinth

Barry M. Schaitkin, MD, Professor, Department of Otolaryngology, University of Pittsburgh School of Medicine, University of Pittsburgh Medical Center Shadyside, Pittsburgh, Pennsylvania
Facial Reanimation Techniques

Harlod F. Schuknecht, MD † , Formerly Professor and Chairman Emeritus, Department of Otology and Laryngology, Harvard Medical School; Emeritus Chief of Otolaryngology, Department of Otolaryngology, Massachusetts General Hospital, Boston, Massachusetts
Cochleosacculotomy

Raymond F. Sekula, Jr., MD, Assistant Professor Neurological Surgery, Department of Neurological Surgery, Allegheny General Hospital, Pittsburgh, Pennsylvania
Operations for Vascular Compressive Syndromes

Robert V. Shannon, PhD, Adjunct Professor, Biomedical Engineering, University of Southern California; Department Head, Auditory Implants and Perception, House Ear Institute, Los Angeles, California
Auditory Implants for the Central Nervous System

M. Coyle Shea, Jr., MD, Associate Clinical Professor, Department of Otolaryngology-Head and Neck Surgery, University of Tennessee Center for the Health Sciences; Active Staff, Baptist Memorial Hospitals; Courtesy Staff, Methodist Hospitals, Memphis, Tennessee
Tympanoplasty—Undersurface Graft Technique: Transcanal Approach

James L. Sheehy, MD † , Formerly Clinical Professor of Surgery and Otolaryngology, University of Southern California School of Medicine, Los Angeles, California
Tympanoplasty—Outer Surface Grafting Technique ; Ossicular Reconstruction ; Mastoidectomy—Intact Canal Wall Procedure ; Tympanoplasty—Staging and Use of Plastic

Clough Shelton, MD, FACS, C. Charles Hetzel, Jr., MD and Alice Barker Hetzel, Presidential Endowed Chair in Otolaryngology; , Professor, Otology, Neuro-Otology and Skull Base Surgery; , Chief, Otolaryngology-Head and Neck Surgery, University of Utah; , Medical Director, Otolaryngology-Head and Neck Surgery and Otology/Neuro-Otology Surgeon, University of Utah Hospital and Clinics, Salt Lake City, Utah
Tympanoplasty—Staging and Use of Plastic ; Laser Stapedotomy , Facial Nerve Tumors ; Middle Fossa Approach

David W. Sim, FRCS Ed (URL), Clinical Tutor, University of Edinburgh, Edinburgh, Scotland
Retrosigmoid Approach to Tumors of the Cerebellopontine Angle

George T. Singleton, MD, Professor Emeritus, Otolaryngology-Head and Neck Surgery, University of Florida College of Medicine; Otolaryngology-Head and Neck Surgery, Shands Teaching Hospital; Otolaryngology-Head and Neck Surgery, Malcolm Randall VA Medical Center, Gainesville, Florida
Perilymphatic Fistula

William H. Slattery, III, MD, Clinical Professor, University of Southern California; Director, Clinical Studies, House Ear Institute; Associate, House Ear Clinic, Los Angeles, California
Implantable Hearing Devices ; Neurofibromatosis

Carl H. Snyderman, MD, Departments of Neurological Surgery and Otolaryngology, University of Pittsburgh School of Medicine; , Minimally Invasive EndoNeurosurgery Center and Center for Skull Base Surgery, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania
Endoscopic Endonasal Approaches to the Skull Base and Paranasal Sinuses

Robert F. Spetzler, MD, Professor, Department of Surgery, Section of Neurosurgery, University of Arizona College of Medicine, Tuscon; Director and J. N. Harber Chairman of Neurological Surgery, Barrow Neurological Institute, Phoenix, Arizona
Vascular Consideration in Neurotologic Surgery

Barry Strasnick, MD, FACS, Professor and Chairman, Department of Otolaryngology-Head and Neck Surgery, Eastern Virginia Medical School, Norfolk, Virginia
Tympanoplasty—Undersurface Graft Technique: Postauricular Approach

Christopher A. Sullivan, MD, Assistant Professor, Otolaryngology-Head and Neck Surgery, Wake Forest University School of Medicine; Staff Surgeon, Otolaryngology-Head and Neck Surgery, North Carolina Baptist Hospital; Assistant Professor, Regenerative Medicine, Wake Forest Institute for Regenerative Medicine, Winston Salem, North Carolina
Rehabilitation of Lower Cranial Nerve Deficits after Neurotologic Skull Base Surgery

Mark J. Syms, MD, Neurologist, Section of Neurotology, Department of Neurosurgery, Barrow Neurological Institute, Phoenix, Arizona
Mastoidectomy—Intact Canal Wall Procedure

Charles A. Syms, III, MD, Clinical Professor, Department of Otolaryngology-Head and Neck Surgery, University of Texas Health Science Center, San Antonio; President, Ear Medical Group, San Antonio, Texas
Mastoidectomy—Intact Canal Wall Procedure

Steven A. Telian, MD, John L. Kemink Professor of Otorhinolaryngology; Director, Division of Otology, Neurology, and Skull Base Surgery; and Medical Director, Cochlear Implant Program, Department of Otolaryngology-Head and Neck Surgery, University of Michigan, Ann Arbor, Michigan
Retrolabyrinthine and Retrosigmoid Vestibular Neurectomy

Fred F. Telischi, MEE, MD, FACS, Professor, Neurological Surgery, Biomedical Engineering, and Otolaryngology, University of Miami Miller School of Medicine; Vice Chairman and Director, University of Miami Ear Institute, Miami, Florida
Intraoperative Neurophysiologic Monitoring

Karen B. Teufert, MD, House Ear Institute, Los Angeles, California
Congenital Malformation of the External Auditory Canal and Middle Ear ; Transcochlear Approach to Cerebellopontine Angle Lesions

Anders M.R. Tjellström, MD, PhD, Department of Otolaryngology, Sahlgrenska University Hospital, Gőteborg, Sweden
The Bone-Anchored Cochlea Stimulator (Baha)

Debara L. Tucci, MD, Associate Professor, Division of Otolaryngology-Head and Neck Surgery, Department of Surgery , Duke University Medical Center, Durham, North Carolina
Extreme Lateral Infrajugular Transcondylar Approach for Resection of Skull Base Tumors

P. Ashley Wackym, MD, FACS, FAAP, John C. Koss Professor and Chairman, Department of Otolaryngology and Communication Sciences, Medical College of Wisconsin; Chief, Section of Otology, Division of Pediatric Otolaryngology, Children's Hospital of Wisconsin; Chief, Department of Otolaryngology-Head and Neck Surgery, Froedtert and The Medical College of Wisconsin Hospital, Milwaukee, Wisconsin; Vice President for Research, Legacy Health System , Portland, Oregon
Spereotactic Radiosurgery of Skull Base Tumors

P. Daniel Ward, MD, MS, Resident, Department of Otolaryngology-Head and Neck Surgery, University of Michigan, Ann Arbor, Michigan
Retrolabyrinthine and Retrosigmoid Vestibular Neurectomy

Frank M. Warren, MD, Assistant Professor, Otolaryngology-Head and Neck Surgery, University of Utah, Salt Lake City, Utah
Facial Nerve Tumors

D. Bradley Welling, MD, PhD, FACS, Professor and Chair, Otolaryngology-Head and Neck Surgery, The Ohio State University, Columbus, Ohio
Surgery of the Endolymphatic Sac

Richard J. Wiet, MD, Professor of Clinical Otolaryngology and Neurosurgery, Northwestern University, and Ear Institute of Chicago, Chicago, Illinois
Complications of Surgery for Chronic Otitis Media

Eric P. Wilkinson, MD, Clinical Assistant Professor of Otolaryngology, University of Southern California Keck School of Medicine; Associate, House Clinic, Los Angeles, California
Canal Wall Reconstruction Tympanomastoidectomy ; Drainage Procedures for Petrous Apex Lesions ; Management of Postoperative Cerebrospinal Fluid Leaks ; Hypoglossal Facial Anastomosis

† Deceased
Acknowledgements
Publication of a book of this scope requires a tremendous effort on the part of many, all of whom I wish to sincerely thank.
First, my thanks to my lovely wife, Charlotte, who supports all my efforts and forgave my absence for the time devoted to this project. No less supportive are our four sons, David, Douglas, Mark, and Steven, who provide diversion and pleasure by taking me hunting and fishing.
Since the publication of the second edition, four additional grandchildren have blessed Charlotte and me. Lauren, Nicholas, Sammy, Kaylee, Daniel, and Megan provide immeasurable pleasure to us. What we have been told about the joy of grandparenting was underemphasized.
My associate editors, Dr. Shelton and Dr. Arriaga, worked tirelessly to bring this volume to fruition.
Anthony Pazos deserves special recognition. He spent countless hours in the temporal bone laboratory learning at first hand the various operations that he then illustrated. All the authors have appreciated his attention to detail and willingness to work with them until everything was “just right.”
The publishers have been extremely supportive throughout the development of this book. From the beginning, they made a major commitment to ensure that this volume would be of the highest quality. I wish to thank particularly Rachel Yard and Scott Scheidt.
Finally, I wish to thank our office staff, who work tirelessly on behalf of our patients and us. I would particularly like to thank Rita Koechowski, my surgery counselor, who not only schedules my surgery but also offers tremendous encouragement and support to all my patients. Her assistant, Patricia McGrath, has been a tremendous help to both of us in supporting our patients.
Finally, I wish to thank my surgical assistants, Matthew Layner and Nancy Aguilar, and my executive assistant, Cathy Weise. She maintains my focus and orientation on a daily basis, and her efforts are greatly appreciated.

Derald E. Brackmann, MD
I would like to thank my wife, Kay, and my children, Jordan and Bill, for their support and encouragement during my career as well as their understanding regarding the demands of my profession.
I would also like to take this opportunity to thank my teachers, friends, and former associates at the House Ear Clinic and my teachers at Stanford, all of whom gave me the skills necessary to practice otologic surgery.
Special recognition goes to the Otolaryngology faculty, residents, and alumni of the University of Utah. Their energy and enthusiasm keeps my professional life fresh and vibrant. It is very gratifying to see their success and advancement in career development.

Clough Shelton, MD
My family's patience and support in this book and all my academic projects continues to motivate and encourage me. My wife Rosemary and children (Becca, Moi, and Toby) participated in this and my other professional activities through tolerating my time away, enduring family moves, and now even offering occasional editorial suggestions on substance and form. Moisés Agusto and Leticia are a continued inspiration.
I particularly want to thank Derald Brackmann for his mentorship and stellar example of skill in otologic surgery and graceful balance of complex competing demands. The physicians and alumni of the House Ear Clinic provide an active network of otologic innovation whose concepts serve as a thread of continuity in this book.
My Louisiana State University residents and partners have provided insightful questions and suggestions that have prompted some of the changes in this edition. Additionally, they have shown that even in the terrific upheaval of post-Katrina Louisiana, calm focus on basic principles ensures quality education and superb patient care as long as we remain flexible to use all resources available.

Moisés A. Arriaga, MD, MBA, FACS
Table of Contents
Instructions for online access
Copyright
Dedication
In Memoriam
Contributors
Acknowledgements
Chapter 1: Otologic Instrumentation
Chapter 2: Canalplasty for Exostoses of the External Auditory Canal and Miscellaneous Auditory Canal Problems
Chapter 3: Malignancies of the Temporal Bone-Limited Temporal Bone Resection
Chapter 4: Malignancies of the Temporal Bone-Radical Temporal Bone Resection
Chapter 5: Congenital Malformation of the External Auditory Canal and Middle Ear
Chapter 6: Surgery of Ventilation and Mucosal Disease
Chapter 7: Diagnosis and Management of the Patulous Eustachian Tube
Chapter 8: Office Management of Tympanic Membrane Perforation and the Draining Ear
Chapter 9: Tympanoplasty-Outer Surface Grafting Technique
Chapter 10: Cartilage Tympanoplasty
Chapter 11: Tympanoplasty-Undersurface Graft Technique: Transcanal Approach
Chapter 12: Tympanoplasty-Undersurface Graft Technique: Postauricular Approach
Chapter 13: Ossicular Reconstruction
Chapter 14: Canal Wall Reconstruction Tympanomastoidectomy
Chapter 15: Surgery of Acute Infections and Their Complications
Chapter 16: Mastoidectomy-Intact Canal Wall Procedure
Chapter 17: Mastoidectomy-Canal Wall Down Procedure
Chapter 18: Tympanoplasty-Staging and Use of Plastic
Chapter 19: Complications of Surgery for Chronic Otitis Media
Chapter 20: Dural Herniation and Cerebrospinal Fluid Leaks
Chapter 21: Total Stapedectomy
Chapter 22: Laser Stapedotomy
Chapter 23: Partial Stapedectomy
Chapter 24: Laser Revision Stapedectomy
Chapter 25: Special Problems of Otosclerosis Surgery
Chapter 26: Avoidance and Management of Complications of Otosclerosis Surgery
Chapter 27: Perilymphatic Fistula
Chapter 28: Management of Bell's Palsy and Ramsay Hunt Syndrome
Chapter 29: Traumatic Facial Paralysis
Chapter 30: Facial Nerve Tumors
Chapter 31: Surgery for Cochlear Implantation
Chapter 32: Implantable Hearing Devices
Chapter 33: The Bone-Anchored Cochlea Stimulator (Baha)
Chapter 34: Surgery of the Endolymphatic Sac
Chapter 35: Middle Cranial Fossa-Vestibular Neurectomy
Chapter 36: Retrolabyrinthine and Retrosigmoid Vestibular Neurectomy
Chapter 37: Translabyrinthine Vestibular Neurectomy
Chapter 38: Posterior Semicircular Canal Occlusion for Benign Paroxysmal Positional Vertigo
Chapter 39: Cochleosacculotomy
Chapter 40: Transcanal Labyrinthectomy
Chapter 41: Chemical Treatment of the Labyrinth
Chapter 42: Superior Semicircular Canal Dehiscence Syndrome
Chapter 43: Overview of Transtemporal Skull Base Surgery
Chapter 44: Operations for Vascular Compressive Syndromes
Chapter 45: Drainage Procedures for Petrous Apex Lesions
Chapter 46: Surgery for Glomus Tumors and Other Lesions of the Jugular Foramen
Chapter 47: Rehabilitation of Lower Cranial Nerve Deficits after Neurotologic Skull Base Surgery
Chapter 48: Middle Fossa Approach
Chapter 49: Translabyrinthine Approach
Chapter 50: Retrosigmoid Approach to Tumors of the Cerebellopontine Angle
Chapter 51: Transotic Approach
Chapter 52: Transcochlear Approach to Cerebellopontine Angle Lesions
Chapter 53: Extended Middle Cranial Fossa Approach
Chapter 54: Anterior and Subtemporal Approaches to the Infratemporal Fossa
Chapter 55: Endoscopic Endonasal Approaches to the Skull Base and Paranasal Sinuses
Chapter 56: Petrosal Approach
Chapter 57: Neurofibromatosis 2
Chapter 58: Auditory Implants for the Central Nervous System
Chapter 59: Extreme Lateral Infrajugular Transcondylar (ELITE) Approach for Resection of Skull Base Tumors
Chapter 60: Management of Postoperative Cerebrospinal Fluid Leaks
Chapter 61: Care of the Eye in Facial Paralysis
Chapter 62: Hypoglossal Facial Anastomosis
Chapter 63: Facial Reanimation Techniques
Chapter 64: Intraoperative Neurophysiologic Monitoring
Chapter 65: Stereotactic Radiosurgery of Skull Base Tumors
Chapter 66: Vascular Considerations in Neurotologic Surgery
Index
Self-Assessment Questions
Chapter 1 Otologic Instrumentation

Jose N. Fayad, Barbara Stahl Hoskins, James E. Benecke, Jr.
Sophisticated micro-otosurgical techniques mandate that the otologic surgeon and surgical team have an in-depth understanding of the operating room (OR) layout and surgical instrumentation. This chapter describes in detail different surgical procedures. The OR setup and instruments necessary for the various types of otologic procedures are described. Appendix 1 provides a comprehensive list of instruments and equipment.

OPERATING ROOM
The OR for otologic surgery requires features that differ from ORs used for nonotologic surgery. The following sections elaborate on the general environment of the OR designed for ear surgery. A word about the sterile field is in order. Respecting the sterile field is vital during routine otologic surgery, and takes on special significance during neurotologic procedures. Maintaining the proper environment means limiting traffic through the OR, and keeping the number of visitors to a minimum. It is preferable for observers to be in a remote room watching the procedures on video. Individuals allowed in the OR should be experienced in sterile technique and should wear jackets over scrubs so that all skin surfaces are covered ( Fig. 1-1 ).

FIGURE 1-1 Observer in jacket.
Before entering the OR, the patient identifies the operative site. The correct ear is marked using a marking pen. The psychological environment of the OR must be respected because many otologic procedures are performed on awake patients under local anesthesia. Members of the surgical team and visitors must use discretion when making comments during surgery.
The first piece of OR equipment to be discussed is the operating table. The surgeon must be comfortable while performing microsurgery. Adequate leg room under the table can be achieved with older OR tables by placing the patient 180 degrees opposite the usual position; in other words, the patient’s head is where the feet would normally be ( Fig. 1-2 ). Newer electric tables easily accommodate the patient and surgeon. Because most otologists spin the OR table 180 degrees after the induction of anesthesia, the new tables allow for spinning the table without unlocking it. Nonetheless, after the patient is properly positioned, the table must be firmly locked in place.

FIGURE 1-2 Operating table with patient’s head at foot of bed.
All ORs are equipped with wall suction. Standard suction devices are acceptable for otologic surgery. It is preferable, however, to use a multiple-canister suction setup, minimizing the number of times the bottles must be emptied ( Fig. 1-3 ). Suction systems have several locations where the amount of suction can be varied, but the surgeon should also employ a control clamp on the suction tubing on the sterile field ( Fig. 1-4 ).

FIGURE 1-3 Multiple-canister suction setup.

FIGURE 1-4 Suction tubing with control clamp.
The tubing that is attached to the suction tips and suction irrigators should be highly flexible. The readily available disposable tubing is not flexible enough for microsurgery, and places awkward torque on the surgeon’s hands. Suction setup problems are common in every OR. The prudent team troubleshoots the system in advance and has access to backup equipment.
Electrocautery equipment should be in a ready-to-use state on all procedures except perhaps stapes surgery. The patient must be properly grounded. It is advantageous to have unipolar and bipolar cautery on the field for all chronic ear and neurotologic procedures. Polytef (Teflon) tips are available for most cautery devices and are desirable. Surgeons have at their disposal a wide array of safe cautery devices, but they must be thoroughly familiar with these electric instruments before use.
The surgical drill is another essential piece of equipment for otologic surgery. The vast array of available drills precludes an in-depth discussion of each system. Generally, otologic drills fall into two categories: air driven and electric. There are advantages and disadvantages to each type, and most surgeons have a distinct preference based on training and experience. For surgeons using air-driven drills, it is preferable to use a central source of nitrogen to power the drill, instead of using room tanks of the gas. Using a central source eliminates the need for changing tanks during long cases.
High-speed drills capable of doing most of the bone work in the temporal bone include the Fisch, Midas Rex, and Anspach drill systems. These drills generally are unsuitable for work in the middle ear, especially around the stapes footplate. For the latter purposes, a microdrill, such as the Skeeter drill or Synergy, is suitable ( Fig. 1-5 ). Whatever drill is used in the middle ear, it must have a variable speed control and a wide array of drill bits.

FIGURE 1-5 Synergy microdrill for footplate work.
Most larger otologic drills are equipped with straight and angled handpieces. Most surgeons prefer straight handpieces for early gross removal of the mastoid cortex, switching to angled handpieces for working deeper in the temporal bone. The Anspach drill system has a handpiece that can be converted from straight to angled simply by rotating the connection. A full complement of cutting and diamond burrs is mandatory. Figure 1-6 shows the Anspach drill system. Most drill systems have attachments that vary in shape, diameter, and length. It is the surgeon’s responsibility to be intimately familiar with the drill system and to have all of the attachments and burrs that might be needed.

FIGURE 1-6 Anspach drill system.
The otologic drill should be held in the hand like a pencil, with the hand resting comfortably on the sterile field. The side of the burr should be used to provide maximum contact between the bone and the flutes of the burr, affording safer and more efficient drilling ( Fig. 1-7 ). The newer drills are remarkably reliable, but, similar to other tools, may malfunction. Drill systems require proper care and inspection before use. A backup system should be readily available.

FIGURE 1-7 Proper holding of the drill.
The introduction of the operating microscope revolutionized otologic surgery. Most otolaryngologists are familiar with the use of the microscope. Several brands of optically superior instruments are available; most are sufficiently similar to share the same general principles.
The otologic surgeon must be familiar with the adjustments on the microscope, and must be prepared to troubleshoot the problems that may arise with the scope. The focal length of the objective lens is a matter of personal preference. Most otologists use a 200 mm or 250 mm objective. If a laser is attached to the microscope, one might consider a 300 mm objective. The objective lens should be selected, confirmed, and properly mounted before draping the microscope. Other adjustments, such as the most comfortable interpupillary distance, also should be done before the scope is draped. Par focal vision should be established so that the surgeon can change magnification without having to change focus. This is accomplished by first setting the diopter setting of both eyepieces to zero. The 40× magnification (or highest available setting) is selected. The locked microscope is focused on a towel using the focus knob only. Without disturbing any of the settings, the magnification is now set at 6× (or the lowest available setting). The eyepieces are individually adjusted to obtain the sharpest possible image. The diopter readings are recorded for future use. The surgeon should have par focal vision when these appropriate eyepieces are used.
The microscope should move easily. All connections should be adjusted so that the microscope does not wander by itself, yet permits movement to any position with minimal effort. Wrestling with the microscope during microsurgery is an extreme distraction.
Proper posture at the operating table is crucial. To perform microsurgical procedures, rule number one is that the surgeon must be comfortable. The surgeon should be seated comfortably in a proper chair with the back support at the correct height. Both feet should be resting comfortably on the floor. Fatigue is avoided by assuming a restful position in the chair, rather than a rigid upright posture ( Fig. 1-8 ).

FIGURE 1-8 A, Proper posture for the surgeon. B, Wrong posture for the surgeon.
The overall OR setup for routine otologic surgery is shown in Figure 1-9 . For neurotologic surgery, more space must be available for additional equipment. Middle cranial fossa procedures require some modifications to the OR setup ( Fig. 1-10 ). Basically, the surgeon and the microscope trade places such that the surgeon is seated at the head of the table. Cooperation and careful orchestration between the surgeon, nursing personnel, and anesthesiologist are required for otologic surgery. The needs of the otologist are best served by having the anesthesiologist at the foot of the bed and the scrub nurse opposite the surgeon. Space for the facial nerve monitoring equipment and personnel is reserved.

FIGURE 1-9 Usual otologic/neurotologic operating room setup.

FIGURE 1-10 Operating room layout for middle fossa surgery.

STAPES SURGERY
The following description of the instrumentation and operative setup for stapes surgery also provides information useful for other middle ear procedures. Under most circumstances, it is preferable to perform stapes surgery under local anesthesia, and surgeons who do so usually employ some type of preoperative sedation. Numerous regimens are available, and their description is beyond the scope of this text. If sedation is administered by the surgeon or nursing personnel, without the assistance of an anesthetist or anesthesiologist, the agents used should be short-acting and reversible.
It is far safer for the patient to be psychologically prepared for the procedure than to be oversedated. At the House Clinic, the associates prefer to perform all local anesthesia cases (including stapes surgery) under monitored anesthesia care. This approach requires the presence of anesthesia personnel in the OR to sedate the patient, as is required for the operation, and to monitor vital functions. The surgeon is relieved from this duty, allowing total concentration on the microsurgery.
About 30 minutes before the operation, the patient is brought to the preoperative holding area. If the surgeon routinely harvests a postauricular graft, this area is now shaved. A plastic aperture drape is applied to the operative site and trimmed so as not to cover the patient’s face ( Fig. 1-11 ). An intravenous line is started, and the patient is now ready to go to the OR. When the patient is on the OR table, the monitors are placed on the patient by the nursing or anesthesia staff. Minimal monitoring includes pulse oximetry, automatic blood pressure cuff, and electrocardiogram electrodes. The ear and plastic drape are scrubbed with an iodine-containing solution, unless the patient is allergic to iodine. A head drape is applied, and the ear is draped with sterile towels so as not to cover the patient’s face; this can be facilitated by supporting the drapes with a metal bar attached to the OR table, or by fixing the drapes to the scrub nurse’s Mayo stand ( Fig. 1-12 ).

FIGURE 1-11 Plastic drape applied for stapes surgery.

FIGURE 1-12 Patient draped in the operating room for stapes surgery.
The patient’s head is now gently rotated as far away from the ipsilateral shoulder as possible, and the table is placed in slight Trendelenburg position. These maneuvers increase the surgeon’s working room and help to straighten the external auditory canal (EAC). The EAC is gently irrigated with saline heated to body temperature. Vigorous cleaning of the canal is avoided until the ear is anesthetized. The local anesthesia is administered with a plastic Luer-Lok syringe that has finger and thumb control holes. A 1½ inch, 27 gauge needle is firmly attached to the syringe. If the ear is injected slowly and strategically, excellent anesthesia and hemostasis can be achieved with a solution of 1% lidocaine with 1:100,000 epinephrine (e.g., 1:40,000). When using stronger concentrations of epinephrine, the patient’s blood pressure and cardiac status must be considered, in addition to the possibility of mixing errors.
The canal is injected slowly in four quadrants starting lateral to the bony-cartilaginous junction. The final injection is in the vascular strip. If one routinely harvests fascia or tragal perichondrium, these areas are now injected.
Before describing stapes surgical instruments, a few general comments are in order. All microsurgical instruments should be periodically inspected to ensure sharp points and cutting surfaces. The instruments for delicate work should have malleable shanks, enabling the surgeon to bend the instruments to meet the demands of the situation.
If the surgeon prefers a total stapedectomy over the small fenestra technique, an oval window seal must be selected. If fascia is used, the tissue is harvested before exposing the middle ear. The tissue is placed on a Teflon block or fascia press to dry. If perichondrium is preferred, this may be harvested immediately before footplate removal. For the small fenestra technique, a small sample of venous blood is obtained when the intravenous line is started. This blood sample is passed to the scrub nurse and placed in a vial on the sterile field.
Various ear specula should be available in oval and round configurations. Sizes typically range from 4.5 to 6.5 mm ( Fig. 1-13 ). It is desirable always to work through the largest speculum that the meatus permits, without lacerating canal skin. Some surgeons prefer to use a speculum holder for stapes and other middle ear procedures. The tympanomeatal flap is started with incisions made at the 6 and 12 o’clock positions with the No. 1, or sickle, knife. These incisions are united with the No. 2, or lancet, knife. This instrument actually undermines the vascular strip instead of cutting it. The strip is cut with the Bellucci scissors. The defined flap is elevated to the tympanic annulus with the large round knife, known as the large “weapon.” When properly identified, the annulus is elevated superiorly with the Rosen needle, and inferiorly with the annulus elevator, or gimmick. Figure 1-14 shows a typical set of stapes instruments, including suction tips.

FIGURE 1-13 Speculum array.

FIGURE 1-14 Stapes instruments
Adequate exposure usually requires removal of the bony ledge in the posterosuperior quadrant. This can be initiated with the Skeeter microdrill and completed with a stapes curette ( Fig. 1-15 ).

FIGURE 1-15 Stapes curette.
From this point on, the steps differ depending on the technique preferred by the surgeon. The diagnosis of otosclerosis should be confirmed on entering the middle ear, and a measurement should be taken from the long process of the incus to the stapes footplate with a measuring stick. The next step is to make a control hole in the footplate with a sharp pick-needle (Barbara needle) or the laser. The incudostapedial joint is separated with the joint knife, the tendon is cut with scissors or laser, and the superstructure is fractured inferiorly and extracted.
For work on the footplate, the surgeon must have a variety of suitable instruments available. A stapedotomy can be created with a microdrill, laser, or needles and hooks. The 0.3 mm obtuse hook is useful for enlarging the fenestra.
For total footplate extraction, a right angle hook or excavator (Hough hoe) is used. The harvested graft is guided into place with a footplate chisel. The prosthesis is grasped with a smooth alligator or strut forceps and placed on the incus. It is positioned on the graft, or into the fenestra, with a strut guide. The wire is secured onto the incus with a crimper, or wire-closing forceps. The McGee crimper is useful, especially if followed by a fine alligator forceps for the last gentle squeeze. A small right angle hook may be necessary to fine-tune the position of the prosthesis ( Fig. 1-16 ).

FIGURE 1-16 Crimpers and footplate hook.
Suction tubes for stapes surgery include Nos. 3 to 7 Fr Baron suctions plus Rosen needle suction tips (18 to 24 gauge) with the House adapter ( Fig. 1-17 ). The Rosen tips are useful when working near the oval window, with the surgeon’s thumb off the thumb port.

FIGURE 1-17 Rosen suction tubes with House adapter; Baron tubes.
Ear packing after stapes surgery is accomplished with an antibiotic ointment to hold the flap in place. A piece of cotton suffices as a dressing, unless a postauricular incision has been made, in which case a mastoid dressing is applied.
For all middle ear procedures, the surgeon should hold the instruments properly. The instrument should rest, like a pencil, between the index finger and thumb, allowing easy rotation around the shank. The hands should always be resting on the patient and the OR table. The middle and ring fingers should rest on the speculum so that the hand moves as a unit with the patient. Proper hand position and holding of instruments should afford the surgeon an unimpeded view ( Fig. 1-18 ).

FIGURE 1-18 Proper holding of instruments as shown by Dr. William House.

TYMPANOPLASTY AND TYMPANOPLASTY WITH MASTOIDECTOMY
The preparation and draping for tympanoplasty with or without mastoidectomy are much the same as for stapes surgery. The major difference is the amount of hair shaved before draping. Usually, enough hair is shaved to expose about 3 to 4 cm of skin behind the postauricular sulcus. The plastic drape is applied to cover the remaining hair ( Fig. 1-19 ).

FIGURE 1-19 Drape (3M 1020) applied for chronic ear surgery.
The patient is positioned on the OR table as described earlier. Whether the procedure is performed under local or general anesthesia depends on the extent of the surgery, the surgeon’s preference, and the desire of the patient. After appropriate sedation or induction of anesthesia, the ear and plastic drape are scrubbed with the proper soap or solution. Some surgeons place a cotton ball in the meatus if a perforation exists, preferring not to allow the preparation solution to enter the middle ear. The field is draped as described earlier, the head is rotated toward the contralateral shoulder, and the table is placed in slight Trendelenburg position ( Fig. 1-20 ). The postauricular area, canal, and tragus (if necessary) are injected with 1% lidocaine with 1:100,000 epinephrine for local and general anesthesia cases.

FIGURE 1-20 Chronic ear surgery draping for local anesthesia.
Most chronic ear procedures begin in a similar fashion. Through an ear speculum, vascular strip incisions are made with the sickle or Robinson knife and united along the annulus with the lancet knife. The vascular strip incisions are completed with a No. 64 or 67 Beaver blade. This same blade can be used to transect the anterior canal skin just medial to the bony-cartilaginous junction. The postauricular incision is made with a No. 15 Bard-Parker blade behind the sulcus. The level of the temporalis fascia is identified, and a small self-retaining (Weitlaner) retractor is inserted. The fascia is cleared of areolar tissue and incised. A generous area of fascia is undermined and removed with Metzenbaum scissors. The scrub nurse can assist by using a Senn retractor to elevate skin and soft tissues away from the fascia. The fascia is thinned on the Teflon block and dehydrated by placing it under an incandescent bulb, carefully monitoring its progress. The fascia may also be dehydrated by placing it on a large piece of Gelfoam and compressing this complex in a fascia press. Figure 1-21 shows the instruments used in the initial stages of chronic ear surgery.

FIGURE 1-21 A, Instruments for making a canal incision. B, Instruments for handling fascia.
Continued postauricular exposure is obtained by incising along the linea temporalis with a knife or with the electrocautery. A perpendicular incision is made down to the mastoid tip. Soft tissues and periosteum are elevated with a Lempert elevator ( Fig. 1-22 ), the vascular strip is identified, and a large self-retaining retractor is inserted. A very large retractor, such as an Adson cerebellar retractor with sharp prongs, is preferred.

FIGURE 1-22 Periosteal elevators.
Next, under the microscope, the anterior canal skin is removed down to the level of the annulus with the large weapon. The plane between the fibrous layer of the drum remnant and the epithelium is developed with a sickle knife, and the skin is pulled free with a cup forceps. The anterior canal skin is placed in saline for later use as a free graft. The ear canal is enlarged with the drill and suction-irrigators. An angled handpiece and medium to small cutting burr are used. Irrigation through the suction-irrigators is done with a physiologic solution such as Tis-U-Wol, lactated Ringer, or saline. Two large (3000 mL) bags of irrigant are hung and connected by way of a three-way stopcock to the delivery system ( Fig. 1-23 ).

FIGURE 1-23 Suction irrigation setup.
For mastoidectomy surgery, the surgeon must have a full array of cutting and diamond burrs, and a complete set of suction-irrigators. It is advisable to have bone wax and absorbable knitted fabric (Surgicel) readily available. Cholesteatoma removal can be accomplished with middle ear instruments such as the gimmick, weapon, and fine scissors.
Although the setup for closing and packing after chronic ear surgery varies with the specifics of the situation, a few generalities should cover most situations encountered by the otologist. To maintain the middle ear space, silicone elastomer (Silastic) sheeting works well and is still readily available. This sheeting comes in various thicknesses, with and without reinforcement. For middle ear packing, absorbable gelatin sponge (Surgifoam) is the usual choice, soaked in saline or an antibiotic otic preparation. Surgifoam is also used to pack the EAC, although some surgeons prefer an antibiotic ointment, as described in the section on stapes surgery. For meatoplasty packing, 1-inch nonadhesive Curity packing strip or nasal packing gauze is saturated with an antibiotic ointment and rolled around the tip of a bayonet forceps; this creates a plug that conforms to the new meatus and is easily removed ( Fig. 1-24 ).

FIGURE 1-24 A, Surgifoam packing. B, Meatoplasty packing.
Wound closure is accomplished in two layers with absorbable sutures. The skin is closed with a running intradermal suture of 1-0 polyglactin 910 (Vicryl) or polyglycolic acid (Dexon) on a cutting needle. Steri-Strips are applied, and the wound is covered with a standard mastoid dressing.
Some additional instruments that prove to be handy in many chronic ear procedures include an ossicles holder, Crabtree dissectors, Zini mirror, right angle hooks, and the House-Dieter malleus nipper ( Fig. 1-25 ). It is impossible to describe instruments for every conceivable situation, but the foregoing should cover most of the needs of the otologist.

FIGURE 1-25 Additional instruments used in chronic ear procedures (see text).

ENDOLYMPHATIC SAC SURGERY
There are many well-described procedures on the endolymphatic sac. The purpose of this chapter is not to outline the surgical options, but rather to discuss the methodology for performing sac surgery. The preparation and draping of the patient for endolymphatic sac surgery are essentially the same as for tympanoplasty with mastoidectomy surgery. In the preoperative holding area, the postauricular area is shaved, exposing at least 4 cm of skin behind the sulcus. Plastic adhesive drapes are applied, and the patient is transported to OR.
Endolymphatic sac surgery is performed under general anesthesia. The field is scrubbed in the usual manner, and the patient is positioned as described for chronic ear surgery.
This is a good time to mention briefly the use of intraoperative facial nerve monitoring and other forms of physiologic monitoring, including eighth cranial nerve and cochlear potentials. Many surgeons use facial nerve monitoring whenever the facial nerve might be in jeopardy. Electrodes for facial nerve monitoring or other forms of monitoring should be positioned before the preparation.
After the preparation for endolymphatic sac surgery, the planned incision is injected with 1% lidocaine with 1:100,000 epinephrine. The incision is made 2 to 3 cm behind the sulcus. Periosteal incisions are made sharply or with the electrocautery. A Lempert elevator elevates soft tissues and periosteum up to the level of the spine of Henle. A House narrow (canal) elevator is used to delineate the EAC, and a large self-retaining retractor is inserted. With drill and suction-irrigator, a complete mastoidectomy is performed. The antrum is not widely opened, but is instead blocked with a large piece of absorbable gelatin sponge (Gelfoam) to prevent bone debris from entering the middle ear.
Bone over the sigmoid sinus and posterior fossa dura is thinned with diamond burrs. The retrofacial air tract is opened widely to locate the endolymphatic sac. The sac is decompressed with a diamond burr. A stapes curette can be used to remove bone over the proximal sac. The occasional bleeding that occurs over the surface of the sac or surrounding dura is best controlled with bipolar cautery. Alternatively, unipolar cautery at a very low setting can be used. The cautery tip is touched to an insulated Rosen or gimmick that is in contact with the offending vessel ( Fig. 1-26 ). Another method used to control small areas of bleeding in endolymphatic sac and chronic ear surgery is to cover the area with pledgets of Gelfoam that have been soaked in topical thrombin.

FIGURE 1-26 Insulated gimmick ( top ) and Rosen ( bottom ).
Before opening the sac, the wound is copiously irrigated with saline or bacitracin solution. Fresh towels are placed around the field. The sac is opened with a disposable Beaver ophthalmic blade (No. 59S, 5910, or 5920). The lumen is probed with a blunt hook or gimmick. The shunt tube preferred by the surgeon is now inserted. Thin Silastic sheeting (0.005 inch) can be used to fashion a shunt. Figure 1-27 shows the materials for the latter steps of endolymphatic sac surgery. As with chronic ear procedures, the wound is closed in layers, usually beginning with 2-0 chromic and finishing with 4-0 Vicryl or Dexon. A standard mastoid dressing is applied. This dressing either is prepared in the OR or is obtained as a prepackaged dressing (e.g., Glasscock dressing).

FIGURE 1-27 Endolymphatic sac instruments and materials.

NEUROTOLOGIC PROCEDURES
This section describes the OR layout for neurotologic procedures, the only exception being middle fossa surgery, which is discussed separately. For procedures involving intracranial structures, extraordinarily meticulous attention to detail is mandatory. The preparation for neurotologic surgery may begin the evening before surgery by having the patient wash his or her hair and scalp with an antiseptic shampoo. The day of surgery, the patient is seen by the surgeon in the holding area so that the ear to be operated on is positively identified. The surgical site is shaved so that at least 6 cm of postauricular scalp is exposed. The area is sprayed with an adhesive, and the plastic drapes are applied ( Fig. 1-28 ). At the same time, the abdomen is shaved from below the umbilicus to the inguinal ligaments, in preparation for harvesting a fat graft. The fat donor site is surrounded by plastic drapes ( Fig. 1-29 ).

FIGURE 1-28 Drapes (3M 1000) applied for neurotologic surgery.

FIGURE 1-29 Abdominal area prepared.
After anesthetic induction, a catheter is inserted, and arterial and central venous lines are placed when indicated. Electrodes for monitoring CN VII and VIII (and possibly other nerves) are positioned. The patient’s head is supported on towels or a “donut” as needed, and rotated toward the contralateral shoulder. The surgical sites are scrubbed, then blotted dry with a sterile towel. The areas are draped off with towels and then covered with plastic adhesive drapes (e.g., Steri-Drape, Ioban, Cranial-Incise). Some surgeons prefer to include another layer of towels around the cranial site, followed by either sheets or a disposable split sheet. It is important to have several layers of draping to prevent saturation of the drapes with fluids down to the level of the patient ( Fig. 1-30 ).

FIGURE 1-30 A-C, Draping sequence for neurotologic surgery.
Because the scrub nurse must handle numerous items attached to tubes and cords, it is helpful to have fastened to the field a plastic pouch into which the drill, suction, and cautery tips can be placed ( Fig. 1-31 ). Two Mayo stands are kept near the field: one for the neurotologic instruments and the other for the fat-harvesting tools ( Fig. 1-32 ).

FIGURE 1-31 SK-100 Surgi-kit for holding instruments.

FIGURE 1-32 A, Mayo stand setup for tumor. B, Mayo stand setup for fat graft.
The postauricular area is injected with the usual local anesthetic, and the plastic drape is cut away with scissors to expose the mastoid and lateral subocciput. As with other procedures, a skin incision is made, hemostasis is obtained, soft tissues and periosteum are elevated, and a large self-retaining retractor is inserted. Bone removal is accomplished using a drill and suction-irrigation. For neurotologic cases, bone removal is more extensive, exposing the sigmoid sinus and a considerable amount of posterior fossa dura behind the sigmoid. It is imperative that the surgeon has immediate access to bone wax and Surgicel. Many surgeons also insist on having immediate access to hemoclips and thrombin-soaked Gelfoam.
The extent of bone removal varies depending on the surgeon’s preference and the nature of the procedure. Some surgeons decompress the sigmoid completely, whereas others leave a thin shell of bone over the sinus (Bill’s island). After appropriate bone removal, the retractor is removed, and the field is vigorously irrigated with bacitracin solution. Bacitracin solution can be prepared by dissolving 50,000 U of bacitracin in 1 L of normal saline. After wound irrigation, fresh towels are placed around the field.
With a wound free of bone dust and debris, the dura can now be opened with a No. 11 Bard-Parker scalpel blade or with the tips of Jacobson scissors. The dura can be pulled away from underlying structures by using a corkscrew-like instrument included in some neurotologic instrument sets ( Fig. 1-33 ). The subdural space is entered, taking care not to violate the arachnoid; this helps to avoid injury to vessels before adequate exposure. The dural flap is carefully developed with Jacobson scissors. Hemostasis is controlled with bipolar cautery. The arachnoid is carefully opened with a sharp hook or the tips of the scissors, allowing the egress of cerebrospinal fluid. Figure 1-33 shows the instruments for dural and arachnoid opening. After opening the arachnoid, one should switch to fenestrated (Brackmann) suction tips ( Fig. 1-34 ). The cerebellum and other intracranial structures should be protected with moist neurosurgical cottonoids. A variety of cottonoids should always be on the stand.

FIGURE 1-33 Brackmann neurotologic instruments.

FIGURE 1-34 Brackmann fenestrated suction-irrigators.
For vestibular neurectomy procedures, the plane between the cochlear and vestibular nerves can be developed with a blunt hook, or the gimmick. The nerve section itself can be completed with a sharp hook or microscissors ( Fig. 1-35 ). The same instruments can be used to define the plane between an acoustic neuroma and the facial nerve. A sharp right angle hook palpates Bill’s bar and sections the superior vestibular nerve fibers along with the vestibulofacial fibers. After establishing the proper plane between the tumor and facial nerve, a blunt hook is used to continue the dissection, avoiding stretching of the facial nerve. Facial nerve monitoring has greatly assisted this part of the dissection. For small tumors, the previously mentioned technique might suffice for total tumor removal. Larger tumors are removed by gutting the tumor extensively, mobilizing the capsule, and removing the capsule in a piecemeal fashion; this is accomplished by morcellizing the tumor with a large crushing forceps, such as the Decker. The Urban rotary suction-dissector is used to extract the pieces ( Fig. 1-36 ). Bayonet forceps direct the tumor into the suction port of the Urban suction-dissector. As the tumor is gutted, the capsule collapses and can be dissected from the brainstem.

FIGURE 1-35 Hooks for neurectomy and tumor dissection.

FIGURE 1-36 Urban dissector.
The Selector ultrasonic aspirator ( Fig. 1-37 ) is another instrument that some surgeons prefer for gutting the tumor. Whatever tool is used, proper use of these sophisticated, potentially dangerous instruments must be learned from user manuals and appropriate training and courses.

FIGURE 1-37 Selector aspirator.
Hemostasis is vital during neurotologic surgery, and the surgeon must have immediate access to all possible items necessary to control bleeding from whatever the source. In addition to unipolar and bipolar cautery, bone wax and precut pieces of Surgicel should be on the Mayo stand. Microfibrillar collagen (Avitene) is another preferred hemostatic agent to have available. Pledgets of Gelfoam soaked in topical thrombin are quite useful. Vascular clips and a reliable clip applicator are useful for controlling bleeding from the petrosal vein and its tributaries ( Fig. 1-38 ).

FIGURE 1-38 Clips and clip applicators.
Infratemporal fossa and other approaches to the skull base are set up in much the same manner as has already been discussed. Incisions are generally long and may extend into the upper cervical region to access major neurovascular structures. Silastic vessel loops should be placed around these structures for control and easy identification. Ligatures of 0 silk and transfixion sutures of 2-0 silk need to be available for jugular vein ligation. Cardiovascular sutures (e.g., 5-0 and 6-0 polypropylene [Prolene]) should also be close by.
The self-retaining retractors described earlier are usually insufficient for skull base surgery. The Fisch infratemporal retractor or pediatric rib retractor are better suited to these tasks, which often include anterior displacement of the mandible. If mandibulotomy is indicated, the appropriate oscillating saw needs to be available.
Some instruments facilitate work on or near the facial nerve. For rerouting the facial nerve, bone is removed with a drill until an eggshell thickness remains. The remaining bone is gently removed with a stapes curette. The nerve can be mobilized with a dental excavator or microraspatory. If a segment of the nerve is to be excised, as in a facial neuroma, this should be done sharply with a fresh knife blade. Likewise, before any neurorrhaphy, the ends of the nerve and graft should be freshened. A 9-0 monofilament suture is used for nerve anastomosis. Appropriate needle holders and forceps must be available ( Fig. 1-39 ). An alternative or adjunct to suturing is to use NeuraGen nerve guides.

FIGURE 1-39 Nerve anastomosis equipment.
Before closing neurotologic and skull base wounds, abdominal fat is removed from the left lower quadrant, most of the dissection being done with electrocautery. The abdominal wound is closed (over a drain if necessary) in layers, with the skin being approximated with a running intradermal 4-0 Vicryl or Dexon suture. The fat is cut into strips and insinuated into the dural defect. Continuous lumbar drainage is rarely necessary to prevent cerebrospinal fluid leakage except in extensive intracranial-extracranial resections. If the neck is opened, a suction drain is inserted into the depths of the wound before closure. Wounds are closed as in other otologic procedures and dressed with a standard mastoid dressing.
Also under the rubric of neurotologic surgery is cochlear implant surgery. Each presently available cochlear implant device has its own unique set of requirements and, possibly, instruments. The surgeon must have proper training and experience to perform cochlear implant procedures. He or she must have all of the necessary special equipment for electrode placement and internal receiver fixation ( Fig. 1-40 ).

FIGURE 1-40 Cochlear implant tools.

MIDDLE CRANIAL FOSSA SURGERY
Middle fossa procedures are discussed separately from other neurotologic procedures because they involve a different OR setup and some different instruments. The most obvious deviation from other procedures is the position from which the surgeon operates. The surgeon and the microscope trade locations, so that the surgeon operates from the head of the bed facing caudally (see Fig. 1-10 ).
As with other neurotologic procedures, middle fossa surgery is performed under general anesthesia. In the preoperative holding area, the ipsilateral scalp is shaved to a distance of 6 cm postauricularly and nearly to the midline of the head above the ear in the temporal fossa. Plastic adhesive drapes are applied, and the patient is taken to the OR. After anesthesia, the surgical site and plastic drapes are scrubbed and blotted dry. The area is covered with another plastic adhesive drape. Towels are positioned to block off the entire temporoparietal scalp, including the auricle and zygomatic arch. Sterile sheets complete the draping ( Fig. 1-41 ). The abdomen is usually prepared as in other neurotologic surgeries.

FIGURE 1-41 Patient draped for middle fossa surgery.
The incision is planned so that it begins in the preauricular incisura below the root of the zygoma. It extends cephalad to the area just above the superficial temporal line. A gentle curve facilitates exposure. Before the incision, as in other cases, the area is infiltrated with local anesthesia.
The plastic drape is cut away to expose the skin. After the skin incision is made, the superficial temporal vessels are identified and ligated. After the temporalis fascia is identified, it is recommended that an inferiorly based temporalis muscle flap be created, instead of splitting the muscle. This flap is centered over the zygoma, is elevated from the calvaria, and is reflected caudally by suturing the end of the flap to the drapes. Preserving the muscle with its neurovascular bundle does not limit the surgeon’s exposure, and allows the use of this muscle if facial reanimation surgery should ever be necessary. The remaining temporalis muscle is reflected laterally, and a self-retaining retractor is inserted. A craniotomy is performed. The size of the bone flap removed is dictated by the amount of exposure necessary. For tumor removal, it is wise to err on the large side.
The bone flap is carefully removed from the dura with an Adson periosteal elevator, or “joker” ( Fig. 1-42 ). The bone flap is placed in bacitracin solution. The craniotomy edges are smoothed with a rongeur, and bleeding is controlled with bone wax.

FIGURE 1-42 Adson periosteal elevator (“joker”).
The joker is used to dissect the dura from the floor of the middle fossa. The surgeon is now ready to insert the House-Urban middle fossa retractor. The surgeon must be familiar with the mechanical workings of this device ( Fig. 1-43 ). The retractor is locked under the bony edges of the craniotomy. The blade housing is positioned so that it allows good visualization of the field without placing excessive traction on the temporal lobe. This usually requires repositioning the retractor several times during the early stages of the dissection. Next, the retractor blade is inserted, and the extradural dissection proceeds. The blade can be tilted with the hand and advanced with the thumb, leaving the other hand free for suctioning. Bleeding can be troublesome from the floor of the middle fossa, especially near the middle meningeal artery. Bipolar cautery, bone wax, Surgicel, and other hemostatic agents should be readily available.

FIGURE 1-43 House-Urban middle fossa retractor.
The surgeon elevates the dura and temporal lobe until the arcuate eminence, superior petrosal sinus, and greater superficial petrosal nerve are visible. Bone over the internal auditory canal (IAC) and geniculate ganglion is removed with a large diamond burr. When the dura over the IAC has been completely skeletonized as far medially as the porus, the wound is irrigated with bacitracin solution, and fresh towels are placed around the field. The dura over the IAC is opened posteriorly (away from the facial nerve) with a sharp hook. For vestibular neurectomy, Bill’s bar is palpated with the same sharp hook that then transects the superior vestibular nerve. Fine microscissors (e.g., Malis, Jacobson) are used to remove a segment of the nerve in continuity with Scarpa’s ganglion. In a likewise fashion, the inferior vestibular and singular nerves are sectioned.
For acoustic tumor removal, significantly more bone removal is required. Having established adequate exposure, the plane between the facial nerve and tumor is developed as in the translabyrinthine approach.
At the conclusion of the procedure, the defect over the IAC can be reconstructed by filling it with small pieces of muscle or abdominal fat and covering it with a small piece of the bone flap that has been cut and trimmed to an appropriate size. The field is inspected for hemostasis, and the middle fossa retractor is removed, allowing the brain to re-expand. The wound is irrigated again with bacitracin. Microplates are used to secure the bone flap in place ( Fig. 1-44 ), and the wound is closed in layers, suturing the temporalis flap back to normal anatomic position. Some surgeons close the skin over a Penrose drain, which is removed the day after surgery. A mastoid dressing completes the closure.

FIGURE 1-44

CONCLUSION
This chapter has provided a detailed description of the OR environment and instrumentation for most procedures that the otologist is likely to encounter. Although these descriptions do not exhaust all possibilities, they have proved to be satisfactory for many otologists. Appendix 1 lists instruments and equipment that have been presented in the text.

APPENDIX 1 INSTRUMENTS AND EQUIPMENT FOR OTOLOGIC SURGERY

General Operating Room Equipment

1. 3M 1000 plastic aperture drapes
2. 3M 1020 aperture drapes
3. 3M Steri-Drape, Ioban drape, or Cranial-Incise drape
4. Pharmaseal preoperative skin preparation tray, No. 4480
5. Suction irrigation setup
6. Suction canisters
7. Electrocautery unit
8. Skytron operating table

Stapes Surgery

1. Assorted Farrior specula
2. Finger-control Luer-Lok syringe
3. 1½ inch, 25 or 27 gauge needle
4. Small Weitlaner retractor
5. Sheehy fascia press
6. House cutting block
7. Scalpel, No. 15 Bard-Parker blade
8. Adson tissue forceps
9. Iris scissors
10. House-Baron suction tubes, No. 3 to 7 Fr
11. House suction tube adapter
12. Rosen suction tubes, 18 to 24 gauge
13. Sickle knife (No. 1 knife)
14. Lancet knife (No. 2 knife)
15. Robinson knife
16. Sheehy-House weapon (large and small)
17. Rosen needle
18. House elevator
19. Gimmick annulus elevator
20. House stapes curette
21. Incudostapedial joint knife
22. Bellucci scissors
23. Straight Barbara pick
24. Measuring struts, 4.0 to 5.0 mm
25. Measuring disk, 0.6 mm
26. Hough hoe
27. Obtuse, 30 degree, 0.25 mm hook
28. Pick, 0.3 mm, 90 degree
29. Strut guide
30. Footplate chisel
31. Skeeter drill; 1.0, 0.7, and 0.6 mm burrs
32. House strut forceps (nonserrated)
33. McGee wire closing forceps (crimper)
34. Antibiotic ointment
35. Cotton balls, Band-Aids, mastoid dressing
36. Speculum holder

Chronic Ear Surgery

1. Assorted Farrior specula
2. Finger-control syringe
3. 1½ inch, 25 or 27 gauge needle
4. Small Weitlaner retractor
5. Large self-retaining retractor (Weitlaner, Adson cerebellar)
6. Scalpel, No. 15 Bard-Parker blade
7. No. 64 or 67 Beaver blade
8. House cutting block
9. Sheehy fascia press
10. House-Baron suction tubes, No. 3 to 7 Fr
11. Adson forceps
12. Iris scissors
13. Small Metzenbaum scissors
14. Sickle knife
15. Lancet knife
16. Robinson knife
17. Sheehy-House weapon (large and small)
18. Rosen needle
19. Gimmick
20. Crabtree dissector (large and small)
21. Lempert elevator
22. House narrow elevator
23. Pick, right angle, 0.6 mm
24. Pick, right angle, 1.5 mm
25. Pick, right angle, 3 mm
26. Bellucci scissors
27. Hartmann forceps
28. House alligator forceps
29. House cup forceps
30. House-Dieter malleus nipper
31. Zini mirrors
32. Sheehy ossicles holder
33. Speculum, endaural (or nasal)
34. Drill with cutting and diamond burrs
35. House suction-irrigators, No. 2.5 × 4 Fr through No. 8 × 12 Fr
36. Needle holder, Webster
37. Suture scissors
38. Suture, 2-0 chromic and 4-0 Vicryl (or Dexon)
39. Surgifoam (saline-soaked and antibiotic-soaked)
40. Curity Packing strip gauze
41. Silastic sheeting, 0.005
42. Gelfilm
43. Steri-Strips
44. Mastoid dressing
45. Bone wax
46. Surgicel
47. Sheehy bone dust collector

Endolymphatic Sac Surgery

1. Finger-control syringe
2. 1½ inch, 25 or 27 gauge needle
3. Scalpel, No. 15 Bard-Parker blade
4. Large self-retaining retractor
5. Lempert elevator
6. House narrow elevator
7. Drill and burrs
8. House suction-irrigators (assortment)
9. Brackmann suction-irrigators, No. 4 × 5 Fr, No. 5 × 7 Fr
10. Stapes curette
11. Gimmick
12. Insulated gimmick
13. Bone wax
14. Surgicel
15. Bipolar cautery
16. Bacitracin irrigation solution
17. Beaver ophthalmic blade (No. 59S, 5910, 5920)
18. Pick, right angle, 1.5 mm
19. Hook, right angle, blunt
20. Rosen needle
21. House alligator forceps
22. Silastic shunt material, 0.005
23. Suture, 2-0 chromic and 4-0 Vicryl (or Dexon)
24. Steri-Strips
25. Mastoid dressing
26. Cranial nerve monitoring equipment

Neurotologic Surgery

1. Finger-control syringe
2. 1½ inch, 25 or 27 gauge needle
3. Scalpel, No. 15 Bard-Parker blade
4. Large self-retaining retractor
5. Lempert elevator
6. House narrow elevator
7. Drill and burrs
8. Assorted House suction-irrigators
9. Assorted Brackmann suction-irrigators
10. Stapes curette
11. Gimmick
12. Insulated gimmick
13. Bone wax
14. Surgicel
15. Bipolar cautery
16. Bacitracin irrigation
17. SK-100 Surgi-Kit (Ethox Corp.)
18. Suture scissors
19. House-Urban dissector
20. Pick, right angle, 1 mm
21. Pick, right angle, 1.5 mm
22. Hook, right angle, blunt, 1.5 mm
23. Bellucci scissors
24. House cup forceps
25. Blakesley nasal forceps (No. 1)
26. House alligator forceps
27. Myringoplasty knife
28. Jacobson scissors
29. Malis scissors
30. Allis forceps
31. Bayonet forceps
32. Adson tissue forceps
33. Microclip applicator
34. Assorted hemostats
35. Metzenbaum scissors
36. Senn retractor
37. U.S. Army retractor
38. House-Urban rotary dissector or Selector
39. Fisch infratemporal fossa retractor
40. Woodson elevator
41. Fisch microraspatory
42. Sagittal saw
43. Needle holder, Castroviejo
44. Needle holder, Crile-Wood
45. Needle holder, Webster
46. Fisch microscissors
47. Titanium needle holders, smooth (2)
48. Janetta forceps
49. Gerald forceps, with and without teeth
50. Avitene
51. Drains, Penrose and Jackson-Pratt
52. Vessel loops
53. Suture, 5-0 and 6-0 vascular Prolene
54. Suture, 0 and 2-0 chromic
55. Suture, 0 and 2-0 silk
56. Suture, 9-0 nylon or Prolene
57. Suture, 4-0 Dexon or Vicryl
58. Neurosurgical cottonoids
59. NeuraGen nerve guide
60. Steri-Strips
61. Mastoid dressing
62. Topical thrombin
63. Surgifoam
64. Special neurotologic instrument sets (e.g., Kartush, Benecke)
65. Cranial nerve monitoring equipment

Middle Cranial Fossa Surgery

1. Finger-control syringe
2. 1½ inch, 25 or 27 gauge needle
3. Scalpel, No. 15 Bard-Parker blade
4. Large self-retaining retractor
5. Lempert elevator
6. House narrow elevator
7. Drill and burrs
8. Assorted House suction-irrigators
9. Brackmann suction-irrigators
10. Stapes curette
11. Gimmick
12. Insulated gimmick
13. Bone wax
14. Surgicel
15. Bipolar cautery
16. Bacitracin irrigation
17. SK-100 Surgi-Kit
18. Pick, right angle, 1 mm
19. Pick, right angle, 1.5 mm
20. Hook, right angle, blunt, 1.5 mm
21. Bellucci scissors
22. Fisch microscissors
23. House cup forceps
24. Metzenbaum scissors
25. House-Urban middle fossa retractor
26. Rongeur, Leksell
27. Adson tissue forceps
28. Microclip applicator
29. Assorted hemostats
30. Avitene
31. Cottonoids
32. Gelfoam
33. Suture, 0 and 2-0 chromic
34. Suture, 4-0 Vicryl (or Dexon)
35. Topical thrombin
36. Mastoid dressing
37. Special neurotologic instrument sets
38. Cranial nerve monitoring equipment
Chapter 2 Canalplasty for Exostoses of the External Auditory Canal and Miscellaneous Auditory Canal Problems

Joseph B. Roberson, Jr., Rodney Perkins
Videos corresponding to this chapter are available online at www.expertconsult.com .
Although clinical disease caused by exostoses of the external auditory canal (EAC) is infrequent, it occurs often enough that a method of surgical management should be in the armamentarium of the otologic surgeon. Because it is not a high-incidence problem or one that is life-threatening, many otolaryngologists use various independent approaches, which frequently result in elimination of or damage to the canal skin. These procedures frequently produce suboptimal results. A well-conceived approach addresses the problem of removal of exostoses, while maintaining the valuable residual skin of the EAC. This chapter begins with clinical observations regarding this condition and then describes an operative procedure that has been very successful in its management.
The etiology of these benign growths of the tympanic bone is strongly associated with the frequency and severity of exposure to cold water. 1 Frequently, these lesions are found in surfers, swimmers, or other individuals with frequent cold water exposure over several years. A widely held belief based on clinical information is that exostoses occur primarily during the years of growth, with their proliferation being enhanced or perhaps even caused by exposure to cold water during this period. This belief tends to be supported by historical information from patients with exostoses, who almost always indicate that they swam in cold water during their youth. 2 - 4 This historical information is strongly corroborated by the high incidence of exostoses in avid surfers who spend hours in the water almost daily. In our clinical experience, this problem occurs almost exclusively in men, who are more likely than women of the same age to have had frequent cold water exposure during their youth.
Most exostoses do not develop to a degree sufficient to cause clinical symptoms. Patients are frequently referred to otologists because the growths are observed, and not understood, by primary care physicians. This is particularly true with exostoses that have a more pedunculated form than the more subtle sessile configuration. When exostoses become more marked, however, they obstruct the natural elimination of desquamated epithelium from the ear canal, and patients usually present with recurrent episodes of external otitis. In their most prolific expression, exostoses can lead to hearing impairment by causing the collection of epithelial debris that tamponades tympanic membrane movement, by impinging on and limiting the mobility of the malleus, or by markedly narrowing the aperture of the canal. These conditions may manifest as a conductive hearing impairment on audiometric examination.
The EAC is part of the hearing pathway. Essentially, the EAC is a tube with resonant characteristics that amplify the incoming sound. The degree of amplification and the frequency at which it occurs are a function of the diameter and the length of the canal. When the diameter becomes small, it can interfere with the passage of sound and cause a hearing impairment. This effect does not become significant, however, until the aperture becomes very small. With apertures less than 3 mm, high-frequency sounds begin to diminish, and further compromise of the channel diameter results in increased impairment and lower frequency loss.

EXOSTOSES OF THE EXTERNAL AUDITORY CANAL

Surgical Indications
Surgery is indicated when chronic or recurrent external otitis exists, or a conductive hearing impairment develops. The presence of chronic and recurrent infection over an extended period seems to debilitate the canal skin, and can compromise the skin’s ability to re-epithelialize in a robust and healthy manner in the postoperative period. For this reason, surgical therapy should be considered when a pattern of recurrent external otitis has been established in these patients. Patients who have significant external canal exostoses without recurrent infection or hearing impairment should be observed periodically, and surgery should be avoided until these symptoms occur.

Preoperative Preparation

Patient Preparation
There are two components of patient preparation for otologic surgery performed under local anesthesia: psychological and pharmacologic.

Psychological Preparation
To reduce anxiety and create rapport, the surgeon should provide the patient with a full explanation of the procedure and its objectives, benefits, and risks. In addition, a surgical nurse or medical assistant should explain what will happen to the patient in the operating room, and describe such things as the operating room environment, use of an intravenous line for medication delivery, placement of monitor electrodes, and draping. By informing the patient of these things and making him or her part of the process, the clinician reduces the patient’s anxiety, encourages cooperation, and may reduce bleeding. Beyond the technical advantages achieved by such preparation, there is an ethical responsibility to inform the patient. In addition, the likelihood of the patient’s becoming litigious because of a poor result is markedly reduced if he or she has been informed about the procedure and its risks and benefits, and has had an opportunity to discuss the risks and benefits with the surgeon before the surgery.

Pharmacologic Preparation
The pharmacologic preparation of the patient can be achieved in many ways. In the average adult who selects intravenous sedation with local anesthesia, we give fentanyl, 50 to 100 μg, and midazolam (Versed), 5 to 10 mg intramuscularly 1 hour before the surgical incision. An intravenous catheter is started in the arm opposite the ear to be operated on before the patient arrives in the operating room, and 5% dextrose in Ringer solution is started with a volutrol. Unless the patient appears very sedated, an additional 50 to 100 μg dose of fentanyl is placed in the volutrol and infused slowly over 30 to 45 minutes. As the surgery proceeds, alternating supplements of intravenous midazolam and fentanyl are infused as needed to maintain sedation.
In most cases, general anesthesia is selected by either the surgeon or the patient. Patients with a history of claustrophobia, patients with poor language skills in the surgeon’s native tongue, and patients with difficult neck mobility are best approached under general endotracheal anesthesia. One advantage of use of general anesthesia is the ability to use facial nerve monitoring during the procedure. Patients receive cefazolin, 1 g intravenously, or another appropriate antibiotic 1 hour before incision.

Site Preparation
The hair is shaved behind the ear to a distance of approximately 1.5 inches posterior to the postauricular fold. The auricle and the periauricular and postauricular areas are scrubbed with povidone-iodine (Betadine) solution or chlorhexidine gluconate (Hibiclens) for iodine-allergic patients. A plastic drape is placed over the area with the auricle and the postauricular area exteriorized through the opening in the drape. This drape is placed over an L-shaped bar that is fixed in the rail attachment of the operating table ( Fig. 2-1 ). For patients under local anesthesia with sedation, a small, low-volume office fan is attached to the bar to provide a gentle cooling breeze to the patient’s face during the procedure. The plastic drape forms a canopy, allowing the patient to see from under the drape and reducing the feeling of claustrophobia. In addition, a foam earpiece from an insert speaker is put into the opposite ear. The earpiece is connected to a compact disk player and input microphone that allows the patient to listen to relaxing music and provides a pathway to converse with the patient, if desired.

FIGURE 2-1

Analgesia
It is important not only to achieve analgesia, but also to maximize canal hemostasis with injections into the external auditory meatus. Using 2% lidocaine (Xylocaine) with 1:20,000 epinephrine solution in a ringed syringe with a 27 gauge needle, a classic quadratic injection is made such that each injection falls within the wheal of the previous injection. Another useful injection is an anterior canal injection, which is made with the bevel of the needle parallel to the bony wall of the external meatus ( Fig. 2-2 ). In a patient with extensive exostoses, this injection is usually made into the lateral base of a large anterior sessile osteoma. After insinuation of the needle, it is advanced a few millimeters, and a few drops are injected extremely slowly. The solution infiltrates medially along the anterior canal wall and provides some analgesia to the auriculotemporal branch of CN V, which is usually unaffected by the quadratic injection and adds to the hemostasis anteriorly. The postauricular area is infiltrated with 2% lidocaine with 1:100,000 epinephrine solution mixed with equal parts of 0.5% bupivacaine.

Surgical Technique
Most surgical approaches for removal of EAC exostoses are through the transmeatal route. 5 - 7 This approach has two disadvantages. It usually results in significant loss of the remaining canal wall skin through damage by the drill, and it does not allow adequate visibility or instrument and drill access to remove the medial portion of the exostotic mass near the tympanic membrane safely. A large sessile anterior exostosis is almost uniformly present in these patients ( Fig. 2-3 ). The approach described here is primarily postauricular and one that maximizes conservation of the canal wall skin and facilitates careful removal of the anterior exostosis, which is usually extremely close to the tympanic membrane.
A curvilinear postauricular incision is made approximately 1 cm behind the postauricular fold ( Fig. 2-4 ). The skin and subcutaneous tissues are elevated anteriorly to the area of the spine of Henle and the bony posterior canal, and a toothed, self-retaining retractor is placed ( Fig. 2-5 ). Locating this area is facilitated by finding the plane of the lateral surface of the inferior border of the temporalis muscle and dissecting in this plane anteriorly to reach the meatus. When this area is reached, the skin overlying the lateral slope of the posterior exostosis is elevated from its surface, and a Perkins bladed tympanoplasty retractor is inserted to hold elevated skin off the surface of the lateral portion of the bony mass ( Fig. 2-6 ).

FIGURE 2-5
Although there may be more than one posterior and anterior exostosis, predominant anterior and posterior exostoses are usually present along with others of lesser mass. These secondary masses may be handled similarly to the primary exostoses, or may be removed directly. To simplify the description here, this operation is divided into two major segments: removal of the posterior exostosis, and removal of the anterior exostosis.

Removal of Posterior Exostosis
By use of a medium-sized cutting burr and an appropriately scaled suction-irrigator, the posterior exostosis is entered along its lateral sloping edge, and the bony removal is progressed medially, keeping a shell of bone over the area being burred anteriorly ( Fig. 2-7 ). The remaining skin over the exostosis medial to the skin elevated earlier is protected from the burr. As this shell becomes thinner, it is advisable to switch to a diamond burr to prevent a sudden breakthrough to the skin, which might occur if one continues with the cutting burr on the excessively thinned bone. The bone removal is continued medially and posteriorly until the estimated normal posterior canal contour and dimension is achieved. As one approaches a medial depth consistent with the posterior annulus of the tympanic membrane (which usually cannot be seen directly at this point), care must be taken to avoid damage to the chorda tympani nerve and the posterior aspect of the tympanic membrane. The surgeon should also keep in mind that some patients’ facial nerve exists lateral to the tympanic annulus at its posteroinferior border. Facial nerve monitoring reduces the possibility of injury to the nerve in a patient unable to tolerate local anesthesia. The thinned bony shell is collapsed, and a small elevator reveals the inside surface of the posterior canal skin that was over the exostosis ( Fig. 2-8 ).
An incision is made midway along the posterior canal skin perpendicular to the long axis of the EAC ( Fig. 2-9 ). The posterior canal skin medial to this incision is positioned onto the new contour of the posterior canal wall ( Fig. 2-10 ). The transmeatal approach is then taken, and incisions are made with a sickle knife superiorly and inferiorly in the canal, extending from the ends of this previous incision laterally to the meatus, and creating a laterally based posterior canal skin flap. This flap is involuted back into the meatal portion of the canal and held there with the Perkins retractor ( Fig. 2-11 ). Attention is turned to the anterior exostosis, which has now been revealed.

FIGURE 2-9

Removal of Anterior Exostosis
By use of a round knife, an incision is made in the skin overlying the anterior exostosis from superior to inferior over the dome of the exostosis and as far medially as can be seen. This incision is connected to the incisions previously made superiorly and inferiorly in the canal that defined the posterior canal skin flap, and this anterior canal flap is elevated laterally ( Fig. 2-12 ). Frequently, the skin of the vascular strip can be left intact if the exostoses do not involve this portion of the canal. By use of a back-angled Perkins tympanoplasty elevator, this laterally based anterior canal skin flap is elevated further to the cartilaginous portion of the anterior canal and is smoothed so as to lie laterally near the posterior canal flap under the retractor ( Fig. 2-13 ).

FIGURE 2-13
With a cutting burr and small suction-irrigator, the anterior exostosis is removed in a manner similar to that of the posterior one, and a thin shell of bone that protects the canal skin is left over the anteromedial portion of the exostosis from the burr ( Fig. 2-14 ). This bone removal is continued to the area of the anterior annulus of the tympanic membrane. The bony shell is collapsed and removed, leaving the intact anterior canal skin ( Fig. 2-15 ). Usually, it is necessary to finish up and smooth an edge of bone that remains at the anterior extent of this dissection to have a smooth contour near the annulus area. To protect the elevated anterior sulcus skin from the burr, a small tympanic membrane–sized piece of silicone elastomer (Silastic) or suture packet foil is placed on the inside surface of the anterior canal skin to hold it against the tympanic membrane during drilling. This prevents the skin flap from getting involved with the burr, and prevents damage to the tympanic membrane that might occur with the burr being used in such close proximity to the membrane. Subsequently, the Silastic is removed, the medial anterior canal skin is placed on the bone, and all skin flaps are folded back into position on the new contours of the bony canal ( Fig. 2-16 ). The medial flaps are packed into place with chloramphenicol (Chloromycetin)-soaked absorbable gelatin sponge (Gelfoam) pledgets, and the postauricular incision is closed with interrupted subcuticular 4-0 polyglactin 910 (Vicryl) suture.
Through the transmeatal route, the laterally based canal skin flaps are packed into place with Gelfoam pledgets. A cotton ball is placed in the meatus, and a mastoid dressing is applied. The patient is returned to the outpatient recovery area and discharged after appropriate recovery.

Postoperative Care
The patient is instructed to remove the mastoid dressing the next morning. The Gelfoam packing is removed using the stereomicroscope on the first office visit 1 week later. Antibiotic-steroid ear drops are prescribed for use twice daily for 1 week and once every 3 days for another 2 to 3 weeks. The second postoperative visit is at 1 month. If there is no evidence of infection, no additional ear drops are recommended. Because most of the patients in whom this procedure is done have had recurrent external otitis, and because time is needed for epithelialization of uncovered bone, the ear canal may remain moist for a longer time than in a typical tympanoplasty. Until the ear canal is completely dry and healed, the patient should be seen every few weeks to inspect and clean debris from the canal as needed.
The canal skin has usually been exposed to numerous infections and has been stretched over the exostoses; it may not be as resilient as normal canal skin. Return to water exposure should be avoided until 1 to 2 months after complete healing has occurred. Frequently, avid surfers return to the water much sooner than instructed, however. Antibiotic drops given after water exposure reduce the risk of early postoperative infection. If the patient is still in the growth years, further repeated exposure of the ear to cold water should be moderated. The bone may reproliferate under these conditions, and further surgery may become necessary. In patients who want to return to frequent surfing or similar water exposure, earplugs should be worn to prevent water entrance. This problem lessens in older surfers because they may be beyond their rapid growth phase, and the economic exigencies of life tend to decrease their frequency of exposure. It is advisable to see the patient annually for 2 years to assess the tendency for the problem to recur, although recurrence is infrequent.

Problems and Complications
Although this procedure is not fraught with serious complications, complications can occur during several aspects of the operation. As the medial extent of the canal is approached in the removal of the posterior exostosis, the course of the chorda tympani nerve must be kept in mind. This portion of the bone removal is done largely without definite landmarks: the surgeon must rely on mental estimation of the distances in arriving at the posterior annulus. The chorda tympani nerve is beneath the bone near this field of dissection and could sustain damage. Also, it is important to remember the course of the facial nerve, which passes posterior and inferior to the canal, although this area is farther from the immediate area of dissection than the chorda tympani nerve. When a burr is used very near the tympanic membrane and the malleus, a diamond burr should be used because it is less likely to run erratically than the cutting burr.

Summary
Exostoses of the EAC usually manifest without attendant compromise in function or clinical disease. When recurrent external otitis or hearing impairment results, however, surgical removal is indicated. Canalplasty has significant advantages over commonly employed transmeatal approaches by maximizing conservation of canal skin and providing surgical access to the anterior medial zone of the canal. Complications are infrequent, but attention to the anatomy of the chorda tympani and facial nerve pathways and careful drill technique in the area of the tympanic membrane are important.
Although surgical techniques involving the EAC have had little attention compared with other reconstructive procedures, they should be in the armamentarium of all otologic surgeons. This technique has proved to be effective for the management of exostoses of the EAC.

MISCELLANEOUS EXTERNAL AUDITORY CANAL CONDITIONS

Medial Third Stenosis
For unknown reasons, some patients develop weeping epitheliitis over the medial third of the EAC. Treatment consists of antibiotic-steroid ear drops that supply broad-spectrum bacterial coverage. Intense treatment, including débridement and the use of topical agents, is usually necessary to bring the process under control. Despite attempts at treatment, progression of the condition may follow a relentless course, resulting in dense fibrosis of the medial segment of the EAC with conductive hearing loss. The mesotympanum and ossicular chain are characteristically spared.
Surgical repair may be necessary when conductive hearing loss produces a functionally significant deficit for the patient. Successful repair is frequently possible, although restenosis may occur, and this possibility should be included in the informed consent. Technically, a postauricular approach is used to allow complete resection of the fibrotic segment medial to noninvolved EAC skin where an incision has been previously created working through a transcanal route ( Fig. 2-17 ). Removal of most of the fibrous layer of the tympanic membrane seems to reduce the chance of postoperative restenosis. Tympanoplasty is performed with a lateral graft or fasciaform technique. Coverage of the resultant exposed bone is mandatory and is provided with a free split-thickness skin graft. The posterior surface of the pinna provides skin of appropriate character within the operative field and can be taken with a No. 10 blade. Skin grafts should overlap the fascia used for tympanic membrane replacement, but should not extend to cover the lateral surface of the reconstructed drum.

FIGURE 2-17
Antibiotic-containing absorbable packing is removed 7 to 14 days later and antibiotic-steroid ear drops are continued for 2 weeks beyond healing to be tapered over time. Close observation postoperatively is necessary to intervene with any signs of restenosis. Recurrent epitheliitis may occur months or years after successful repair.

Collapsing Canal
Stenosis of the cartilaginous portion of the lateral EAC may produce symptoms for some patients. In severe cases, conductive hearing loss may result when closure to less than 2 mm occurs. More commonly, accumulation of debris and a warm, moist environment lead to recurrent external otitis. Although this condition occurs naturally, an iatrogenic component is frequently present. After a postauricular incision, the natural tension of the cartilaginous canal may be unopposed by inadequately reapproximated deep layers such as the mastoid periosteum. Gradual stenosis may occur until symptoms become evident many years after the surgical procedure. Operative repair includes removal of cartilage from the anterior concha and posterior cartilaginous canal from the postauricular area with imbrication of the deep tissue layers overlying the mastoid cortex, similar to imbrication of the subcutaneous musculoaponeurotic system in a facelift. The skin of the ear canal need not be violated in such a procedure. Postoperative stenting for 2 weeks also is helpful in restoring a normal contour to the canal. In some patients with only lateral soft tissue and cartilage involvement, the stenosis may be addressed via a transcanal route, avoiding a postauricular incision.

Keratosis Obturans
Exuberant accumulation of desquamated skin may produce bony erosion and gradual expansion of the bony EAC. 8 The process may progress to the point of erosion into structures adjacent to the canal, such as the temporomandibular joint or mastoid. Erosion lateral to the eardrum may cause loss of support of the fibrous annulus of the tympanic membrane and a characteristic “jump rope sign” inferiorly (which can also be seen after curetting for a stapes procedure more superiorly). Poor epithelial migration has been proposed as the cause of the disorder. Frequent cleaning may retard the process. Cleaning may be much easier if the typically inspissated and adherent material is softened with mineral oil for several days before the clinical appointment. Surgical intervention is rarely indicated, unless severe erosion exposes vital structures.

Osteonecrosis and Osteoradionecrosis of the Tympanic Bone
Radiation and occasionally chronic vasculitis devascularize a portion of the tympanic bone, producing skin loss and bone exposure. The low-grade osteomyelitis can be managed conservatively with topical antimicrobials and mild débridement. Addition of oral antibiotics may improve the chance of healing lesions in the early phases. Frequently, bone involvement progresses, however, and can lead to further skin loss. A culture and sensitivity test is indicated before institution of topicals and later with deterioration of healing to look for resistant organisms. One must always consider malignancy in such a clinical situation, and biopsy is prudent in many cases.
Operative repair is indicated for progression of bone exposure or associated cellulitis or both. Removal of all devitalized bone with the postauricular approach is necessary. The margins of the canal skin are freshened similar to what is performed in a tympanoplasty. Autogenous fascia is placed directly on the freshly drilled bone, and the skin is returned to anatomic position overlying it. The external canal is packed with antibiotic-containing absorbable sponge, which is removed in 7 to 10 days when antibiotic drops are initiated, which are continued until complete healing occurs.

Scutum Defects
Cholesteatoma of the pars flaccida produces bone erosion in many patients. Repair of the EAC is necessary to prevent re-retraction and cholesteatoma formation through the canal defect. Small defects (<2 mm) may be repaired with double-layered fascia. Large defects must be addressed for best long-term patient outcome. Repair may be accomplished with a composite cartilage graft or a fascial sleeve and bone pâté.
Cartilaginous repair is possible with cartilage harvested from the base of the tragus. The perichondrium is left attached to one side of the cartilage, which is carved to match the bony defect similar to the piece of a puzzle. The composite graft is inserted in the defect after elevation of the canal skin and eardrum from the lateral surface of the handle of the malleus. The graft is positioned such that the perichondrium faces the elevated skin and eardrum, and the cartilage extends into the defect ( Fig. 2-18 ).

FIGURE 2-18
Alternatively, bone formation may be stimulated with placement of autogenous bone chips (bone pâté harvested with a microdrill and mixed with antibiotic) within a U-shaped fascial sleeve. 9 This technique requires removal of bone lateral to the heads of the ossicles in the epitympanum and sculpting of the posterior surface of the bony external canal to allow placement of the fascia ( Fig. 2-19 ).

FIGURE 2-19

Post-Traumatic Suture Dehiscence
Temporal bone trauma may produce partial dislocation of either the temporosquamous or the temporomastoid suture lines. When visible on examination, these signs indicate a temporal bone fracture. Rarely, surgical intervention is necessary for entrapped epithelium.

REFERENCES

1. Kroon D.F., Lawson M.L., Derkay C.S., et al. Surfer’s ear: External auditory exostoses are more prevalent in cold water surfers. Otolaryngol Head Neck Surg . 2002;126:499-504.
2. Adams W. The aetiology of swimmer’s exostoses of the external auditory canals and of associated changes in hearing: I. J Laryngol . 1951;65:133-153.
3. Harrison D. Exostosis of the external auditory meatus. J Laryngol . 1951;65:704-714.
4. Fowler E.P.Jr., Osmun P.M. New bone growth due to cold water in the ears. Arch Otolaryngol Head Neck Surg . 1942;36:455-466.
5. Rauch S.D. Management of soft tissue and osseous stenosis of the ear canal and canalplasty. In: Nadol J.B.Jr., Schuknecht H.F., editors. Surgery of the Ear and Temporal Bone . New York: Raven Press; 1993:117-125.
6. Shambaugh G.E.Jr., Glasscock M.E.III. Operations on the auricle, external meatus, and tympanic membrane. In: Shambaugh G.E.Jr., Glasscock M.E.III, editors. Surgery of the Ear . Philadelphia: Saunders; 1980:194-215.
7. Dibartolomeo J.R. Exostoses of the external auditory canal. Ann Otol Rhinol Laryngol . 1979;88(Suppl 61):2-20.
8. Piepergerdes J.C., Kramer B.M., Behnke E.E. Keratosis obturans and external auditory canal cholesteatoma. Laryngoscope . 1980;90:383-390.
9. Althaus S.R. Tympanomastoid surgery: A technique for repairing posterior osseous canal wall defects with autologous temporalis fascia and bone pâté. Otolaryngol Head Neck Surg . 1985;93:529-535.
Chapter 3 Malignancies of the Temporal Bone—Limited Temporal Bone Resection

Moisés A. Arriaga, John P. Leonetti
Videos corresponding to this chapter are available online at www.expertconsult.com .
Although carcinoma of the temporal bone is uncommon and aggressive, the best outcome depends on careful evaluation and planning that result in a complete resection with pathologically clear surgical margins. The most common lesion is primary squamous cell carcinoma of the external auditory canal (EAC); however, direct extension by pinna and salivary gland lesions, metastatic lesions, and adenocarcinomas of the glandular adnexa of the ear canal and pinna are potential lesions. Tumors involve the temporal bone through primary growth, direct extension, and metastatic spread. The consequences of these lesions include morbidity owing to anatomic remodeling, intracranial extension, perineural spread, vascular encasement and dural invasion, and ultimately death.
Historically, carcinoma of the temporal bone was an ominous diagnosis. Advancements in diagnostic and surgical technique have led to greatly improved outcomes. The successful resection of T1 disease has shown survival outcomes of 95%, and the treatment of T2 and T3 disease has shown survivals of 85% when a clear surgical margin is combined with postoperative radiation therapy. 1
A multidisciplinary approach to the diagnosis and treatment of these lesions offers the best possible outcome. Surgery and postoperative radiation represent the principal treatment arms; however, interest in a possible combined role for chemotherapy is increasing. 2 The type of resection needed is determined by the extent of disease. A sound oncologic resection can be achieved through a lateral temporal bone resection, subtotal temporal bone resection, or total temporal bone resection with such additional simultaneous procedures as parotidectomy, facial nerve resection, mandibulectomy, and cervical lymphadenectomy as indicated. When the surgery has been planned, reconstructive options should be explored. Great strides have been made over the past century in the surgical and nonsurgical management of temporal bone neoplasms, but they remain a significant treatment challenge.

TUMOR CONSIDERATIONS
The incidence of tumors of the temporal bone is 200 new cases per year with a frequency of 6 cases per 1 million. Squamous cell carcinoma accounts for 86% of these tumors. Possible etiologic factors include industrial exposure to petroleum-based products, topical disinfectants, and chronic infection. Basal cell carcinoma, adenoid cystic carcinoma, adenocarcinoma, and ceruminous carcinoma occur less frequently. 3 - 5 Tumors of mesenchymal origin are as rare, with rhabdomyosarcoma occurring most frequently. 6 Salivary gland tumors can originate from ectopic rests of salivary tissue within the middle ear (pleomorphic adenoma has been described in that location), or from minor salivary glands within the EAC, but both are rare. 7
Salivary gland tumors are more likely to involve the temporal bone through direct extension from the parotid gland. The anatomic relationship between the temporal bone and parotid gland is responsible for this tendency. The parotid gland is located in close proximity to the mastoid and tympanic portions of the temporal bone. It communicates directly with the cartilaginous EAC through the fissures of Santorini and foramen of Huschke. 8 The stylomastoid foramen, carotid canal, jugular foramen, petrotympanic fissure, and eustachian tube provide avenues for intratemporal extension. In primary temporal bone carcinoma, these anatomic pathways are particularly significant as routes for extension beyond the temporal bone to the adjacent parotid tissue and soft tissue at the base of the skull base.
In rare cases of temporal bone involvement by benign tumors of the parotid gland, symptoms of a facial mass, trismus, or compression of the parapharyngeal space by tumor usually precede temporal bone involvement. 9 Additionally, benign masses have a tendency to compress or remodel adjacent tissue, rather than invade it. This tendency allows for extirpation of a benign parotid neoplasm, in some cases, without requiring a formal temporal bone resection. These lesions can be removed through traditional parotidectomy techniques. Disarticulation of the mandibular condyle, resection of the EAC, or mastoidectomy may be necessary to assist with resection. Pleomorphic adenoma of the tail of the parotid gland can manifest as a subcutaneous mass of the floor of the lateral portion of the EAC. This situation is best managed with combined superficial parotidectomy with mastoidectomy and postauricular canalplasty.
Temporal bone involvement by malignancies of salivary gland origin is aggressive and involves adjacent tissue more readily. Tumors can develop insidiously and relatively asymptomatically, with 75% manifesting with a painless mass and only 6% to 13% manifesting with facial nerve palsy. Symptoms may not be present until after temporal bone invasion has occurred. Pain, dysphagia, and dysphonia can occur after direct invasion of the skull or involvement of the lower cranial nerves at the jugular foramen. Direct extension into bone, fissures, and foramina are potential routes of spread. Mass lesions of the poststyloid parapharyngeal space can traverse the carotid canal and jugular foramen, and neurotrophic tumors, such as adenoid cystic carcinoma, follow the facial nerve as an avenue toward the stylomastoid foramen. Carcinoma of the auricle, anterior scalp, or face that has spread to the intraparotid lymphatics can involve the temporal bone in a similar fashion. In a review of 27 cases of advanced and recurrent parotid neoplasms requiring temporal bone resection, Leonetti and colleagues 9 found that adenocarcinoma occurred most commonly followed by adenoid cystic carcinoma and mucoepidermoid carcinoma.
Malignancies involving the temporal bone present a formidable problem. Without treatment, these lesions result in a high incidence of morbidity and almost certain death. Extension into the otic capsule and petrous bone can result in hearing loss, vestibulopathy, cranial neuropathies, and hemorrhage. Malignant spread into the middle and posterior fossa and extension into the petroclival region or cavernous sinus portend a grim prognosis even with aggressive surgical efforts. In cases of distant metastatic disease, a temporal bone resection may still be indicated for palliation.

HISTORY AND PHYSICAL EXAMINATION
A high index of suspicion by the examiner is necessary for prompt diagnosis and treatment in temporal bone carcinoma. Symptoms of fullness, pain, or trismus without clear explanation or rapid resolution are suspicious for carcinoma. Refractory pain is a hallmark of temporal bone carcinoma. An unexplained mass of the pinna, ear canal, or middle ear should prompt closer evaluation. An insidious symptom of carcinoma that frequently causes a delayed diagnosis is persistent ear drainage. Before the advent of computed tomography (CT), most temporal bone carcinomas were diagnosed after mastoidectomy for presumed chronic otitis media. Such nononcologic intervention frequently resulted in spread of the lesion to adjacent soft tissue structures.

BIOPSY
The only way to diagnose temporal bone carcinoma definitively is by biopsy. Although it is possible to obtain a biopsy specimen of an exuberant lesion of the EAC in the office, we recommend imaging before performing any deep tissue biopsies or removing any soft tissue lesions of the middle ear to prevent inadvertent damage to the carotid, jugular bulb, or facial nerve. False-negative biopsy specimens are an important consideration in temporal bone carcinoma. These lesions are often secondarily infected, and superficial biopsy specimens may reveal only chronic inflammatory changes. If initial biopsy results are negative, we recommend performing deeper tissue biopsies in an operating room to ensure that an adequate sample has been obtained.

DIAGNOSTIC TESTS
Imaging studies and audiometric testing are crucial. Magnetic resonance imaging (MRI) and CT provide accurate information helpful in the staging of disease and determining the extent of resection needed. A preoperative hearing assessment establishes a functional baseline, the need for postoperative middle ear reconstruction when appropriate, and the potential for postoperative deficits. Angiography should be performed in all cases in which the carotid artery is at risk. When carotid resection is anticipated, cerebral blood flow analysis should be used to determine resectability and the need for revascularization. Consideration should also be given to embolization when intraoperative hemorrhage is a concern. When the work-up is complete, proper TNM staging can occur, which provides a basis for discussing treatment options and prognosis with the patient.
The close proximity of vital structures within and adjacent to the temporal bone requires an accurate assessment of the involved anatomy. CT and MRI are indispensable in this regard. The ability of CT to detail bony structures and the superb soft tissue contrast offered by MRI play complementary roles during the work-up. Together, CT and MRI are helpful in establishing tumor extent, the involvement of critical structures, and the best surgical plan. 10
The use of high-resolution CT with fine cuts is recommended. Images with a thickness of 0.625 to 1.25 mm produce the best assessment of the skull base. Direct axial and coronal scans should be obtained. When advanced scanning technologies are available, reconstructed images provide resolution that is equivalent to the original data set. CT is essential to preoperative staging. Arriaga and colleagues 11 showed that CT can “achieve 98% accuracy in predicting pathologic involvement in temporal bone resection specimens.” CT scans have limitations, however. Distinguishing mucosal inflammation from tumor and the extension of tumor without bony erosion remains difficult. In previously operated areas, positron emission tomography (PET) combined with CT has proven useful for distinguishing scar from neoplasm in identifying tumor recurrence and guiding treatment. 12
MRI should be used to examine tumor relative to dura, brain, cerebrospinal fluid, and skeletal muscle. MRI also offers the advantage of imaging in multiple planes. Multiplanar imaging is useful when evaluating lesions that traverse the skull base through direct extent or perineural spread. T1 and T2 fat-saturated sequences should be obtained. T1 images help to determine spatial relationships and bone marrow involvement, whereas T2 images with fat saturation help to delineate tumors that enhance brightly. Postgadolinium T1-weighted images with fat saturation should also be obtained to determine the presence and extent of perineural involvement. This involvement can manifest as foraminal widening or enhancement, replacement of fat density, or increased signal intensity.
Audiologic testing shows the functional status of the middle and inner ear. This information is useful during surgical planning and preoperative patient counseling. Conductive losses may be attributable to the presence of a malignancy in the external or middle ear. Anacusis, tinnitus, and vertigo suggest inner ear involvement. If a reduction or elimination of hearing is anticipated, the patient should be informed in advance. Ossicular chain reconstruction or a bone-anchored hearing aid may be indicated when conductive hearing is sacrificed, but sensorineural hearing is spared.
A four-vessel angiogram with venous runoff should be used in cases of carotid encasement, or when disease mandates dissection of the petrous carotid. Arterial stenosis and contour irregularity at the site of the lesion suggest malignant involvement. Close inspection of the carotid canal on CT and CT angiography is useful for carotid assessment. Temporary balloon occlusion coupled with a cerebral blood flow quantification study helps to determine when carotid sacrifice would be tolerated. Quantification studies include PET, functional MRI, and xenon-CT. Xenon-CT is the best-studied modality. 13 An occlusional cerebral blood flow less than 30 mL/100 g/min requires carotid bypass with prophylactic or intraoperative saphenous grafting or consideration of preoperative carotid stenting. 14 Cerebral blood flow less than 30 mL/100 g/min or the development of neurologic symptoms during the test indicates a high risk of perioperative stroke. These findings either preclude the surgical option or require that prophylactic revascularization be done if surgery is performed. The venous side of imaging must not be ignored. If the torcular Herophili is not patent, permitting venous drainage from the ipsilateral sigmoid-transverse system to the opposite sigmoid-transverse-jugular system, venous infarction may occur. Specific attention should be focused on the adequacy of contralateral venous drainage.

STAGING
The American Joint Committee on Cancer states that a staging system should provide a sound basis for therapeutic planning for cancer patients by describing the survival and resultant treatment of different groups in comparable form. A lack of uniformity regarding preoperative staging and treatment plans made the study of temporal bone cancer difficult. This situation has changed with the demonstration that CT accurately predicts the degree of neoplastic involvement. The supplementation of these observations with clinical findings enabled the formation of a reliable system for staging carcinoma of the EAC. 11 Attempts to modify this system have been made. Moody and coworkers 15 proposed upstaging patients with preoperative facial nerve paralysis or paresis to T4 status when the primary tumor originates in the EAC. They proposed that the extension of tumor through tissue separating the facial nerve and EAC and tumor involving the horizontal segment of the nerve are ominous signs. 15 Although this and other modifications to the original system by Arriaga and colleagues 11 have been suggested, the original system has provided a useful framework for staging these lesions ( Table 3-1 ), and validation of the various systems is still pending.
TABLE 3-1 Arriaga—University of Pittsburgh Tumor Lymph Node Metastasis Staging System Proposed for Squamous Cell Carcinoma of the External Auditory Canal T STATUS T1—Tumor limited to external auditory canal without bony erosion or evidence of soft tissue extension T2—Tumor with limited external auditory canal bony erosion (not full-thickness) or radiographic finding consistent with limited (<0.5 cm) soft tissue involvement T3—Tumor eroding osseous external auditory canal (full-thickness) with limited (<0.5 cm) soft tissue involvement, or tumor involving middle ear or mastoid, or patients presenting with facial paralysis T4—Tumor eroding cochlea, petrous apex, medial wall of middle ear, carotid canal, jugular foramen, or dura, or with extensive (>0.5 cm) soft tissue involvement N STATUS Involvement of lymph nodes is a poor prognostic finding and automatically places patient in advanced stage (i.e., stage III [T1, N1] or stage IV [T2, T3, and T4, N1] disease) M STATUS Distant metastasis indicates poor prognosis and immediately places patient in stage IV
This system can be used to plan the surgical management of the temporal bone when involved secondarily by a cancer of the parotid gland. Although the data are not as clear for salivary gland cancers or pinna lesions extending to the temporal bone as for primary temporal bone lesions, the same staging criteria should be applied to decisions regarding the extent of the anatomic resection and the need for radiation therapy. Patients can be counseled about prognosis and survival based on results with primary cancer arising in the temporal bone, while carefully evaluating the status of the primary source of origin and possible metastases to cervical lymphatics.

SURGICAL TREATMENT
Surgery with postoperative radiation is the principal treatment for temporal bone carcinoma. The surgical procedure depends on the extent of disease because the medial extension of tumor dictates the aggressiveness: partial temporal bone resection, subtotal temporal bone resection, or total temporal bone resection. When tumors involve the temporal bone secondarily through direct extension, temporal bone resection accompanies the surgical management of the primary tumor. Similarly, if parotid gland involvement is likely from a primary temporal bone lesion, parotidectomy is also indicated.
Partial temporal bone resection includes removal of the entire external auditory meatus. It is indicated for cancer of the temporal bone that is limited to the external canal. The facial nerve, stapes, and promontory provide the medial limit of resection. The incisions and soft tissue management for all temporal bone resections depend on the planned management of the pinna. If the pinna is extensively involved and is to be sacrificed, a postauricular incision combined with a preauricular incision permits excision of the pinna—usually the pinna is resected in continuity with the temporal bone resection and parotidectomy specimen. If the pinna can be preserved, a circumferential incision around the soft tissue of the ear canal is performed, and the opening is sutured closed to prevent contamination by tumor spillage during manipulation of the specimen ( Fig. 3-1 ).

FIGURE 3-1
The actual temporal bone resection begins by performing a complete mastoidectomy with accurate identification of the tegmen mastoideum and sigmoid sinus. The course of the facial nerve is dissected by exposing it with careful drilling of the fallopian canal from the lateral semicircular canal to the stylomastoid foramen. An extended facial recess approach provides wide access to the middle ear space by following the fibrous annulus inferiorly as the anterior limit of the dissection. Inferiorly and superiorly, the objective is to bring the dissection into the soft tissues of the glenoid fossa. As the inferior dissection proceeds anteriorly, the surgeon must consider the position of the jugular bulb and carotid artery. Usually the level of the fibrous tympanic annulus is safely lateral to the important vascular structures; however, preoperative CT imaging and intraoperative vigilance are necessary to avoid injury to those vessels. Superiorly, the zygomatic air cells are also dissected, and drilling proceeds superiorly from the antrum toward the zygomatic root, and through the epitympanum to the soft tissue of the temporomandibular joint. Superior to the EAC, the dissection proceeds lateral to the incus and malleus, and the surgeon takes care to avoid middle fossa dura by remaining close to the superior aspect of the EAC.
When the superior and inferior approaches to the glenoid fossa have been completed, the incudostapedial joint is separated; the tensor tympani is cut, and the ligamentous attachments of the ossicles are divided. At this point, the anterior portion of the external canal is its only remaining attachment ( Figs. 3-2 and 3-3 ). This bone is fractured free of the carotid with gentle pressure or tapping with an osteotome. If a chisel is used, it is important to angle the instrument lateral to the carotid so that inadvertent injury of the vessel can be avoided. When the specimen has been removed, and the middle ear has been fully exposed, the eustachian tube is obliterated by filling it with muscle or fascia.

FIGURE 3-3
During the procedure, it is important to remain cognizant of the tumor, taking care to avoid it during the dissection. While drilling the epitympanum, it is important to remain lateral to the geniculate ganglion and medial to the annulus. An intact tympanic membrane should be preserved with the specimen for tumors limited to the EAC; this reduces the likelihood of tumor spillage. When involvement of the facial nerve is present, specimens of the proximal and distal margins should be examined histologically with sufficient tissue resection until the margins are free of tumor.
If the nerve is sacrificed, an interposition graft connects the proximal and distal tumor-free portions of the nerve. The sural nerve and the greater auricular nerve serve as excellent donor sites. The greater auricular nerve is used more often because of its proximity to the surgical field, but if there is malignant lymphadenopathy in the neck, the sural nerve should be used instead. Care is necessary during graft orientation to position the graft so that regenerating fibers are not lost through side branching, orienting the graft with the distal end of the graft in apposition with the proximal segment.
If the parotid gland is involved secondarily from extension of a temporal bone carcinoma or as the primary lesion that has extended to the temporal bone, the involved parotid tissues should be removed in continuity. In contrast to most decision making in surgical otology, the primary objective is an oncologically complete resection with clear margins; functional considerations such as hearing function and facial nerve function are secondary in priority. Tumor involvement of the facial nerve, deep lobe of parotid, or glenoid fossa necessitates a more aggressive resection. Gross tumor involvement of the glenoid is best managed by simultaneous resection of the mandibular condyle and zygomatic root, which facilitates dissection of the intratemporal and parapharyngeal spaces, and prevents the violation of soft tissue attachments between the parotid, temporomandibular joint, and EAC.
Consideration should also be given to management of the cervical lymphatics. Generally, primary temporal bone cancers rarely metastasize to the cervical lymphatics. Secondary involvement of the parotid by a primary temporal bone carcinoma and primary cancers of salivary gland origin have inherently different lymphatic drainage than carcinoma limited to the temporal bone, however, making dissection of the cervical lymph nodes prudent.
Subtotal temporal bone resection is necessary if the middle ear or facial nerves are involved. Involvement of the middle ear space requires a subtotal temporal bone resection. The dissection extends medially into the otic capsule and petrous portions of the temporal bone to obtain negative margins. The medial extent of dissection is defined by the internal auditory canal. At this extent of tumor involvement, adherence to the ideal of an en bloc resection is affected by the three-dimensional anatomy of the temporal bone. The technical steps of a subtotal temporal bone resection depend on the exact location of tumor involvement, but may result in piecemeal removal of the most medial extent of tumor with frozen section control.
It is most practical to begin with an en bloc partial temporal bone resection, and then adjust the resection medially. If resection of the jugular bulb or extensive carotid dissection is planned, control of the internal carotid artery and jugular vein is obtained inferiorly. Anteriorly, the vertical portion of the petrous internal carotid artery is identified by drilling away the cochlea and hypotympanum. When resection of the sigmoid sinus and jugular bulb is necessary, careful planning of handling these vascular structures limits unnecessary blood loss. The sigmoid must be occluded proximally, and the jugular vein must be ligated distally. If dural entry is planned, the sigmoid can be ligated with sutures by exposing the dura anterior and posterior to the sigmoid sinus. Alternatively, bone can be preserved from the midportion of the sigmoid and proximally toward the sigmoid-transverse junction.
Absorbable knitted fabric (Surgicel) can be packed extraluminally to occlude the sinus. Brisk bleeding from the inferior petrosal sinus and condylar vein occurs with opening of the jugular bulb, and the surgeon should be prepared with additional Surgicel packing. Although the initial packing involves significant material, the surgeon can gradually remove most of the packing leaving only the small portions occluding the openings of the inferior petrosal sinus and condylar vein in the bulb, and limit the risks to the lower cranial nerves in the pars nervosa of the jugular bulb from excessive packing and pressure. An additional strategy to prevent bleeding from the jugular bulb is preoperative coil embolization of the openings of the inferior petrosal sinus and condylar vein. 16 The final resection margins proceed along the floor of the middle fossa connecting the glenoid fossa, internal auditory canal, and posterior-superior mastoid.
When the cancer has progressed beyond the limits of a subtotal temporal bone resection, a total temporal bone resection may be indicated. This topic is addressed in more detail in Chapter 4 . Total temporal bone resection is rarely performed because of the high level of morbidity and a lack of well-documented survival benefit except in specific circumstances, such as verrucous squamous carcinoma, in which the aggressiveness is entirely local and indolent. The surgery involves freeing the temporal bone at the petrous apex. Before extirpation, the intratemporal portion of the internal carotid artery must be dissected to the foramen lacerum, and the internal jugular vein must be ligated. Sacrifice or reconstruction of the internal carotid artery may be performed based on the results of preoperative testing.
A subtemporal craniotomy is performed exposing the transverse sinus. The dura covering the cerebellum is incised, and the transverse sinus is ligated and divided near the superior petrosal sinus, being particularly careful to avoid injury to the vein of Labbé. The tentorium is divided sharply along the petrous bone in a plane superior and parallel to the superior petrosal sinus. The seventh and eighth cranial nerves are divided at the internal auditory canal. With the cerebellum retracted medially, an intradural incision is used to divide CN IX, X, and XI, and free the specimen at its posterior dural attachment. When the surrounding structures have been freed, a chisel is placed in the foramen ovale and directed posteriorly in a trajectory lateral to foramen lacerum; this frees the temporal bone at its apex.

RECONSTRUCTION
Reconstructive options should be explored preoperatively, but as in all oncologic surgeries, the reconstructive plan must never compromise the completeness of oncologic resection. Consideration should be given to the probable need for postoperative radiation, which should begin within 6 weeks of the resection. Additional concerns include cosmesis and the durability of the repair. Intraoperative findings might dictate a more complex reconstruction than anticipated. Careful planning improves the preparation for various potential defects. We prefer to involve a head and neck reconstructive surgeon for this portion of the procedure to avoid reconstructive consideration influencing the adequacy of the oncologic resection.
Partial temporal bone resections may be reconstructed with split-thickness skin grafts lining the mastoid and middle ear and sutured to the remaining soft tissue of the meatus. The graft should be placed to line the ear canal and mastoid bowl. Its medial extent can be carefully draped over the oval window or stapes remnant. Reconstruction of the ossicular chain can be done later. This reconstruction may require frequent postoperative care, however, and delayed healing can affect the timing of postoperative radiation. Vascularized temporal-parietal fascia or postauricular soft tissue (Palva flap) can be used to provide a vascularized bed for skin graft healing. Alternatively, the cavity can be obliterated with temporalis muscle or another rotational flap, such as a pectoralis major or sternocleidomastoid flap; however, this most likely would preclude reconstruction of the conductive hearing mechanism ( Figs. 3-4, 3-5, and 3-6 ).
Subtotal temporal bone resection and total temporal bone resection require added soft tissue to obliterate dead space, prevent the leakage of cerebrospinal fluid, and provide protection against complications related to radiation therapy, the most serious of which is osteoradionecrosis. Smaller wounds involving resection of the pinna and external canal may be closed by a posterior scalp or cervicofacial advancement flap. If additional bulk is needed, a muscle or myocutaneous flap can be rotated on a vascularized pedicle, or inset via microvascular anastomosis.
Smaller defects may be amenable to closure using a temporalis muscle rotational flap. A trapezius, latissimus, or pectoralis major muscle rotational flap may become necessary as the size of the defect increases. Extensive defects may require a rectus abdominis muscle or perforator-based adipose free flap for closure. The arterial and venous anastomosis should be sutured to the external carotid artery and jugular vein. In wounds requiring additional skin, a split-thickness skin graft can be placed over the muscular portion of the reconstructive flap. If dura is resected, the dural defect and eustachian tube must be obliterated. This obliteration is accomplished with abdominal fat or free tissue transfer, and serves to shield the central nervous system from environmental insult.

COMPLICATIONS
Hemorrhage is a common risk in temporal bone resection. The otologic surgeon should be very familiar with the different techniques to control unplanned venous bleeding from the sigmoid sinus, superior petrosal sinus, and jugular bulb. With the sigmoid sinus, gentle pressure with absorbable gelatin sponge (Gelfoam) or Cottonoid is usually adequate. Great care must be exercised to not allow packing to dislodge within the lumen of the sigmoid sinus, unless the jugular vein has already been ligated in the neck. The jugular bulb does not respond to the same hemostatic strategies as the sigmoid sinus because the vessel wall is much thinner. Venous bleeding can be responsible for massive blood loss, and losses of 2500 mL can be encountered. As mentioned previously, excessive bleeding most commonly occurs at the inferior petrosal sinus, but this bleeding can be controlled with proper technique. The excessive use of packing at the jugular foramen can result in injury to CN IX, X, and XI, so this should be done with caution. 17
Injury to the carotid artery should be managed with direct pressure and placement of temporary clips proximal and distal to the insult. Systemic and intra-arterial heparin should be given. The injury should be repaired with 8-0 monofilament suture. If minor leaks persist after closure, topical hemostatic agents can be applied. If successful repair of the vessel cannot be achieved, the preoperative balloon occlusion test should be used to guide management. Vascular surgery and neurosurgical consultation are imperative. If there is significant carotid involvement, preoperative stent placement has been suggested to avoid vascular complications. 14
Facial nerve sacrifice or excessive manipulation of the nerve can result in facial asymmetry and inadequate eye closure. During the immediate postoperative period, the eye should be protected with lubrication, use of a moisture chamber, or mechanical lid closure. If the nerve is sacrificed, an interposition graft using the ipsilateral greater auricular nerve or sural nerve should be performed. If the greater auricular nerve is unavailable, the sural nerve can be used instead. Successful nerve interposition can restore function to a House-Brackmann scale grade III, but may take 12 to 18 months to occur. Placement of a gold weight implant or spring, lateral tarsorrhaphy, or tensing of the lower eyelid may be necessary during the reinnervation period. Facial-hypoglossal anastomoses can also help restore facial function. When lower cranial nerve deficits exist, this should be done with caution. A loss in the function of CN XII can have devastating consequences on an already impaired swallowing apparatus.
Tumor involving the jugular foramen may result in preoperative or postoperative paresis or palsy of CN IX and X. Such lesions can manifest in the airway and cause nutritional difficulties. Temporary or permanent tracheotomy and the placement of a gastrostomy tube may be necessary to compensate for the associated deficits. The combination of an insensate supraglottis, vocal fold motion impairment, and inadequate swallow reflex can result in aspiration with fatal consequences. Vocal fold medialization may restore safe deglutition. In more severe cases of swallowing or laryngeal dysfunction, a laryngotracheal separation may be necessary.
If dura has been excised or violated, the resulting defect must be repaired immediately. Primary closure should be instituted whenever possible. If necessary, the dural defect should be obliterated with fat, fascia, or free tissue transfer. Postoperative leakage of cerebrospinal fluid can be managed conservatively for 7 to 10 days with appropriate measures. Bed rest, elevation of the head of the bed, stool softeners, and placement of a lumbar drain can be useful in reducing intracranial pressure. 18 If the leak persists beyond this period, the wound should be explored surgically, and closure of the dural defect should be reattempted.

RADIATION
Plans for the use of postoperative radiation should be made during the preoperative work-up. The use of adjuvant radiation should be anticipated whenever the middle ear is involved with disease. If intraoperative findings confirm the need for radiation, it should be administered in a timely fashion. Radiation therapy should not be delayed, or withheld in lieu of a recurrence, because this can result in decreased therapeutic efficacy. Closure of the surgical defect with viable, durable tissue is necessary to prevent development of osteoradionecrosis, which can be a devastating and sometimes fatal complication. In addition, careful postoperative hygiene and maintenance (cleaning and débridement with otomicroscopy) of the reconstructed area is essential to reduce likelihood of chronic infection that can predispose to osteoradionecrosis. Dosages typically range from 5000 to 6000 rad, and fields should be designed to include the area of resection and involved nodal groups.
The rarity of temporal bone malignancy makes the study of treatment protocols difficult, but encouraging results have been reported. T1 lesions successfully treated with surgery alone have a 95% 5-year survival, with no benefit from the addition of radiation. Some T2 and T3 lesions treated with radiation after complete surgical removal have shown an 85% 5-year survival. The 5-year survival of patients with more advanced lesions decreases to less than 50%. Cancer requiring a total temporal bone resection carries a dismal prognosis, with a 50% 1-year survival and reports of 0% 2-year survival. 5, 6, 19

CHEMOTHERAPY
The role of chemotherapy in the treatment of temporal bone malignancy has not been determined, but interest in its use is growing. Because of the low incidence and the histologic diversity of temporal bone malignancies, few meaningful studies have been conducted. Temporal bone malignancies of salivary gland origin, similar to salivary malignancies in other sites, do not usually respond to currently available chemotherapeutic agents. Squamous cell carcinoma of the temporal bone may respond to platinum-based agents, but typically the results are not durable, and other modalities must be used. For these reasons, most patients with temporal bone cancer are treated with surgery, radiation, or a combination of the two, and chemotherapy is usually reserved for palliation in patients with distant metastases or recurrences.
Nakagawa and coworkers 2 published data that suggest a possible role for preoperative chemoradiation therapy in the treatment of T3 and T4 squamous cell carcinoma when staged according to the Arriaga system. The radiation-enhancing effect of chemotherapy may be useful in reducing the tumor burden and improving control of the surgical margin. Nakagawa and coworkers 2 showed improved survival rates for T4 lesions not involving dura, pyramidal apex, carotid canal, or lymph nodes that are as good as survival rates in patients with T3 lesions. The poor outcomes associated with the treatment of advanced temporal bone malignancy mandate further investigation into the possible role of chemotherapy as a treatment modality.

REHABILITATION OF LOWER CRANIAL NERVE DEFICITS
The details of surgical rehabilitation of lower cranial nerve deficits are discussed elsewhere. Generally, in limited temporal bone resection, the function of CN IX, X, XI, and XII can be preserved. Their sacrifice has significant quality-of-life and function implications for speech, voice, and swallowing. In addition to involvement of a head and neck surgeon with expertise in laryngeal restoration, thyroplasty and palatal rehabilitation, team members should include speech-language pathologists with experience in diagnosing and treating lower cranial nerve dysfunction. Strategies such as modified barium swallow and flexible endoscopic evaluation of swallowing are important components of a comprehensive assessment.
The impact of radiation sequelae such as xerostomia on swallowing should not be underestimated. 20 Nonetheless, postoperative radiation is a crucial part of the comprehensive management of a patient with temporal bone carcinoma.

CONCLUSION
Successful management of temporal bone carcinoma depends on adequate pretreatment evaluation and staging. Most patients require limited temporal bone resection followed by postoperative radiation. In contrast to other otologic procedures, the management priorities in malignancy require that the otologic surgeon should ensure that the resection is oncologically sound, and consider hearing, vestibular, and facial function as secondary priorities.

REFERENCES

1. Kinney S.E., et al. Malignancies of the temporal bone: Limited temporal bone resection. In: Brackmann D.E., Shelton C., Arriaga M.A., et al, editors. Otologic Surgery . Philadelphia: Saunders, 1994.
2. Nakagawa T., Kumamoto Y., Natori Y., et al. Squamous cell carcinoma of the external auditory canal and middle ear: An operation combined with preoperative chemoradiotherapy and a free surgical margin. Otol Neurotol . 2006;27:242-249.
3. Moffat D., De la Cruz A., Evans P.H.R. Management of tumours of the temporal bone. In: Evans P.H.R., editor. Principles and Practice of Head and Neck Oncology . London: Martin Dunitz, 2003.
4. Brackmann D.E., Arriaga M.A. Posterior fossa skull base neoplasms. In Cummings C., Fredrickson J., Krause C., Schuller D., editors: Cummings Otolaryngology–Head and Neck Surgery , 4th ed, St. Louis: Mosby, 2005.
5. Prasad S., Janecka I.P., et al. Malignancies of the temporal bone: Radical temporal bone resection. In: Brackmann D.E., Shelton C., Arriaga M.A., editors. Otologic Surgery . Philadelphia: Saunders, 1994.
6. Marsh M.M., Jenkins H.A. Temporal bone neoplasms and lateral cranial base surgery. In Cummings C., Fredrickson J., Krause C., Schuller D., editors: Cummings Otolaryngology–Head and Neck Surgery , 4th ed, St. Louis: Mosby, 2005.
7. Peters B.R., Maddox H.E., Batsakia J.G. Pleomorphic adenoma of the middle ear and mastoid with posterior fossa extension. Arch Otolaryngol Head Neck Surg . 1988;114:676-678.
8. Prasad M., Kraus D. Acinic cell carcinoma of the parotid gland presenting as an external auditory canal mass. Head Neck . 2004;26:85-88.
9. Leonetti J.P., Smith P.G., Anand V., et al. Subtotal petrosectomy in the management of advanced parotid neoplasms. Otolaryngol Head Neck Surg . 1993;108:270-276.
10. Glenn L. Innovations in neuroimaging of skull base pathology. Otolaryngol Clin North Am . 2005;38:613-629.
11. Arriaga M., et al. Staging proposal for external auditory meatus carcinoma based on preoperative clinical examination and computed tomography findings. Ann Otol Rhinol Laryngol . 1990;99:714-721.
12. Shintani S.A., Foote R.L., Lowe V.J., et al. Utilizing of PET/CT imaging performed early after surgical resection in the adjunct treatment planning from head and neck cancer. Int J Radiat Oncol Biol Phys . 2008;70(2):322-329.
13. Janecka I.P., Sekhar L.N., Horton J.A. General blood flow evaluation. In: Cummings C.W., Fredrickson J., Krause C., Schuller D., editors. Otolaryngology–Head and Neck Surgery Update II . St. Louis: Mosby–Year Book; 1990:54-63.
14. Sanna M., Khrais T., Menozi R., et al. Surgical removal of jugular paraganglioma after stenting of the intratemporal internal carotid artery: A preliminary report. Laryngoscope . 2006;116:742-746.
15. Moody S.A., Hirsch B.E., Myers E.N. Squamous cell carcinoma of the external auditory canal: An evaluation of a staging system. Am J Otol . 2000;21:582-588.
16. Carrier D., Arriaga M.A., Dahlen R. Preoperative embolization of anastomosis of the jugular bulb: A new adjuvant in jugular foramen surgery. AJNR Am J Neuroradiol . 1997;18:1252-1256.
17. Brackmann D.E., Arriaga M.A., et al. Surgery for glomus and jugular foramen tumors. In: Brackmann D.E., Shelton C., Arriaga M.A., editors. Otologic Surgery . Philadelphia: Saunders, 1994.
18. Nuss D.W., Constantino P.D. Cerebrospinal fluid leaks: Comprehensive diagnosis and management. Otolaryngol Head Neck Surg . 1993;108:539.
19. Pensak M., Willging J.P. Tumors of the temporal bone. In: Jackler R., editor. Neurotology . St. Louis: Mosby, 1994.
20. Koukourakis M.I., Danieldis V. Preventing radiation induced xerostomia. Cancer Treat Rev . 2005;31:546-554.
Chapter 4 Malignancies of the Temporal Bone—Radical Temporal Bone Resection

Sanjay Prasad, Ivo P. Janecka
Primary malignancies of the temporal bone were first recognized in the late 18th century and histologically first confirmed in the 1850s. These lesions are uncommon, with only 250 cases having been reported in the English literature by 1974. 1 The overall prevalence in the general population is 6 cases per 1 million. 2 Because of their infrequent occurrence, these tumors are often misdiagnosed and treated as chronic external otitis or chronic mastoiditis. They are usually discovered at a later stage, when more radical treatment is required. The infrequent occurrence of the disease poses a challenging obstacle to any attempt at a clinical study regarding treatment.
Secondary malignancies of the temporal bone from regional spread of parotid cancers occur far more commonly. The fissures of Santorini provide a conduit for regional spread through the anterior cartilaginous ear canal.
Basal cell carcinoma and squamous cell carcinoma are the more common malignancies to affect the temporal bone. Basal cell carcinoma is thought to occur secondary to actinic exposure, and commonly involves the external ear or ear canal or both. Squamous cell carcinoma can arise primarily from the external canal or middle ear, or both, or spread into the temporal bone from a primary lesion in the parotid gland. In contrast to squamous cell carcinoma of the upper aerodigestive tract, squamous cell carcinoma of the temporal bone is not related to tobacco or alcohol use. Predisposing factors to these lesions are few. Chronic infection within the temporal bone is the most commonly cited factor.
Adenoid cystic carcinoma can arise either from the ear canal and middle ear or from the parotid gland and spread secondarily into the temporal bone. These lesions have a tendency toward perineural spread. Ceruminous adenoma, adenocarcinoma, and mucoepidermoid carcinoma are other lesions that can affect the temporal bone.
Regional spread to cervical nodes and distant metastases are uncommon. Depending on the extent of the disease, radical resection coupled with radiation treatment offers the best treatment. The efficacy of chemotherapy has not been clearly established, and it may play a role only in recalcitrant disease.
Radical temporal bone resection refers to one of three operations that can be offered to patients with this disease. A lateral temporal bone resection (LTBR) refers to the removal of the external auditory canal (EAC), tympanic membrane, malleus, and incus. Subtotal temporal bone resection (STBR) refers to the additional removal of the otic capsule, and total temporal bone resection (TTBR) refers to the additional removal of the petrous apex with or without the carotid artery.
LTBR is well accepted for lesions that involve the EAC or tympanic membrane or both. Controversy arises in defining the optimal management of neoplasms that invade the mesotympanum. Some authors advocate LTBR with gross removal of middle ear disease followed by radiation therapy, whereas others prefer more radical surgery (STBR or TTBR), followed by radiation therapy. When the tumor has invaded the petrous apex, involvement of dura mater, brain parenchyma, or internal carotid artery (ICA) is usually present.
This chapter focuses on preoperative diagnostic evaluation, the surgical techniques of STBR and TTBR, postoperative management, and potential complications. Rehabilitation and adjuvant treatment for recalcitrant disease are briefly discussed. Finally, we present a literature review of squamous cell carcinoma of the temporal bone in an effort to define the optimal management for middle ear disease and discuss the prognostic significance of dural, brain, and ICA involvement.

DIAGNOSTIC EVALUATION
The diagnostic evaluation begins with a thorough history and physical examination, with special emphasis on the chronology of developing cranial neuropathies. The pathway of tumor spread occasionally can be deduced from a careful history. Facial nerve function, hearing, and balance function should be carefully documented. Examination includes palpation of the parotid gland and cervical lymph glands for the presence of local spread and regional metastases. Patients should be questioned and tested for temporal lobe signs (e.g., memory loss, dysphasia, left-sided neglect, hemiparesis, and olfactory hallucinations) and cerebellar signs (e.g., ocular dysmetria, truncal ataxia, nystagmus, and dysdiadochokinesia).
Imaging allows determination of the extent of tumor involvement. High-resolution axial and coronal computed tomography (CT) imaging at 1.5 mm thickness can identify areas of bony involvement. Enhanced and unenhanced magnetic resonance imaging (MRI) can determine intracranial involvement.
Histologic confirmation of the lesion is essential in further treatment planning. Biopsy specimens of lesions involving the EAC or periauricular skin can be easily obtained. Needle aspiration biopsy of parotid lesions can also be performed.
Angiography is used when involvement of the major vessels is suspected on preoperative imaging, or when surgical exposure of the petrous carotid artery is anticipated. The venous phase of the study can provide important information regarding blood flow through the dural venous sinuses. Embolization of feeding vessels is rarely required because most lesions are relatively avascular.
Cerebral blood flow evaluation is indicated when involvement of the ICA is present. Patency of the anterior and posterior communicating arteries on angiography is an inadequate evaluation for collateral flow. Our current method of preoperative carotid artery testing is described. 3 A 30-minute temporary balloon occlusion of the ICA allows identification of patients who would most likely tolerate carotid artery sacrifice. Transfemoral introduction of a nondetachable intravascular balloon, inflated in the ICA, is performed in the patient while sensory, motor, and higher cortical functions are assessed.
Patients who develop a neurologic deficit during temporary occlusion are at high risk for stroke after carotid sacrifice. Preoperative or intraoperative extracranial-to-intracranial arterial bypass should be considered. Repeating the temporary balloon occlusion before surgical extirpation should also be considered. Conservative treatment options should also be discussed with these patients.
Patients who tolerate a 30-minute balloon occlusion of the ICA are at low risk for development of a stroke, provided that a long “distal” stump is avoided. Permanent ICA occlusion can be performed angiographically. Hypotension and hypovolemia in the perioperative period should be avoided if permanent ICA occlusion is performed.

PREOPERATIVE PREPARATION
Preoperative preparation sets the stage for the operative and postoperative course. The evening before surgery, the operative site is shampooed and scrubbed with hexachlorophene. Intravenous phenytoin or phenobarbital and cefuroxime are used for prophylactic anticonvulsant and antibiotic coverage. To facilitate intraoperative cranial nerve monitoring, short-acting neuromuscular blocking agents are used only for the induction of anesthesia, and not during the operation.
On the morning of the operation, sequential compression stockings are placed on both legs to help decrease the incidence of thromboembolic disease. After insertion of a central venous catheter and an arterial line, the patient is intubated, and the endotracheal tube is secured. The operating table is turned 90 degrees from the anesthesiologist, giving him or her access to the contralateral arm. The head is positioned on a horseshoe (Mayfield) head holder to allow repositioning during the course of the operation. Temporary bilateral tarsorrhaphies are placed to prevent corneal abrasions. The operative site, which includes the temporal fossa, lateral half of the face, postauricular area, neck, and ipsilateral thigh and lower leg (for the potential use of tensor fascia lata and sural nerve), is shaved and scrubbed with an iodine-based solution. Bipolar facial electromyographic electrodes are placed in areas where facial function exists.

SURGICAL PROCEDURE
Incisions vary according to the extent of the tumor ( Fig. 4-1 ). For lesions contained within the temporal bone, a C-shaped incision extending from the temporal fossa postauricularly into the neck is used. A blind-sac closure of the EAC helps contain the specimen. When tumor invasion of the conchal cartilage or periauricular skin is suspected, an appropriate skin island is incorporated into the overall design. The EAC skin is sutured shut to avoid tumor spillage. The outline of the incisions should preserve the blood supply to the remaining auricle. The anterior and posterior skin flaps are elevated ( Fig. 4-2 A). The superficial temporal fat pad is elevated with the anterior skin flap in a subperiosteal plane over the zygomatic arch. The superficial temporal and middle temporal arteries are ligated.

FIGURE 4-1 Incisions vary according to whether the tumor is contained in the temporal bone.
FIGURE 4-2. A, The facial nerve can be divided peripherally at the distal branches or centrally at the facial nerve trunk, depending on involvement of the parotid gland. B, After osteotomies and removal of the zygomatic arch and mandibular segments, dissection in the infratemporal fossa continues. EAC, external auditory canal.
The facial nerve can be handled differently, depending on tumor invasion of the parotid gland. When the gland is involved, peripheral branches of the facial nerve are identified with the help of the facial nerve monitor and then divided. The stumps of the anterior segments are secured to the anterior skin flap. The entire parotid gland is dissected off the masseteric fascia, provided that the latter is free of disease, and mobilized posteriorly, while the attachment to the EAC is maintained. When the parotid gland is suspected to be free of tumor, the facial nerve trunk is located in the usual manner at the tympanomastoid suture and divided. The parotid gland, along with the distal stump of the facial nerve, is dissected free of the EAC and mobilized anteriorly off the masseteric fascia.
The jugulodigastric region is explored, and cervical lymph nodes are sent for frozen section pathologic analysis. Regional metastases determine the need for a formal cervical lymphadenectomy. The ninth cranial nerve, the greater auricular nerve, or cervical cutaneous nerves can be used as cable grafts for facial nerve reconstruction. CN IX, X, XI, and XII; the internal jugular vein; and the external carotid artery and ICA are dissected in an inferosuperior direction toward the temporal bone. The sternocleidomastoid and digastric muscles are detached from their attachment to the mastoid.
The masseter is detached from the zygomatic arch, allowing exposure of the zygoma and mandible. Zygomatic and mandibular osteotomies (see Fig. 4-2 A) can then be performed. The meniscus of the temporomandibular joint is separated from the glenoid fossa, and the chorda tympani nerve emerging from the petrotympanic fissure is divided. The stylomandibular and sphenomandibular ligaments are divided and allow removal of the mandibular segment ( Fig. 4-2 B). The temporalis muscle is elevated in a subperiosteal fashion and reflected inferiorly. The temporalis muscle must be separated from the lateral pterygoid muscle, and care should be taken not to injure the deep temporal arteries supplying blood to the temporalis muscle. The lateral and medial pterygoid muscles are resected either en bloc with the specimen or separately, depending on tumor invasion.
In a subperiosteal manner, the contents of the infratemporal fossa are elevated off the floor of the middle fossa to expose the middle meningeal artery and vein in the foramen spinosum and the mandibular division of the trigeminal nerve in the foramen ovale. The contents of the foramen spinosum are bipolarly coagulated and divided. Frequently, the venous plexus of the foramen ovale requires bipolar coagulation and packing with oxidized cellulose. The lesser petrosal nerve can be seen emerging from the innominate canal, on its way to the otic ganglion.
The stylohyoid, stylopharyngeus, and styloglossus muscles (Riolan’s bouquet) are detached from the styloid process, which is then rongeured away. The branches of the external carotid artery are dissected in the infratemporal fossa. The anterior tympanic and deep auricular branches of the internal maxillary artery are often divided before identification, and may require bipolar coagulation. The internal maxillary artery is preserved up to the branches of the deep temporal artery. When the internal maxillary artery must be sacrificed, brisk backflow from the anterior stump indicates that the temporalis muscle may derive its blood supply from reversed flow via the pterygoid system. If brisk backflow is not observed, the temporalis muscle cannot be relied on to reconstruct the surgical defect, and microvascular free flap options must be considered. The cartilaginous eustachian tube is divided, and the anterior end is sutured closed to prevent postoperative cerebrospinal fluid rhinorrhea ( Fig. 4-3 A).

FIGURE 4-3 A, Further dissection in the infratemporal fossa allows division and ligation of the eustachian tube and exposure of the petrous carotid artery. B, The petrous carotid artery is dissected further according to whether a subtotal or total temporal bone resection is performed. ICA, internal carotid artery; STBR, subtotal temporal bone resection.
The ICA is dissected toward the carotid canal, and care is taken not to injure CN IX, which crosses its anterior surface. Kerrison rongeurs are used to uncover the vertical and horizontal petrous segments of the carotid artery ( Fig. 4-3 B). Occasionally, bleeding from the pericarotid venous plexus requires bipolar coagulation. The caroticotympanic artery is also divided when the petrous carotid artery is separated from the specimen. The extent of petrous carotid mobilization depends on whether STBR or TTBR is performed. When STBR is performed, the vertical petrous carotid artery is mobilized from the carotid foramen and canal. When TTBR is performed, the vertical and horizontal petrous carotid artery is mobilized out of the carotid canal to the foramen ovale.
A temporal craniectomy is performed, and the intracranial portion of the middle meningeal vessels is coagulated (see Fig. 4-3 B). The patient is hyperventilated to keep the P co 2 at 25 mm Hg for adequate brain relaxation. Mannitol and furosemide can improve brain relaxation. Subtemporal dural elevation proceeds in a posteroanterior direction. The greater superficial petrosal nerve and accompanying petrosal artery are coagulated and divided to lessen traction on the geniculate ganglion. The lesser petrosal nerve and superior tympanic artery are similarly divided. Subtemporal dural elevation proceeds as far medially as possible to expose the superior petrosal sinus. When carcinomatous involvement of the middle fossa dura is suspected, an intradural approach keeps the involved dura attached to the specimen.
The extent of the mastoidectomy depends on whether tumor is present in the mastoid air cells. Care is taken to avoid exposure of tumor in the mastoid. In this case, the confluence of the transverse, sigmoid, and superior petrosal sinuses is decorticated to expose posterior fossa dura on either side of the sigmoid sinus. When posterior fossa dural involvement is suspected, a presigmoid intradural approach with gentle retraction of the cerebellum ( Fig. 4-4 A) allows exposure of the vessels and nerves in the cerebellopontine angle that are keeping the involved dura attached to the specimen. When the mastoid air cells are thought to be free of tumor, a translabyrinthine approach to the IAC is used ( Fig. 4-4 B). The anterior inferior cerebellar artery is retracted after the labyrinthine artery is bipolarly coagulated and divided. The superior and inferior vestibular nerves, cochlear nerve, facial nerve, and nervus intermedius (nerve of Wrisberg) are divided. A segment of the proximal facial nerve stump can be sent for frozen section pathologic examination if it is suspicious for carcinoma. The dome of the jugular bulb must be separated from the specimen when the dural venous sinuses are spared.

FIGURE 4-4 A ( left and right ), When tumor is thought to be present in the mastoid, a presigmoid intradural approach (enlarged view on the right) to the porus acusticus is used. B, When the mastoid is thought to be free of tumor, a translabyrinthine approach allows exposure of the internal auditory canal. AICA, anterior inferior cerebellar artery; ICA, internal carotid artery.
The surgical technique from here varies according to whether the dural venous sinuses or the ICA is preserved. When both are preserved, and STBR is being performed, the bone between the bony canal of the carotid artery at the junction of the vertical and horizontal segments ( Fig. 4-5 A) and the fundus of the IAC is removed with a high-powered drill. Separation of the petro-occipital synchondrosis sometimes requires insertion of an osteotome just above the jugular bulb. This step releases the specimen en bloc from attachment to the clivus. Packing oxidized cellulose intraluminally toward the cavernous sinus controls bleeding from the inferior petrosal sinus.

FIGURE 4-5 A, A drill, inserted at the junction of the vertical and horizontal petrous carotid canal, is aimed toward the fundus of the internal auditory canal (IAC) to allow removal of the subtotal temporal bone specimen. B, A drill, inserted at the horizontal petrous carotid canal just posterior to the foramen ovale, is directed slightly posteriorly to avoid entry into the foramen lacerum. This releases the total temporal bone specimen.
FIGURE 4-6. When the dural venous sinus is sacrificed, the internal jugular vein is mobilized toward the cranial base as the sigmoid sinus is intraluminally packed.
When both vascular structures are preserved, and TTBR is being performed, the bone between the posterior edge of the foramen ovale and spheno-occipital synchondrosis is removed ( Fig. 4-5 B). The petro-occipital synchondrosis may require an additional osteotomy before the specimen is delivered.
When the dural venous sinuses are sacrificed, the internal jugular vein is double ligated in the upper cervical area and mobilized toward the jugular bulb ( Fig. 4-6 ). The superior petrosal sinus and sigmoid sinus are divided and intraluminally packed with oxidized cellulose. Care is taken not to overpack the sigmoid sinus proximally to avoid obstruction of the vein of Labbé; this can cause hemorrhagic necrosis of the temporal lobe. Similarly, excessive packing of the inferior petrosal sinus can lead to cavernous sinus thrombosis. The sigmoid sinus is opened toward the jugular bulb and resected. Intraluminal rather than extraluminal packing of the inferior petrosal sinus is preferred to avoid injury to cranial nerves traversing the jugular foramen.
The results of the temporary balloon occlusion determine whether the ICA can be safely resected. When the patient is at high risk for stroke after sacrifice of the ICA, the patient requires revascularization to ensure adequate cerebral blood flow. An extracranial-to-intracranial arterial bypass, such as a superficial temporal artery–to–middle cerebral artery bypass, must be considered.
The middle and posterior fossa dura is inspected for carcinomatous involvement. Any involved areas are resected, and margins are sent for frozen section pathologic examination. The temporal lobe and cerebellum are also examined, and limited involvement of the inferior temporal gyrus and cerebellum can be resected. When intradural hemostasis is achieved, the dura is closed in a watertight manner using pericranium, fascia lata, or cadaveric dura.
Reconstruction includes restoration of facial nerve continuity and closing the dead space after tumor resection. The greater auricular nerve, cervical cutaneous nerve, or CN XI can be used as a cable graft from the facial nerve in the IAC to the peripheral branches. When greater length is required, the sural nerve can be harvested from the lower leg. Use of vascularized tissue, rather than autogenous fat, is preferred to fill in the surgical defect. The temporalis muscle can be rotated into the defect. Split-thickness skin grafts can be used for cutaneous defects. A small bolus dressing is placed to ensure adequate adhesion. When the temporalis is unavailable, plastic surgery teams can harvest microvascular free flaps. Jackson-Pratt drains are installed under the neck and scalp skin flaps to ensure tissue coaptation.

POSTOPERATIVE CARE
After extubation in the operating room, the patient is examined for neurologic deficits. Unanticipated neurologic deficits are studied further by noncontrast CT imaging to evaluate the presence of intracranial edema or bleeding. Antibiotics are continued postoperatively until the drains are removed, or if an infectious process dictates otherwise. Dexamethasone is continued for 48 hours and then tapered over 5 days.
When the ICA has been sacrificed, great care is taken to avoid even minor hypotensive and hypovolemic periods. These events can reduce the cerebral blood flow through the remaining contralateral carotid artery and lead to cerebral ischemia.
Intermittent spinal drainage, through a lumbar drain installed at the end of the procedure, reduces the pressure in the subarachnoid space and accelerates healing of dural defects. Continuous spinal drainage can cause overdrainage and pneumocephalus and is not used. Depending on patient tolerance, 35 to 50 mL of spinal fluid is drained every 8 hours for 48 hours. The drain is then clamped for 24 hours and removed.

POTENTIAL COMPLICATIONS
Inadvertent carotid artery injury can be managed initially by local pressure to the site of entry and placement of temporary clips on either side. After systemic heparinization, the tear is examined, irrigated with heparinized saline, and repaired using 8-0 Novofil suture. Before placement of the last suture, the lumen is irrigated with heparinized saline to clear any clots. The hemoclips are released, and any minor leaks are managed with oxidized cellulose. If the tear is beyond repair, the results of the preoperative temporary balloon occlusion dictate further management.

ADJUVANT TREATMENT
Treatment of temporal bone malignancies extending into the middle ear should consist of surgical resection of all visible disease followed by external-beam radiotherapy. Occasionally, large, aggressive tumors invading brain parenchyma, the dominant carotid artery, or dural venous sinus are encountered, and total tumor removal is impossible without serious neurologic deficits. In these instances, brachytherapy catheters can be inserted and used.

REHABILITATION
Facial palsy after temporal bone resection requires careful assessment and treatment. A temporary tarsorrhaphy at the conclusion of the operation affords early corneal protection. When the periorbital edema subsides, a gold weight implant in the upper eyelid can offer long-term corneal protection. Elderly patients also may require lower eyelid tightening procedures. Facial nerve recovery can be expected at 12 to 18 months. The best facial function a patient can expect with a cable graft, in our hands, is House-Brackmann grade III.
Excessive packing of the inferior petrosal sinus can lead to lower cranial nerve dysfunction (CN IX, X, and XI) that can be debilitating. Some patients require temporary tracheostomy and gastrostomy, and others can be treated with polytetrafluoroethylene (Teflon) injection of the vocal fold or an Isshiki thyroplasty. 4

FOLLOW-UP
Patients are seen every month for the first year, and repeat imaging (CT and MRI) is obtained at 6 months and yearly thereafter. Enhancing tumors are best visualized by contrast-enhanced fat-suppression MRI, which helps differentiate transposed flaps from tumor recurrence. Any suspicious areas require biopsies either directly or by needle aspiration techniques with or without CT guidance.

RESULTS
Temporal bone neoplasms occur infrequently. The limited experience makes analysis of treatment difficult. Because of this difficulty, we reviewed the literature for all cases of squamous cell carcinoma of the temporal bone, 5 analyzed the extent of disease present, studied the different treatment strategies employed, and reported on outcome. Our findings are presented.
All publications in the English language from 1915 to 1992 dealing with the treatment of squamous cell carcinoma of the temporal bone were reviewed; 96 publications 1, 6 - 100 were encountered, of which 26 articles 75 - 100 contained enough information on 144 patients. Various parameters were then analyzed. The major reason for exclusion of a study was the lack of a descriptive table in which the extent of disease, type of treatment, and follow-up for each patient were carefully documented.
Several conclusions about overall survival could be made. When disease was confined to the EAC, no statistically significant difference in 5-year survival was found between patients treated with LTBR (48.6%) and patients treated with STBR (50%). When disease extended into the middle ear, patients who had STBR had better 5-year survival (41.7%) than patients who had LTBR (28.6%) ( Fig. 4-7 ). The experience with carcinoma that invaded the petrous apex was limited. Four patients treated with TTBR had a 50% 1-year survival and 0% 2-year survival. One patient treated with STBR was dead of disease at 1 year.

FIGURE 4-7 Treatment-specific survival for patients with carcinoma extending to the middle ear. TBR, temporal bone resection.
(From Prasad S, Janecka IP: Efficacy of surgical treatments for squamous cell carcinoma of the temporal bone. Otol Head Neck Surg 110:270-280, 1994.)
The value of preoperative or postoperative radiation therapy was also analyzed. When disease was confined to the EAC, the addition of either preoperative or postoperative radiation therapy to LTBR did not significantly improve 5-year survival (48% with radiation therapy, 44.4% without radiation therapy) ( Fig. 4-8 ). This was the only group in which a conclusion regarding radiation treatment could be made.

FIGURE 4-8 Survival of patients with carcinoma confined to the external auditory canal treated with lateral temporal bone resection (TBR) with or without preoperative or postoperative radiation therapy (RT).
(From Prasad S, Janecka IP: Efficacy of surgical treatments for squamous cell carcinoma of the temporal bone. Otol Head Neck Surg 110:270-280, 1994.)
The prognostic value of dural involvement was also studied. Resection of involved dura mater did not improve overall 5-year survival (11.1% with or without resection). Margin status was not always reported.
Four patients had extension of disease to involve the ICA. Of the two patients treated with TTBR and ICA sacrifice, one died of postoperative cerebral ischemia, and the other died of disease at 14 months of regional and distant failure. The other two patients who were treated in a method that spared the ICA died of disease shortly after resection.
Two patients with carcinomatous invasion of the temporal lobe treated with limited resection also died of disease shortly after resection. No patient was encountered who had resection of involved cerebral or cerebellar tissue.
Site of failure was also studied. Of 54 patients who died of disease, 45 had local failure, 5 had locoregional failure, 3 had regional failure alone, and 1 had regional distant failure.
Several other aspects of this disease could not be studied because of the lack of information provided by the authors. First, the histologic differentiation of the tumor and its relationship to overall survival could not be analyzed. Second, the method of temporal bone removal, whether by en bloc resection, piecemeal resection, or a drillout, and its relationship to survival could not be ascertained. The status of the margins of resection and relationship to overall survival remains to be studied.

SUMMARY
Radical resection of the temporal bone requires thorough knowledge of the intricate anatomy of the temporal bone and surrounding structures. There is no substitute for laboratory dissection before embarking on such an operation. Thorough preoperative imaging, delineation of the extent of tumor involvement, and preoperative carotid artery testing are imperative.
The indications for the operation are slowly evolving as we gain experience and collate data for analysis. From our literature review regarding squamous cell carcinoma, 5 it seems that cancerous involvement of the middle ear is best treated by STBR rather than LTBR and gross removal of middle ear disease. When the tumor involves the petrous apex, we believe that TTBR can allow total tumor extirpation and possibly prolonged survival, although the latter remains to be proved. Prospective, randomized studies are needed to define the value of margin-free dural, carotid artery, and brain parenchymal resection. The value of adjunctive radiation therapy for extensive lesions also requires further study.

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68. Spector J.G. Management of temporal bone carcinomas: A therapeutic analysis of two groups of patients and long-term follow-up. Otolaryngol Head Neck Surg . 1991;104:58-66.
69. Ariyan S., Sasaki C.T., Spencer D. Radical en bloc resection of the temporal bone. Am J Surg . 1981;142:443-447.
70. Arena S. Tumor surgery of the temporal bone. Laryngoscope . 1974;84:645-670.
71. Brooker G.B. Bilateral middle ear carcinomas associated with Waldenström’s macroglobulinemia. Ann Otol Rhinol Laryngol . 1982;91:299-303.
72. Towson C.E., Shofstall W.H. Carcinoma of the ear. Arch Otolaryngol Head Neck Surg . 1950;51:724-738.
73. Robinson G.A. Malignant tumors of the ear. Laryngoscope . 1931;41:467-473.
74. Kinney S.E., Wood B.G. Malignancies of the external ear canal and temporal bone: Surgical techniques and results. Laryngoscope . 1987;97:158-164.
75. Buckmann L.T., Barre W. Carcinoma of the middle ear and mastoid. Ann Otol Rhinol Laryngol . 1943;52:194-201.
76. Liebeskind M.M. Primary carcinoma of the external auditory canal, middle ear, and mastoid. Laryngoscope . 1951;61:1173-1187.
77. Stokes H.B. Primary malignant tumors of the temporal bone. Arch Otolaryngol Head Neck Surg . 1990;32:1023-1030.
78. Rosenwasser H. Neoplasms involving the middle ear. Arch Otolaryngol Head Neck Surg . 1940;32:38-53.
79. Grossman A.A., Donnelly W.A., Smithman M.F. Carcinoma of the middle ear and mastoid process. Ann Otol Rhinol Laryngol . 1947;56:709-721.
80. Mattick W.L., Mattick J.W. Some experience in management of cancer of the middle ear and mastoid. Arch Otolaryngol Head Neck Surg . 1951;53:610-621.
81. Wahl J.W., Gromet M.T. Carcinoma of the middle ear and mastoid. Arch Otolaryngol Head Neck Surg . 1953;58:121-126.
82. Crabtree J.A., Britton B.H., Pierce M.K. Carcinoma of the external auditory canal. Laryngoscope . 1976;86:405-415.
83. Hanna D.C., Richardson G.S., Gaisford J.C. A suggested technique for resection of the temporal bone. Am J Surg . 1967;114:553-558.
84. Adams G.L., Paparella M.M., Fiky F.M. Primary and metastatic tumors of the temporal bone. Laryngoscope . 1971;81:1273-1285.
85. Sataloff R.T., Myers D.L., Lowry L.D., Spiegel J.R. Total temporal bone resection for squamous cell carcinoma. Otolaryngol Head Neck Surg . 1987;96:4-14.
86. Nadol J.B., Schoknecht H.F. Obliteration of the mastoid in the treatment of tumors of the temporal bone. Ann Otol Rhinol Laryngol . 1984;93:6-12.
87. Arriaga M., Hirsch B.E., Kamerer D.B., Myers E.N. Squamous cell carcinoma of the external auditory meatus (canal). Otolaryngol Head Neck Surg . 1989;101:330-337.
88. Michaels L., Wells M. Squamous cell carcinomas of the middle ear. Clin Otolaryngol . 1980;5:235-248.
89. McCrea R.S. Radical surgery for carcinoma of the middle ear. Laryngoscope . 1972;82:1514-1523.
90. Gacek R.R., Goodman M. Management of malignancy of the temporal bone. Laryngoscope . 1977;87:1622-1634.
91. Scholl L.A. Neoplasms involving the middle ear. Arch Otolaryngol Head Neck Surg . 1935;22:548-553.
92. Clairmont A.A., Conley J.J. Primary carcinoma of the mastoid bone. Ann Otol Rhinol Laryngol . 1977;86:306-309.
93. Beal D.D., Lindsay J.R., Ward P.H. Radiation-induced carcinoma of the mastoid. Arch Otolaryngol Head Neck Surg . 1965;81:9-16.
94. Coleman C.C. Removal of the temporal bone for cancer. Am J Surg . 1966;112:583-590.
95. Parsons H., Lewis J.S. Subtotal resection of the temporal bone for cancer of the ear. Cancer . 1954;7:995-1001.
96. Miller D., Silverstein H., Gacek R.R. Cryosurgical treatment of carcinoma of the ear. Trans Am Acad Ophthalmol Otolaryngol . 1972;76:1363-1367.
97. Tabb H.G., Komet H., McLaurin J.W. Cancer of the external auditory canal: Treatment with radical mastoidectomy and irradiation. Laryngoscope . 1964;74:634-643.
98. Lodge W.O., Jones H.M., Smith M.E.N. Malignant tumors of the temporal bone. Arch Otolaryngol Head Neck Surg . 1955;61:535-541.
99. Ward G.E., Loch W.E., Lawrence W. Radical operation for carcinoma of the external auditory canal and middle ear. Am J Surg . 1951;82:169-178.
100. Newhart H. Primary carcinoma of the middle ear: Report of a case. Laryngoscope . 1917;27:543-555.
Chapter 5 Congenital Malformation of the External Auditory Canal and Middle Ear

Antonio De la Cruz, Karen B. Teufert
Videos corresponding to this chapter are available online at www.expertconsult.com .
Congenital aural atresia is characterized by aplasia or hypoplasia of the external auditory canal (EAC), often associated with absence or deformity of the auricle (microtia) and the middle ear, with occasional inner ear abnormalities. Aural atresia occurs in 1 in 10,000 to 20,000 live births 1 - 5 ; unilateral atresia is three times more common than bilateral atresia. This disorder occurs more commonly in males and on the right side. 1 EAC atresia is more often bony rather than membranous, and bony atresia is regularly accompanied by malformation of the middle ear cavity and structures of the middle ear. 6 - 9 More severe forms of congenital microtia are usually associated with EAC atresia; rarely, canal atresia may be seen in patients with a normal pinna. 10 Generally, a more severe external deformity implies a more severe middle ear abnormality. 11, 12
Kiesselbach, in 1883, is often credited with the first deep operation attempting to correct this malformation. 8 Lascaratos and Assimakopoulos 13 noted that the Byzantine physician Paul of Aegina performed a surgical treatment of congenital aural atresia. 14 The procedure done by Kiesselbach resulted in facial paralysis. Because of the lack of middle ear microsurgery and the high complication rate, congenital aural atresia surgery was considered dangerous and to be avoided for the most part. In 1914, Page 15 reported hearing improvement after surgery in five of eight patients. This report was followed in 1917 by Dean and Gittens, 16 who reported an excellent hearing result in a patient and reviewed the various types of operations that had been tried by other surgeons. The prevailing attitude toward surgical correction in these cases remained generally pessimistic, however, despite these and other occasional reports of successful operations, until 1947. That year, Ombredanne 17 in France and Pattee 18 in the United States each reported a series of patients successfully operated on to improve hearing. Pattee’s technique included removal of the incus to “mobilize” the stapes 18 ; Ombredanne 17 added fenestration of the lateral semicircular canal.
With the advent of tympanoplasty techniques in the 1950s, interest in atresiaplasty increased as the teachings of Wullstein and Zollner carried over into surgery of the congenital ear. 8 Larger series with greater success rates were reported as surgeons attempted to improve their results, using ossiculoplasty, mastoidectomy, differing degrees of bone removal, and different types and techniques of graft placement. 2, 4, 17, 19 - 26 Ombredanne 27 went on to report on more than 600 aplasia cases by 1971 and 1600 cases with major and minor malformations by 1976. 8 Gill’s report of 83 cases in 1969 2 and Jahrsdoerfer’s 1978 article 8 are considered landmarks. Crabtree, 28 Jahrsdoerfer, 29, 30 Marquet, 31, 32 and De la Cruz 6, 33 and their colleagues all reported on large surgical series, with modifications of classification and operative techniques.
Although techniques of canalplasty, meatoplasty, tympanoplasty, and ossiculoplasty have improved considerably, surgical correction of congenital aural atresia remains one of the most challenging operations performed by otologists. This is a complex surgical problem, requiring application of all tympanoplasty techniques and a thorough knowledge of the surgical anatomy of the facial nerve, oval window, and inner ear, and their congenital variants. 1, 6, 8, 17, 21, 26, 27, 29- 31, 33- 40 The temporomandibular joint is displaced posteriorly by the lack of development of the EAC, narrowing the distance between the glenoid fossa and the anterior wall of the mastoid tip. 19, 41 Fusion of the incus and malleus is common, but because of its dual origin, the stapes footplate is usually normal. 4, 42
The surgical repair of aural atresia is recommended at age 6 years. 6 The timing of repair must take into account any planned auricular reconstruction procedures. Criteria for patient selection must be stringent when attempting to achieve closure of the air-bone gap to within 20 to 30 dB. Preoperative counseling and several postoperative visits are essential for optimal results. In this chapter, we discuss these issues and provide guidelines for patient evaluation and selection, surgical techniques, and postoperative management.

EMBRYOLOGY
A review of the normal embryologic development of the ear aids in understanding the myriad of possible combinations of malformations encountered in congenital aural atresia. The inner ear, middle ear, and external ear develop independently and in such a way that deformity of one does not presuppose deformity of another. 9, 43 Most frequently, abnormalities of the outer and middle ear are encountered in combination with a normal inner ear. 44, 45
Microtia is a result of first and second branchial arch anomalies. Growth of mesenchymal tissue from the first and second branchial arches forms six hillocks around the primitive meatus that fuse to form the auricle ( Table 5-1 ). By the end of the third month, the primitive auricle has been completed. The external auditory meatus develops from the first branchial groove. During the second month, a solid core of epithelium migrates inward from the rudimentary pinna toward the first branchial pouch. This core, the precursor of the EAC, starts to hollow out and take shape in the sixth month. It canalizes in the seventh month, causing the developing mastoid to become separated from the mandible. Its subsequent posterior and inferior development carries the middle ear and facial nerve to their normal positions. 1, 43, 46 - 48 Some of the literature supports the notion that microtia grade can indicate the status of middle ear development in aural atresia. The better developed the external ear is, the better developed is the middle ear.
TABLE 5-1 Development of the Auricle First Branchial Arch Second Branchial Arch First hillock—tragus Fourth hillock—antihelix Second hillock—helical crus Fifth hillock—antitragus Third hillock—helix Sixth hillock—lobule and lower helix
The first branchial pouch grows outward to form the middle ear cleft. The plaque of tissue where this cleft meets the epithelium of the EAC forms the tympanic membrane. While the pouch is forming the eustachian tube, tympanic cavity, and mastoid air cells, Meckel’s cartilage (first branchial arch) is forming the neck and head of the malleus and incus body. Reichert’s cartilage (second branchial arch) forms the remainder of the first two ossicles’ long processes and the stapes superstructure. The footplate has a dual origin from the second arch and the otic capsule. The ossicles attain their final shape by the fourth month. By the end of the seventh to eighth month, the expanding middle ear cleft surrounds the ossicles and covers them with a mucous membrane. 1, 45, 49
The facial nerve is the nerve of the second branchial arch. At 4.5 weeks, this developing nerve divides the blastema, which is the condensation of the second arch mesenchymal cells, into the stapes, the interhyale (stapedius muscle precursor), and the laterohyale (precursor of the posterior wall of the middle ear). The nerve’s intraosseous course is dependent on this bony expansion. 45, 47 The membranous portion of the inner ear develops during the third to sixth week from an auditory placode on the lateral surface of the hindbrain. The surrounding mesenchyme transforms into the bony otic capsule. 50
Congenital aural atresia can range in severity from a thin membranous canal atresia to complete lack of tympanic bone, depending on the time of arrest of intrauterine development. 1, 51, 52 The common finding of a normal inner ear is explained because the inner ear is formed by the time of external/middle ear development arrest. Facial nerve course abnormalities are often seen.

CLASSIFICATION SYSTEMS
Of historical significance is a classification in congenital aural atresia developed in 1955 by Altmann. 51 In this system, atresias are categorized into three groups, as follows:
Group 1 (mild): Some part of the EAC, although hypoplastic, is present. The tympanic bone is hypoplastic, and the ear drum is small. The tympanic cavity is either normal in size or hypoplastic.
Group 2 (moderate): The EAC is completely absent, the tympanic cavity is small, and its content is deformed, and the “atresia plate” is partially or completely osseous.
Group 3 (severe): The EAC is absent, and the tympanic cavity is markedly hypoplastic or missing.
Altmann’s classification system is purely descriptive, and most surgical candidates fall into groups 2 and 3.
The De la Cruz classification includes surgical feasibility guidelines using only high-resolution computed tomography (CT), taking into consideration mastoid pneumatization, inner ear normality, and facial nerve and footplate relationship. 6 The malformations are divided into minor and major malformations ( Table 5-2 ). The clinical importance of this classification is that surgery in cases of minor malformations has a good possibility of yielding serviceable hearing, whereas cases of major malformations are frequently inoperable, but treatable with the bone-anchored hearing aid (BAHA) system. 3
TABLE 5-2 De la Cruz Classification of Congenital Aural Atresia Minor Malformations 1. Normal mastoid pneumatization 2. Normal oval window/footplate 3. Good facial nerve–footplate relationship 4. Normal inner ear Major Malformations 1. Poor pneumatization 2. Abnormal or absent oval window/footplate 3. Abnormal course of facial nerve 4. Abnormalities of inner ear
From De la Cruz A, Linthicum FH Jr, Luxford WM: Congenital atresia of the external auditory canal. Laryngoscope 95:421-427, 1985.
Jahrsdoerfer and colleagues 53 developed a widely used point grading system to guide surgeons in preoperative assessment of the best candidates for hearing improvement ( Table 5-3 ). This system takes into account the parameters of mastoid pneumatization, presence of the oval and round windows, facial nerve course, status of the ossicles, and external appearance. Point allocation is based primarily on the findings on high-resolution CT. Jahrsdoerfer and colleagues 53 proposed that when the preoperative evaluation of the patient is itemized into this grading system, the best results (>80% success) are achieved with a score of 8 or better. A score of 7 indicates the patient is a fair candidate, a score of 6 indicates the patient is a marginal candidate, and with a score less than 5 the patient becomes a poor candidate.
TABLE 5-3 Jahrsdoerfer’s Grading System of Candidacy for Surgery of Congenital Aural Atresia Parameter Points Stapes present 2 Oval window open 1 Middle ear space 1 Facial nerve normal 1 Malleus-incus complex present 1 Mastoid well pneumatized 1 Incus-stapes connection 1 Round window normal 1 Appearance of external ear 1 Total available points 10 Rating Type of Candidate 10 Excellent 9 Very good 8 Good 7 Fair 6 Marginal ≤5 Poor
From Jahrsdoerfer RA, Yeakley JW, Aguilar EA, et al: Grading system for the selection of patients with congenital aural atresia. Am J Otol 13:6-12, 1992.
Ishimoto and associates 54 evaluated the relationship between hearing level and temporal bone abnormalities in patients with microtia, using Jahrsdoerfer’s CT scoring system and high-resolution CT scans of the temporal bone. They found that the hearing level in microtic ears correlated with the formation of oval/round windows and ossicular development, but not with the degree of middle ear aeration, facial nerve aberration, or severity of microtia.
Schuknecht’s 55 system of classification of congenital aural atresia is based on a combination of clinical and surgical observations. Type A (meatal) atresia is limited to the fibrocartilaginous part of the EAC. Meatoplasty is the surgical procedure of choice, and when performed in a timely fashion prevents formation of canal cholesteatoma and conductive hearing loss. In type B (partial) atresia, there is narrowing of the fibrocartilaginous and bony EAC, but a patent dermal tract allows partial inspection of the tympanic membrane. The tympanic membrane is small and partly replaced by a bony septum. Minor ossicular malformations exist, and hearing loss may be mild to severe. Type C (total) atresia includes all cases with a totally atretic ear canal, but a well-pneumatized tympanic cavity. There is a partial or total bony atretic plate, the tympanic membrane is absent, the heads of the ossicles are fused, there may be no connection to a possibly malformed stapes, and the facial nerve is more likely to have an aberrant course over the oval window. Type D (hypopneumatic total) atresia is a total atresia with poor pneumatization, common in dysplasias such as Treacher Collins syndrome. There are abnormalities of the facial nerve canal and the bony labyrinth. These patients are poor candidates for hearing improvement surgery.
Chiossone’s 56 classification is based primarily on the location of the glenoid fossa. In type I, the fossa is in the normal position; in type II, it is moderately displaced; in type III, the fossa overlaps the middle ear; and in type IV, in addition to the fossa overlapping the middle ear, there is lack of mastoid pneumatization. Patients with types I and II are ideal surgical candidates. Type III cases have a tendency toward graft lateralization. Patients with type IV are not surgical candidates. In atresiaplasty surgery, a classification scheme is useful for surgical planning, patient counseling, and comparison of outcomes.

INITIAL EVALUATION AND PATIENT SELECTION
When aural atresia is noted in a newborn, several issues must be addressed. Where one congenital abnormality is found, others must be sought. A high-risk registry for hearing loss is helpful in this regard. 57 After the degree of aural deformity is assessed by physical examination, evaluation of auditory function in unilateral and bilateral atresia should be performed using auditory brainstem response audiometry within the first few days of life. An 11% to 47% incidence of inner ear abnormality is associated with congenital aural atresia. 12 Occasionally, in unilateral cases, there is a total sensorineural hearing loss (SNHL) on the side of the normal-appearing ear, which might otherwise be missed. 6, 33
In bilateral cases, a bone-conduction hearing aid should be applied as soon as possible, ideally in the third or fourth week of life. In unilateral cases in which the opposite ear hears normally, a hearing aid is unnecessary. A child with aural atresia and associated cephalic abnormalities (e.g., hemifacial microsomia and Treacher Collins, Crouzon, or Pierre Robin syndrome) should be recognized. 57 - 61 In this subset, surgical correction has poor results, 55 and a long-term bone-conduction hearing aid or BAHA in these nonoperable bilateral congenital aural atresia situations is beneficial (see later). 3
Prompt and careful counseling of the parents of a child with sporadic (nonsyndromal) congenital aural atresia is necessary to alleviate concerns regarding possible occurrence in subsequent children (no more than the general population), to answer questions regarding future auricular reconstruction, and, most important, to ensure that proper hearing amplification is instituted in a timely fashion. The child should be enrolled in special education at an early age to maximize speech and language acquisition, in preparation for “mainstreaming” at preschool age. Radiologic and surgical evaluations are deferred until the child is 6 years old (see later).
In the initial evaluation of an older individual with congenital aural atresia, the most crucial elements remain the functional and anatomic integrity of the inner ear. Audiometry and high-resolution thin-section (≤1 mm) CT in coronal and axial views are necessary. Prognosis for hearing improvement depends on the presence and degree of malformations. Auricular reconstruction must be done before hearing reconstruction to avoid interfering with the blood supply to the surrounding soft tissue, which is indispensable for microtia repair. Reconstruction with alloplastic materials, such as porous high-density polyethylene (Medpor), can be done before or after atresiaplasty because intact blood supply is not indispensable.
A patient with congenital aural atresia may present with an infected or draining ear or acute facial palsy; 14% have congenital cholesteatoma. 6 The priority in these cases is removal of the cholesteatoma and resolution of the infection. Preoperative audiometry and high-resolution CT scanning may be necessary at an earlier age in children with repeated infections in the atretic ear. 6, 55, 62
There are two requirements for planning surgery in congenital aural atresia: radiographic three-dimensional evaluation of the temporal bone and audiometric evidence of cochlear function. 8, 63 Other conditions mandating prompt surgical intervention are congenital cholesteatoma, a draining postoperative atretic ear, and acute facial palsy. The CT scan should always be reviewed for cholesteatoma, which necessitates surgery at any age. 55, 62, 64 It is not included in any of the grading systems because these are used only for predicting hearing results in elective atresiaplasty surgery.

TIMING OF AURICULAR RECONSTRUCTION AND ATRESIAPLASTY
In bilateral or unilateral atresia, auricular reconstruction and atresiaplasty are recommended at 6 years of age. Before this age, there may be a tendency to form exostosis-like bony growth that may occlude the EAC, and there is less patient cooperation. By age 6, the costal cartilage has developed sufficiently to allow for reconstruction of the auricle, and the mastoid has become as pneumatized as possible. The microtia repair should be done first because the complex flaps and use of autologous rib graft demand excellent blood supply. 65, 66 Many surgeons do not perform cartilage microtia reconstruction on an ear with previous reconstruction attempts. 64 The hearing restoration surgery is performed 2 months after the last step of the microtia repair. Rehabilitation of auricular defects can be done using an osseointegrated percutaneous mastoid implant prosthesis, with and without bone-conduction aids, such as BAHA. 3, 48, 67 - 69 Alloplastic materials have been used for microtia repair in the past, but there is a high risk of extrusion associated with their use. Newer materials, such as Medpor, seem to be very well tolerated, however. 70 - 72 As noted earlier, Medpor reconstruction can be done before or after atresiaplasty because intact blood supply is not indispensable.
In unilateral cases, atresiaplasty surgery may be indicated in a patient with “minor” unilateral atresia with normal middle ear, ossicles, and facial nerve, and excellent pneumatization. In such patients, atresiaplasty may be offered in childhood with the parents’ consent. 33 We often see older adults with unilateral atresia who request surgery when their normal ear begins having high-frequency hearing loss (presbycusis).

Bone-Anchored Hearing Appliances
Implantable bone hearing aids available for clinical use were introduced in 1977 in Sweden. BAHA, using Branemark System implants in combination with a hearing aid, has proved to be a favorable means of providing hearing rehabilitation for certain groups of patients, including patients with a congenital ear malformation. BAHAs are suitable for patients who are poor atresiaplasty candidates because of the severity of their malformations. BAHA is a better alternative than a conventional bone hearing aid. Conventional bone hearing aids have several drawbacks: discomfort because of constant pressure from the steel spring, worse sound quality because of higher frequency attenuation by the skin, and poor esthetics and insecure positioning of the device. BAHA works without pressure on the skin and provides direct bone transmission without air interface. Other implants are discussed in detail elsewhere in this textbook.
Surgery for BAHA can be performed under local or general anesthesia and is a one-stage procedure. To implant BAHA, a small transcutaneous titanium abutment is implanted behind the ear, where it osseointegrates to the mastoid bone. After a 3-month healing period the BAHA processor can then be connected.
Audiologic indications for BAHA include a pure tone average bone-conduction threshold better than or equal to 45 dB hearing level (HL) (average 500 Hz, 1000 Hz, 2000 Hz, and 3000 Hz). A maximum speech discrimination score better than 60% when using PB (Phonetically Balanced) word lists is recommended. From an audiologic point of view, the side with the best cochlear function (the best bone-conduction threshold) should be used. Patients with a bone-conduction threshold of 25 to 45 dB HL would be expected to improve, but might not achieve levels in the normal range. Patients with a bone-conduction threshold of less than 30 dB HL (similar to most atresias) can be expected to experience hearing improvements that restore hearing levels to normal ranges. Patients must be able to maintain the abutment-skin interface of BAHA. Careful consideration must be given to the patient’s psychological, physical, emotional, and developmental capabilities to maintain hygiene. Titanium implants can be installed in most patients because allergy to titanium is extremely rare. Alternative treatments should be considered for patients with a disease that might jeopardize osseointegration.
For patients with bilateral hearing loss, BICROS (Bilateral Contralateral Routing of Signal) hearing aid is an additional microphone that can be used as an accessory to an implanted BAHA fixture and sound processor to overcome the head shadow effect. The accessory microphone is placed in the contralateral ear to the BAHA fixture. The signal is routed from the accessory microphone to the BAHA sound processor via a wire worn behind the neck. It is intended to improve hearing by eliminating the head shadow effect, but it does so with little success and is not well accepted by patients. 73
We do not generally recommend implantable hearing aids in children because the surgical scars may preclude any future microtia repair. However, the BAHA titanium implant is ideally placed 5 to 6 cm behind and 3 cm above the ear canal in a hair-bearing area. This placement seems to allow for the possibility of transplanting costal cartilage to an area with unscarred skin for future microtia repair. On the other hand the titanium implants for a bone-anchored ear epithesis are ideally placed 18 to 20 mm behind the (future) ear canal; this interferes with the skin of a future auricle, if reconstruction is contemplated. 73
Numerous studies have reviewed results with BAHA in atresia patients. 3, 74 - 77 In one series, 45 atresiaplasty surgeries were compared with 39 BAHA surgeries. 3 Of 44 ears followed for more than 2 years after atresiaplasty, hearing gain was less than 10 dB in 55% and 10 to 30 dB in 43%. Surgical outcome correlated with Altmann classification: the worse the Altmann classification stage, the worse the surgical outcome. Within 5 years, 24 ears were reoperated on. Of the 39 patients supplied with BAHA, 16 had had prior atresiaplasty work. All BAHA patients in the series considered the implant to be superior to conventional bone-conduction hearing aids, and superior to hearing improvement obtained surgically, for the difficult cases for whom atresiaplasty had been unsuccessful. Van der Pouw and colleagues 74 described experience with bilateral BAHA in four patients with bilateral inoperable congenital aural atresia, three of whom had Treacher Collins syndrome. Bilateral BAHA application resulted in improved performance in all tested audiologic parameters, including sound localization, speech recognition in quiet, speech recognition in noise, and a cued listening task.
Kunst and associates 75 reported on the audiologic outcome of BAHA in 20 patients with congenital unilateral conductive hearing impairment, with a mean air-bone gap of 50 dB. Small, although not statistically significant, improvements in localization scores were observed in favor of BAHA. Some patients with congenital unilateral conductive hearing impairment had such good directional hearing and speech-in-noise scores in the unaided situation that no overall significant improvement occurred after BAHA fitting. Compliance with BAHA use was remarkably high, however, suggesting patient perceived benefit.
House and Kutz 76 reported the incidence of complications associated with implantation of BAHA in 149 patients and the management of these complications. There were no intraoperative or perioperative complications. Significant postoperative complications requiring intervention occurred in 12.8% of patients. Skin overgrowing the abutment occurred in 7.4%, and all but one of these patients required revision in the operating room. Skin overgrowth was a late complication, occurring an average of 12 months (range 3 months to 2 years) after the initial procedure. Implant extrusion from failure to osseointegrate occurred in 3.4%. Two patients had local wound infections requiring oral antibiotics.
One study evaluated hearing results in pediatric patients managed with EAC reconstruction or BAHA. 77 The investigators also evaluated the medical cost-effectiveness of each procedure. They reviewed 36 ears that underwent surgical canal reconstruction and 6 patients who underwent BAHA placement. Most (93%) of the patients undergoing EAC reconstruction required some form of amplification postoperatively. The investigators concluded that BAHA can achieve acceptable hearing (<15 dB) in school-aged children with normal bone curves, and it can match the bone curves for children with SNHL. The two-staged BAHA system placement may be provided at almost one third the cost to the medical system of surgical EAC reconstruction, on a decibel-for-decibel basis, with single-stage placement yielding even greater cost savings. Implantable hearing appliances seem to offer a good alternative for patients with inoperable atresia and for patients in whom the operative prognosis is poor.

PREOPERATIVE EVALUATION AND PATIENT COUNSELING
Early diagnosis with auditory brainstem response and auditory enhancement with bone-conduction hearing aids in bilateral cases should be done in the first weeks of life. 78 Corrective surgery begins at 6 years of age. Imaging is deferred until age 6. Microtia repair is performed before atresiaplasty. The size of the mastoid on physical examination can be estimated by palpation of the mastoid tip, suprameatal spine of Henle (if present), condyle, and zygomatic arch. This is a useful measure because the new ear canal is constructed at the expense of the mastoid air-cell system.
The preoperative imaging study is a high-resolution CT scan of the temporal bone in coronal and axial planes ( Fig. 5-1 ). 5, 12, 63, 79 The CT scan must be examined carefully by the otologic surgeon together with the otoradiologist. 41, 80 The four important imaging elements that are most helpful to the surgeon planning reconstruction of a congenitally malformed ear are (1) the degree of pneumatization of the temporal bone; (2) the course of the facial nerve, including the relationship of the horizontal portion to the footplate, and the location of the vertical segment; (3) the presence of the oval window and stapes footplate; and (4) the status of the inner ear. 5, 6, 63 CT also provides information on thickness and form of the atretic bone, size and status of the middle ear cavity, and soft tissue contribution to the atresia, 6 but these are less critical for the repair.

FIGURE 5-1 Congenital aural atresia, right ear. Coronal high-resolution CT shows atretic external auditory canal and normally developed mastoid system, with normal inner ear.
Proponents of three-dimensional reconstruction CT for preoperative evaluation believe that three-dimensional imaging clearly shows the relationships between the condyle, zygomatic arch, temporal bone, temporomandibular joint, and fallopian canal. We have not found it to be of practical use, however.
Lack of pneumatization is the major cause of inoperability in congenital aural atresia. 6, 33 Normal pneumatization is present in most cases. The facial nerve over the oval window may prevent ossiculoplasty and hearing improvement. If the oval window or footplate are absent, surgery with fenestration of the lateral semicircular canal or placement of a hearing aid is indicated. There is potential for facial nerve injury in atresia surgery. 81 The nerve may describe a more acute angle rather than its usual 90 to 120 degrees at the mastoid genu, and often lies more lateral than usual ( Fig. 5-2 ). 82 On high-resolution CT, it is important not to “identify” mistakenly the vertical lie of the facial nerve in the marrow bone leading to the styloid process and the hypoplastic mastoid process ( Fig. 5-3 ). 83 Even in atretic ears in which the facial nerve does not have an abnormal course, a significantly reduced distance is found between the facial canal and the temporomandibular joint, 41 and the facial canal and the posterior wall of the cavum tympani. 47

FIGURE 5-2 Facial nerve in congenital aural atresia. A, Normal intratemporal facial nerve anatomy. B, Intratemporal facial nerve anatomy in congenital aural atresia.

FIGURE 5-3 Pitfalls in congenital aural atresia surgery: facial nerve on coronal high-resolution CT. Arrows point to a vertical segment of the facial nerve in the left ear.
To be considered a surgical candidate, the patient must have sufficient cochlear function as determined by auditory brainstem response or routine audiometry; a normal-appearing inner ear on CT scan; and, preferably, a well-developed mastoid, and good oval window/footplate and facial nerve relationship. The patient and parents are counseled regarding the success of atresiaplasty repair and the chances of successful hearing improvement. Patients with a degree of malformation equivalent to an 8 or better on the Jahrsdoerfer grading scale are given a greater than 80% chance of hearing improvement. The risk to the facial nerve is small, made more so by the use of the facial nerve monitor intraoperatively. 33, 82 Patients are informed that a split-thickness skin graft (STSG) from the hypogastrium is used to line the new EAC. Initially, frequent postoperative visits are necessary. The possibilities of a facial nerve paralysis (<1%), profound SNHL (approximately 7%, no dead ears), postoperative canal stenosis (<4%), tympanic membrane graft lateralization (<4%), and ossicular chain refixation (<4%) are noted. 84, 85

SURGICAL APPROACH
Early atresiaplasty operations failed because of poor tympanoplasty techniques, large mastoidectomies, and faulty skin grafting techniques. 18 Advances in meatoplasty added to the success rate of atresiaplasty surgery, however. 19, 86 Although fenestration remains a rare option in bilateral congenital absence of the oval window, modern methods of ossiculoplasty are used preferentially and yield superior results. 6, 8, 19, 23, 26, 28, 31, 34- 36, 87- 89
General endotracheal anesthesia is used; muscle relaxants are avoided. Facial nerve monitoring is used in all cases. The patient is in the otologic position, and the head is turned away. A large shave of the postauricular area is performed, and the auricle and postauricular area are prepared with povidone-iodine and draped. Additionally, the hypogastrium is shaved, aseptically prepared, and draped for the skin graft donor site.
A postauricular temporo-occipital incision is made. In cases in which microtia repair has been done, care is taken not to expose the costal cartilage graft or alloplastic material used in the auricular reconstruction. Subcutaneous tissue is elevated anteriorly to the temporomandibular joint. An incision is made in the periosteum, which is elevated forward exposing the mastoid cortex and, anteriorly, the temporomandibular joint space ( Fig. 5-4 ). Care is taken to avoid injury to an anomalous facial nerve exiting the temporal bone in this area. Temporalis fascia is harvested, trimmed of excess soft tissue if needed, and placed aside to dry. The temporomandibular joint space is explored to verify that the facial nerve or tympanic bone is not lying within it.

FIGURE 5-4 Incision, harvesting temporalis fascia, T-incision, and elevation of periosteum. TMJ, temporomandibular joint.
The literature has fostered the belief that there are separate and distinct approaches to the bony work necessary in atresiaplasty: the anterior approach, the transmastoid approach, and modification of the anterior approach. 6, 8, 24, 33, 35, 57, 64 We believe that strict distinction between these surgical approaches is unnecessary because each can be used alone or in combination to facilitate the atresiaplasty.

Surgical Technique
If a remnant of tympanic bone is present, drilling for the new ear canal begins at the cribriform area. If no such remnant exists, drilling of a 12 mm cylindrical-shaped canal begins at the level of the linea temporalis, just posterior to the glenoid fossa. Dissection proceeds anteriorly and medially, keeping in mind the lack of landmarks in atretic bone. The middle fossa plate is identified and followed to the epitympanum, where the fused malleus head/incus body mass is identified ( Fig. 5-5 ). Care is taken to avoid exposure of the temporomandibular joint space or to avoid opening an excessive number of mastoid air cells. A radical mastoidectomy–like approach should be avoided. When the ossicular mass is identified, the atretic bone is removed with diamond microdrills and curettes to expose the ossicles completely ( Fig. 5-6 A).

FIGURE 5-5 Removal of atretic plate and adhesions, exposing the ossicles, and drilling for the new ear canal.

FIGURE 5-6 A and B, The ossicular mass is dissected free of the atretic plate, and a 2 mm space is created around the ossicles. MF, middle fossa.
It is important to minimize drilling on the ossicular mass because transmission of high-speed drill energy to the inner ear may result in high-tone SNHL. An argon laser is used to free the malleus-incus complex from its soft tissue attachments to reduce potential drill trauma to the inner ear. The ossicular mass in the epitympanum is meticulously dissected free of the atresia plate and left intact. Although the temporomandibular joint often limits anterior dissection, particular effort is made to try to create a space of 2 mm or greater, anterior to the ossicular mass ( Fig. 5-6 B). The horizontal facial nerve always lies medial to the ossicular mass. While dissecting the inferior and posterior aspect of the canal, an aberrant facial nerve may be encountered as it passes laterally through the atretic bone. Drilling for the new ear canal continues until it measures about 12 mm. This circumference is most difficult to achieve medially, where the facial nerve, temporomandibular joint capsule, and middle fossa plate limit larger exposure.
Reconstruction with the patient’s own ossicular chain is performed in almost all cases, even if the ossicular chain is deformed. If the ossicular chain is intact, it is left in place and used for ossicular reconstruction. When this is impossible, a total or partial ossicular reconstruction prosthesis to either a mobile footplate or the stapes head is used for reconstruction. The prosthesis is covered with cartilage before grafting the new drum. Occasionally, the stapes footplate may not be seen well because of anomalous facial nerve anatomy, making placement of an ossicular prosthesis difficult or dangerous. In these instances, gentle transposition of the facial nerve has been described, but more commonly hearing restoration can be accomplished with lateral semicircular canal fenestration or the patient can be counseled to use a hearing aid only. 4, 8, 17, 26, 31, 36, 42
Drilling continues to create an EAC. It must be one and one third times the size of a normal canal (12 mm versus 9 mm) to allow for contracture healing in the postoperative period. While creating the EAC, care is taken not to open mastoid cells or enter the temporomandibular joint unnecessarily.
A dermatome is used to obtain a 0.008-inch thick, 6 × 6 cm STSG from the hypogastrium. Pressure with a gauze sponge soaked in 1% lidocaine with epinephrine 1:100,000 and thrombin solution aids hemostasis of the donor site. When dry, the donor site is dressed with a sterile Tegaderm dressing. 90 This dressing reduces most of the pain associated with other methods of donor site care. One edge of the skin graft is cut in a zigzag fashion to create four or five triangular points ( Fig. 5-7 ). To assist inspection of the skin graft in the final stages of the procedure, the tips of each point and the two corners on the opposite edge are colored with a skin marker.

FIGURE 5-7 Split-thickness skin graft (STSG) used to line new external auditory canal (EAC).
The dried temporalis fascia is trimmed to size, ideally a 20 × 15 mm oval, and a small 4 mm “tab” is cut into the anterior-inferior aspect of the graft in an attempt to prevent lateralization. 91 Nitrous oxide is discontinued 30 minutes before grafting begins. The fascia is placed over the ossicular chain medial to the malleus, if present, or over the cartilage that covers the prosthesis ( Fig. 5-8 ). The tab of the graft is placed medially into the protympanum to help prevent lateralization of the new eardrum.

FIGURE 5-8 Temporalis fascia graft with tab used over an ossicular mass or a partial ossicular replacement prosthesis and cartilage. F, temporalis fascia.
Next, the new ear canal is circumferentially lined with the STSG so that all the bone is completely covered ( Fig. 5-9 ). The triangular corners of the skin graft are placed medially and partially overlap the fascia. The colored points help ensure that no skin lies folded on itself, and that the entire width of the graft is used. A single layer of antibiotic-soaked absorbable gelatin sponge (Gelfoam) holds the fascia and skin graft in place. To reproduce the anterior tympanomeatal angle, a disk of absorbable gelatin film (Gelfilm) is placed over the fascia and skin graft. Lateralization is the most common delayed cause of a poor hearing outcome, usually occurring in the first 12 months after surgery. When the graft starts lateralizing, it pulls away from the ossicles, and the original good hearing results slowly deteriorate. After the fascia and skin graft are in proper position, three 0.020 inch silicone elastomer (Silastic) strips are placed to line the skin ( Fig. 5-10 ). The Silastic strips help prevent adhesions between the skin graft and the ear canal packing, and ensure good contact between the skin graft and ear canal bone. A 9 × 15 mm Merocel wick is placed in the bony canal.

FIGURE 5-9 A and B, Split-thickness skin graft (STSG) in place over fascia, lining new external auditory canal, and disk of Gelfilm over fascia and skin graft.

FIGURE 5-10 A-C, Split-thickness skin graft (STSG) and Silastic strips with ear wicks to maintain contact with bony external auditory canal and wide meatus.
A 12 mm meatus is created, anticipating that a third of its diameter will reduce because of normal healing. Before starting the meatoplasty, the ear is turned back, and the periosteum is brought back in place with one absorbable suture at the superior level of the new ear canal; this stabilizes the pinna and helps ensure that the meatus is at the same level as the new ear canal. Skin, subcutaneous tissue, and cartilage are removed in a 12 mm diameter core over the new meatus. An attempt is made to avoid exposing the grafted cartilage or other materials used for auricular reconstruction. The lateral edge of the STSG is brought through the meatoplasty, and the lateral portion of the new ear canal and the meatus are packed with a large 15 × 25 mm Ambrus wick (Ambrus Merocel, Medtronic Xomed Surgical Products, Jackonsiville, Florida) this applies diffuse pressure over the entire lateral skin graft and widely packs the meatoplasty. Five tacking sutures of 5-0 braided polyester (Ticron) attach the lateral edge of the skin graft circumferentially to the meatal skin. Finally, 6-0 fast-absorbing plain gut is used in a running manner between each Ticron suture ( Fig. 5-11 ).

FIGURE 5-11 Skin graft sutured into place at meatus. EAC, external auditory canal; STSG, split-thickness skin graft.
The periosteum is sutured back into position. The postauricular incision is closed using absorbable sutures (3-0 polyglactin 910 [Vicryl]). Steri-Strips cover the incision, a mastoid dressing is applied, anesthesia is reversed, monitoring equipment is removed, and the patient leaves the operating room.
Silastic sheets and Merocel wicks have helped decrease the incidence of tympanic membrane lateralization by maintaining the tympanic membrane graft in position and the incidence of postoperative EAC stenosis by covering all exposed areas of bone that may cause granulation tissue formation. 85 The Merocel wicks, which are now available in many sizes for canal stenting, help prevent postoperative infection and granulation tissue by allowing administration of topical antibiotics to the entire EAC.

Transmastoid Approach (Canal Wall Down Technique)
The transmastoid approach is of historical interest only ( Fig. 5-12 ). It has not been used since 1975. In this approach, the drilling starts as posterior as possible from the temporomandibular joint. It starts at the linea temporalis and follows the sinodural angle to the ossicular mass. Mastoid air cell exenteration and lowering of the facial ridge to the facial nerve allows the creation of an EAC with a canal wall down technique. Bone pâté and soft tissue obliteration of the large mastoid cells is performed before undertaking meatoplasty and canal skin grafting. The transmastoid approach resulted in a large mastoid cavity with frequent postoperative drainage, and patients were not allowed to swim.

FIGURE 5-12 Transmastoid approach: of historical interest only. TMJ, temporomandibular joint.

POSTOPERATIVE CARE
The mastoid dressing is removed on the first postoperative day. The Steri-Strips are left in place over the postauricular incision for 7 days. The patient is counseled to keep the operative site dry and to change the cotton ball over the canal/meatus packing four times daily. The Tegaderm over the skin graft donor site is left on for at least 3 weeks and requires no special attention. Epithelialization occurs under the plastic, and the typical pain associated with older methods of donor site dressing is absent. 90 The patient is given a 5-day course of oral antibiotics.
The patient is seen 1 week after surgery, at which time the postauricular strips and the tacking Ticron sutures at the meatus are removed. Any dried blood or crusting on the lateral end of the meatus pack should be trimmed. The donor site is inspected. The postauricular site can now be washed, but water precautions continue to apply to the ear canal. We continue to see the patient on a weekly basis. At 2 weeks, the Merocel packs and Silastic are removed, and the meatus is repacked with antibiotic-soaked Gelfoam. At this point, the patient should apply antibiotic suspension to the packing in the ear canal twice a day for 8 to 12 weeks. Usually by 3 weeks, the abdominal donor site has completed the initial re-epithelialization, and the Tegaderm may be removed.
By 6 to 8 weeks postoperatively, nearly all of the Gelfoam is usually gone, and the canal is healing well. The first postoperative audiogram is obtained at that time and repeated in 6 months, at 1 year, and yearly thereafter.

PITFALLS
Clear communication between the surgeon and the anesthesiologist ensures that the patient is not paralyzed during the procedure, so that facial nerve monitoring, which is essential in these cases, can be effective. When the monitor is turned off transiently owing to the use of electrocautery, we monitor the facial nerve manually with a hand on the patient’s face. In a poorly pneumatized mastoid, the otic capsule may be difficult to distinguish from surrounding bone, so care is taken not to fenestrate the semicircular canals accidentally. Postoperative care is crucial to achieve proper healing. Patients should understand beforehand that they must follow the postoperative instructions strictly, and that they must keep all scheduled postoperative visits. We check the circumference of the pack each week and allow air to enter the EAC. If the meatus appears to be narrowing, usually at the third month, it should be dilated every 2 weeks and restented with a Merocel wick for a period of several months to 2 years. This practice usually eliminates the need of reoperation. Early identification and treatment of infection is also necessary to prevent graft failure and canal stenosis.

RESULTS
Numerous publications have described atresiaplasty results in more than 500 patients from our institution over time. 6, 33, 84, 85, 92 Our most recent reviews were published in 2003 and 2004 and included 116 atretic ears operated at the House Ear Clinic. 84, 85 Closure of the air-bone gap to 30 dB at short-term (<6 months) follow-up occurred in 58.5% of primary surgeries and 56% of revisions. 84 The long-term (≥6 months) postoperative air-bone gap was 30 dB or less in 50.8% and 39.1% respectively. There was no significant change in air-bone gap from short-term to long-term follow-up for either primary or revision cases. Soft tissue stenosis occurred in 8% of primary surgeries and 3.4% of revisions, and tympanic membrane lateralization occurred in 3.4% and 3.4% respectively, an improvement from the previous series reported in 1995.
The lower complication rates resulted from anchoring the fascia graft medial to the malleus handle, placing the tabs created in the graft into the hypotympanum and protympanum, using a Gelfilm disk to form an anterior tympanomeatal angle and to keep the graft in position, and using thinner STSG and Merocel Ambrus ear packs. One of the most common causes of postoperative hearing loss after congenital aural atresia surgery is ossicular chain refixation; this occurred in 11.5% of primary cases and 6.9% of revision cases. To try to avoid refixation, we vaporize fibrous ligaments and bony adhesions with argon laser in the final phases of ossicular dissection.
By 1994, all the modifications used in current practice (use of argon laser, thinner STSG, Silastic sheets in the EAC, and Merocel wicks) were routinely being employed. On this basis, the patients were divided into two groups: old cases performed before the changes in surgical technique ( n = 36), and new cases that included surgeries performed after these changes were introduced ( n = 80). 85 We compared complication rates and hearing results before and after the introduction of the new techniques. Overall, the new group had better hearing results and lower rates of complications. Closure of the air-bone gap to 30 dB or less at short-term follow-up occurred in 63.1% of surgeries performed after modifications in the surgical technique and 44.5% of surgeries performed before the modifications. Soft tissue stenosis and bony growth of the EAC were seen in 3.8% of surgeries performed after and 13.9% of surgeries performed before the surgical technique changes. Tympanic membrane lateralization occurred in none of the cases performed after and in 11.1% of the surgeries performed before the surgical technique changes. Ossicular chain refixation occurred in 3.8% of surgeries performed after and 25% of surgeries performed before the modifications. There were no dead ears and no facial palsies in either group.
Shih and Crabtree 93 reviewed long-term surgical results for 39 ears. Hearing averages of 25 dB, 40 dB, and 46 dB were achieved for mild, moderate, and severe atresia. Restenosis occurred in 33%, and 31% had recurrent cavity/canal skin infections. This rate was reduced with the use of STSG.
Digoy and Cueva 94 reviewed their short-term (<1 year) and long-term (>1 year) surgical and hearing results for congenital aural atresia in 45 patients (54 ears). Approximately 50% of their patients achieved a speech reception threshold of 30 dB or better in the short term and long term. The average improvement in air-bone gap was 22 dB. Short-term and long-term outcomes were not significantly different. Patients with an intact ossicular chain did not seem to have a significant advantage in hearing compared with patients with a reconstruction prosthesis. They reported meatal stenosis in 7% and tympanic membrane lateralization in 18% of the cases.
Persistent or recurrent conductive hearing loss after an initial satisfactory improvement can occur after this procedure and is usually secondary to lateralization of the tympanic membrane or ossicular chain refixation. Modifications used in the surgical technique, such as Silastic sheets, Merocel wicks, Gelfilm disks and tabs in the fascia graft placed in the protympanum, have helped decrease the incidence of these two complications and achieve better hearing results. Stenosis of the ear canal is one of the most common postoperative complications. The subsequent routine use of STSG, covering all exposed bony and soft tissue surfaces, allows for quicker epithelialization and healing with a reduction in postoperative infection and stenosis. The use of Merocel packs and Silastic sheets has also helped decrease soft tissue stenosis. The Merocel wick placed in the EAC exerts enough pressure to hold the skin graft against the bone, and the Silastic sheets used to line the ear canal make the skin look smooth, with no bubbles, after the packing is removed.

COMPLICATIONS AND THEIR MANAGEMENT
Complications of atresiaplasty at our institution for cases operated with the most current technique include lateralization of the tympanic membrane in 3.4%, stenosis of the meatus in 3.8%, high-tone SNHL in 7.5%, and facial nerve palsy in less than 1%. 84, 85 Other authors have reported meatal stenosis in 7% and tympanic membrane lateralization in 18% of their cases. 94
Care is taken at the time of surgery to help minimize the incidence of lateralization. Modern techniques of tympanoplasty are applied during the reconstruction. Nitrous oxide is discontinued 30 minutes before grafting. The graft is anchored medially to the malleus, and tabs are placed into the protympanum. An accurately sized Gelfilm disk is used in an attempt to recreate an anterior tympanomeatal angle, minimizing blunting and keeping the graft in position. Silastic sheets and Merocel wicks placed in the EAC also help minimize the incidence of lateralization. The patient must be followed carefully for at least 24 months because lateralization has been known to occur up to 12 months postoperatively.
The incidence of stenosis has been greatly reduced with the use of one-piece STSG covering all exposed bone, and Silastic sheets and Merocel wicks in the EAC. 85 Local care and prevention of infection avoid graft failure and early restenosis. Careful inspection of the meatus and early restenting with large Merocel wicks can obviate reoperation.
Bony EAC stenosis with a “bumpy” exostosis-like appearance tends to occur more frequently in young patients 84 ; this is probably due to active bone growth at this age, resulting in an exuberant bone regrowth in the newly created EAC. This problem seems to be greatly underreported in the literature.
Although laser is used in an attempt to reduce noise trauma to the inner ear and manipulation of the ossicular chain, cases with SNHL and noise-induced hearing loss are still observed. To reduce the risk of inner ear trauma, it is crucial to minimize drilling on the ossicular chain when dissecting it away from the atretic bone, but noise transmission during ear canal creation cannot be completely avoided.
With high-resolution CT, the oval window can be identified, and problems of SNHL resulting from oval window drill-out can be anticipated. Patients with severe malformations, in whom surgery would be fraught with problems, can be counseled against surgical intervention and fitted with hearing aids or BAHA. With CT, the facial nerve position and trajectory inside the temporal bone can be identified, and, along with facial nerve monitoring, use of this information can reduce the incidence of facial nerve paralysis further.

UNILATERAL ATRETIC EAR
Controversy remains over whether children with unilateral atresia should undergo surgery. Jahrsdoerfer 8 and De la Cruz and coworkers 6 have argued for atresia surgery in selected patients with unilateral atresia. Other authors support this position. 95 In the past, Schuknecht, 96 Crabtree, 28 and Bellucci 52 recommended against operating on children with unilateral atresia. These authors argued that the benefit to be gained is minimal in the presence of a contralateral normal-hearing ear. Hearing results at that time were unpredictable and often did not approach the 20 dB air-bone gap needed for useful hearing in the atretic ear. Risks of surgery, including facial nerve injury, also precluded operating on the unilateral atretic ear. In a review of more than 1000 operations for aural atresia with and without cholesteatoma, however, Jahrsdoerfer and Lambert 97 showed that the risk was minimal (1%).
The incidence of major complications (total SNHL and facial nerve injury) and of other complications (tympanic membrane graft lateralization and restenosis) has decreased over the years, but these are still potential complications. The decision to operate on the unilateral atretic ear must weigh these potential complications along with the possibility of a draining ear. Nevertheless, with excellent preoperative imaging, improved surgical techniques, and advances in technology, we believe the results of atresia surgery are now more predictable. Closure of the air-bone gap to within 30 dB in a properly selected patient can be consistently achieved, and hearing remains stable over the length of follow-up. 84 A review examining long-term stability of hearing results in patients operated on for aural atresia does show some drop-off in hearing thresholds (speech reception threshold) over time, however. 84, 85, 98 In the hands of an experienced otologic surgeon with an anatomically favorable patient who (with the parents) understands the risks of potential complications and the need for postoperative care, atresiaplasty in the patient with unilateral atresia is a rewarding operation for the surgeon and the patient. Surgical correction of unilateral atresia offers the benefits of a clean, dry ear with binaural hearing, including sound localization and improved hearing in noise.

SUMMARY
The treatment of congenital aural atresia poses a challenge. Early identification, appropriate hearing amplification, and speech and language therapy are crucial in bilateral cases. Cooperation with the auricular reconstruction surgeon allows for the best esthetic and functional success. Strict radiologic and clinical criteria are necessary to select appropriate candidates for atresiaplasty. Classification of patients into categories of minor and major malformations provides a guide for prognosis for hearing improvement and potential risks of surgery. A thorough understanding of the embryologic development of the ear and adherence to the surgical principles of tympanoplasty, canalplasty, and facial nerve surgery enable optimal and safe hearing restoration. Maintenance of good initial surgical results and avoidance of late complications require diligent postoperative office care. BAHAs provide a good alternative for patients who are poor atresiaplasty candidates.

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52. Bellucci R.J. Congenital aural malformations: Diagnosis and treatment. Otolaryngol Clin North Am . 1981;14:95-124.
53. Jahrsdoerfer R.A., Yeakley J.W., Aguilar E.A., et al. Grading system for the selection of patients with congenital aural atresia. Am J Otol . 1992;13:6-12.
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56. Chiossone E. Surgical management of major congenital malformations of the ear. Am J Otol . 1985;6:237-242.
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58. Fernandez A.O., Ronis M.L. The Treacher Collins syndrome. Arch Otolaryngol . 1964;80:505-520.
59. Rapin I., Ruben R.J. Patterns of anomalies in children with malformed ears. Laryngoscope . 1976;86:1469-1502.
60. Ruben R.J., Toriyama M., Dische M.R., et al. External and middle ear malformations associated with mandibulo facial dysostosis and renal abnormalities: A case report. Ann Otol Rhinol Laryngol . 1969;78:605-624.
61. Sanchez-Corona J., Garcia-Cruz D., Ruenes R., Cantu J.M. A distinct dominant form of microtia and conductive hearing loss. Birth Defects . 1982;18:211-216.
62. Miyamoto R.T., Fairchild T.H., Daugherty H.S. Primary cholesteatoma in the congenitally atretic ear. Am J Otol . 1984;5:283-285.
63. Jahrsdoerfer R.A., Yeakley J.W., Hall J.W.III, et al. High-resolution CT scanning and auditory brain stem response in congenital aural atresia: Patient selection and surgical correlation. Otolaryngol Head Neck Surg . 1985;93:292-298.
64. Jahrsdoerfer R.A., Hall J.W. Congenital malformations of the ear. Am J Otol . 1986;7:267-269.
65. Brent B. The correction of microtia with autogenous cartilage grafts, I: The classic deformity. Plast Reconstr Surg . 1980;66:1-12.
66. Brent B. Auricular repair with autogenous rib cartilage grafts: Two decades of experience with 600 cases. Plast Reconstr Surg . 1995;90:355-374.
67. Gates G.A., Hough J.V., Gatti W.M., Bradley W.H. The safety and effectiveness of an implanted electromagnetic hearing device. Arch Otolaryngol . 1989;115:924-930.
68. Hakansson B., Liden G., Tjellstrom A., et al. Ten years of experience with the Swedish bone-anchored hearing system. Ann Otol Rhinol Laryngol Suppl . 1990;151:1-16.
69. Niparko J.K., Langman A.W., Cutler D.S., Carroll W.R. Tissue-integrated prostheses in the rehabilitation of auricular defects: Results with percutaneous mastoid implants. Am J Otol . 1993;14:343-348.
70. Naumann A. Plastic surgery to correct deformities of the ear. MMW Fortschr Med . 2005;147:28-31.
71. Romo T.3rd, Presti P.M., Yalamanchili H.R. Medpor alternative for microtia repair. Facial Plast Surg Clin North Am . 2006;14:129-136.
72. Kelley P.E., Scholes M.A. Microtia and congenital aural atresia. Otolaryngol Clin North Am . 2007;40:61-80.
73. Tjellstrom A., Hakansson B. The bone-anchored hearing aid: Design, principles, indications, and long-term clinical results. Otolaryngol Clin North Am . 1995;28:53-72.
74. van der Pouw K.T.M., Snik A.F.M., Cremers C.W.R.J. Audiometric results of bilateral bone-anchored hearing aid application in patients with bilateral congenital aural atresia. Laryngoscope . 1998;108:548-553.
75. Kunst S.J., Leijendeckers J.M., Mylanus E.A., et al. Bone-anchored hearing aid system application for unilateral congenital conductive hearing impairment: audiometric results. Otol Neurotol . 2008;29:2-7.
76. House J.W., Kutz J.W.Jr. Bone-anchored hearing aids: incidence and management of postoperative complications. Otol Neurotol . 2007;28:213-217.
77. Evans A.K., Kazahaya K. Canal atresia: “Surgery or implantable hearing devices? The expert’s question is revisited.”. Int J Pediatr Otorhinolaryngol . 2007;71:367-374.
78. Sortini A.J. Hearing aids for children with bilateral congenital ear canal atresia. Hear Instrument . 1981;6:20-23.
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80. Andrews J.C., Anzai Y., Mankovich N.J., et al. Three-dimensional CT scan reconstruction for the assessment of congenital aural atresia. Am J Otol . 1992;13:236-240.
81. Crabtree J.A. The facial nerve in congenital ear surgery. Otolaryngol Clin North Am . 1974;7:505-510.
82. Linstrom C.I., Meiteles L.Z. Facial nerve monitoring in surgery for congenital auricular atresia. Laryngoscope . 1993;103:406-415.
83. Chandrasekhar S.S., De La Cruz A., Lo W.W.M., Telischi F.J. Imaging of the facial nerve. In: Jackler R.A., Brackmann D.E., editors. Neurotology . St. Louis: Mosby–Year Book; 1993:341-359.
84. De la Cruz A., Teufert K.B. Congenital aural atresia surgery: Long-term results. Otolaryngol Head Neck Surg . 2003;129:121-127.
85. Teufert K.B., De la Cruz A. Advances in congenital aural atresia surgery: Effects on outcome. Otolaryngol Head Neck Surg . 2004;131:263-270.
86. Chole R.A. Meatoplasty using inferiorly based island pedicle flap for congenital aural atresia. Laryngoscope . 1983;93:954-955.
87. Colman B.H. Congenital malformations of the ear—aspects of management. J Otolaryngol Soc Austral . 1978;4:197-200.
88. Wigand M.E. Tympano-meatoplastie endurale pour les atresies congenitales severes de l’oreille. Rev Laryngol . 1978;99:14-28.
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94. Digoy G.P., Cueva R.A. Congenital aural atresia: Review of short- and long-term surgical results. Otol Neurotol . 2007;28:54-60.
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98. Lambert P.R. Congenital aural atresia: Stability of surgical results. Laryngoscope . 1998;108:1801-1805.
Chapter 6 Surgery of Ventilation and Mucosal Disease

Bradley W. Kesser, M. Jennifer Derebery, Rick A. Friedman
Bilateral myringotomy with placement of ventilation tubes is the most common surgical procedure performed in the United States. An estimated 1.05 million tympanostomy tube procedures are performed annually in the United States. 1 In addition, otitis media is the most common diagnosis of patients who make office visits to physicians in the United States—the diagnosis increased from about 10 million visits in 1975 to 25 million in 1990. 2 The annual visit rate for children younger than 2 years statistically increased by 224% during one study period. 3 Otitis media with effusion (OME) incurs approximately $5 billion annually in direct and indirect costs. 1 Because of the magnitude of the disease and its impact on society, and conflicting reports over the most appropriate and cost-effective management of the problem, 1, 3 - 5 consensus on the treatment of OME has been difficult to achieve. Attempts have been made to devise an algorithm for the management of OME in young children, 6 and these guidelines have been recently reviewed and updated (see later). 7, 8 This chapter reviews the terminology, epidemiology, pathophysiology, and medical and surgical treatment of OME.

TERMINOLOGY
The term otitis media, in its broadest sense, refers to any inflammatory process in the middle ear. The etiology of the inflammation can be (and usually is) infectious in nature, but it can also involve rarer systemic inflammatory diseases (e.g., Wegener’s granulomatosis or type I Gel and Coombs hypersensitivity). The inflammation can be marked by the presence or absence of an effusion, or fluid in the middle ear space. The fluid can be serous (thin, watery, often golden), purulent (pus), or mucoid (thick, viscid “glue”).

Acute Otitis Media without Effusion
Acute otitis media (AOM) without effusion is characterized by an inflamed middle ear mucosa and tympanic membrane in the absence of an effusion; this can be seen in the early stages of AOM or during its resolution. The tympanic membrane appears dull, erythematous, hypervascular, and inflamed; normal landmarks are often lost. In infants and children, AOM without effusion is usually caused by the same organisms that are isolated from acute OME. 9 Treatment principles are the same and are discussed later.

Acute Otitis Media with Effusion
Acute OME occurs most frequently in infants. Redness with or without bulging of the tympanic membrane, fever, irritability, and pain are the hallmark signs and symptoms. An older child with acute OME has a red tympanic membrane and middle ear effusion, but may not have pain or fever. The middle ear effusion is generally purulent. Casselbrant and associates 10 reported a cumulative incidence of acute OME of 43% in a study of 198 newborns followed monthly until the age of 2 years. In the Greater Boston Otitis Media Study Group, infants had an average of 1.2 and 1.1 episodes per year, with 46% of children having had 3 or more episodes by the age of 3 years. 11
Recurrent AOM refers to frequent bouts of AOM. The child most likely has intercurrent, persistent (chronic) OME. The effusion becomes infected, and the child develops AOM. Recurrent AOM is an indication for surgical intervention (see later).

Otitis Media with Effusion
Otitis media with effusion simply refers to fluid in the middle ear without signs or symptoms of ear infection. Asymptomatic OME can be classified as acute (<3 weeks), subacute (3 weeks to 3 months), or chronic (>3 months). 12 Acute and chronic refer to the temporal course of the disease, not to severity. Synonyms of OME include secretory otitis media, nonsuppurative otitis media, or serous otitis media; the most commonly used term is OME.

Chronic Suppurative Otitis Media
Chronic suppurative otitis media (CSOM) is a stage of ear disease in which there is chronic infection of the middle ear and mastoid, and in which a central perforation of the tympanic membrane (or a patent tympanostomy tube) and discharge (otorrhea) are present. 13 To meet the requirement for “chronic,” the otorrhea should be present for 6 weeks or longer. The infection involves the mastoid and the middle ear, and usually drains through a central perforation. Chronic otorrhea through a nonintact tympanic membrane (perforation or ventilation tube) may or may not be accompanied by cholesteatoma. Cholesteatoma may or may not result in CSOM. CSOM should not be confused with chronic OME; in the latter, no perforation is present, and the fluid is not purulent.

Idiopathic Hemotympanum
The clinical hallmark of idiopathic hemotympanum is the dark blue–appearing tympanic membrane. There is usually no antecedent history of trauma, but trauma can induce this condition. Idiopathic hemotympanum represents a tissue response of the temporal bone to the presence of a foreign body—cholesterol crystals. Three etiologic factors are thought to be responsible: interference with drainage, hemorrhage, and obstruction of ventilation. Chronic OME is the principal precursor. Cholesterol granuloma is the histopathologic correlate. These cholesterol cysts can take an aggressive course with bone erosion and osteitis. Treatment is generally surgical drainage (see later).

EPIDEMIOLOGY
Teele and colleagues 11, 14, 15 found that 13% of children in their study groups had at least one episode of AOM by age 3 months; that percentage increased to 67% by 12 months. By age 3 years, 46% of children had three or more episodes of AOM. The highest incidence of AOM was found in children 6 to 11 months old. Most children with multiple recurrences of otitis media have their first episode before age 12 months.
An episode of AOM is a significant risk factor for the development of OME. Many investigators have documented persistent middle ear effusion after a single episode of AOM. 14 - 17 Middle ear effusion has been shown to persist after an episode of AOM for 1 month in 40% of children, 2 months in 20%, and 3 or more months in 10%. 15

Risk Factors
Risk factors for OME include male gender, recent upper respiratory infection, allergic rhinitis, first-degree relative with allergy, bottle feeding, cigarette smoke in the house, increased number of siblings in the house, and, probably the most important, daycare. 18 Children in a public daycare facility have a fivefold increase in otitis media at age 2 years compared with children in home care. 19 Whites and Hispanics are more susceptible than African Americans; Native Americans and Inuit are at even greater risk.
Skeletal and anatomic factors also predispose to OME. Cleft palate—either overt or submucous—is a significant risk factor. Other craniofacial anomalies, including Treacher Collins syndrome, Apert’s syndrome, Down syndrome and the mucopolysaccharidoses, put children at greater susceptibility to middle ear disease, presumably because of immaturity, dysfunction, and anatomic course of the Eustachian tube. Children with immunodeficiencies are also at greater risk. IgG subclass deficiencies, acquired immunodeficiency syndrome, complement deficiencies, and immunosuppression secondary to medication all predispose to otitis media. Ciliary dysfunction and cystic fibrosis are also known risk factors.

Microbiology
Bluestone and coworkers 20 obtained aspirates of middle ear effusions by tympanocentesis in infants and children with AOM or OME. Of aspirates from ears with AOM, 35% grew Streptococcus pneumoniae, 23% grew Haemophilus influenzae, and 14% grew Moraxella catarrhalis . 20 S. pneumoniae remains the most common bacterium causing AOM. 21 - 23 Introduction of the pneumococcal vaccine may significantly reduce the incidence of pneumococcal disease, including otitis media. 24 - 26
Asymptomatic middle ear effusion (OME) had been previously thought to be sterile. Newer, more sensitive cultures and the introduction of polymerase chain reaction (PCR) testing have shown bacteria and bacterial DNA in asymptomatic middle ear effusions. 27 These investigators found that 77% of middle ear effusions had evidence of the three major organisms by PCR (with or without being culture positive), whereas only 28% were culture positive. The most common bacteria were H. influenzae (54.5%), M. catarrhalis (46.4%), and S. pneumoniae (29.9%). 27 By comparison, in an earlier study of ears with OME, 30% of aspirates did not grow bacteria, 45% grew “other” strains, 15% had H. influenzae, 10% had M. catarrhalis, and 7% grew S. pneumoniae . 20 Other bacteria include Staphylococcus aureus and gram-negative enteric bacilli. In infants younger than 6 weeks, gram-negative bacilli cause about 20% of AOM episodes. 21
The bacteriology of CSOM with or without cholesteatoma is different. Most frequently isolated bacteria include Pseudomonas aeruginosa (most common), S. aureus, Corynebacterium, Klebsiella pneumoniae, and anaerobes. 23 With better culture techniques, anaerobes have been increasingly isolated from chronic suppurating ears; these organisms include Bacteroides spp., Peptococcus spp., Peptostreptococcus spp., and Propionibacterium acnes . 23

PATHOPHYSIOLOGY

Acute Otitis Media
Retrograde reflux of material from the nasopharynx through the Eustachian tube is thought to account for the introduction of microorganisms into the middle ear. Bacteria colonize the nasopharynx, but infect the host as a result of a breakdown in barrier or protective factors in the nasopharynx, Eustachian tube, and middle ear.
AOM is principally a sequela of a viral upper respiratory infection. The upper respiratory infection impairs ciliary motility and breaks down mucosal barriers that prevent bacterial adherence and growth. Poor clearance of secretions results in stasis and allows bacteria to infect the host. Pathogenic bacteria that appear in the nasopharynx after an upper respiratory infection are the same as the bacteria cultured from middle ear effusions ( S. pneumoniae and H. influenzae ). 28 The adenoid seems to be the source of infecting bacteria in middle ear disease; Pillsbury and associates 29 showed higher bacterial colony counts in the adenoids of children with recurrent otitis media than in children undergoing adenoidectomy for adenoid hypertrophy without otitis media. During an upper respiratory infection, sneezing, blowing the nose, and swallowing in the presence of nasal obstruction may create a pressure differential between the nasopharynx and middle ear, forcing bacteria through the Eustachian tube into the middle ear.
Finally, Eustachian tube dysfunction is held accountable for OME. The Eustachian tube has three functions: (1) clearance of secretions from the middle ear into the nasopharynx, (2) protection of the middle ear from nasopharyngeal pathogens, and (3) equalization of pressure between the atmospheric pressure (in the nose) and middle ear pressure. The middle ear is an aerated “sinus.” It too must be ventilated and cleared of secretions—the Eustachian tube serves this capacity. In children, the Eustachian tube is short, horizontal, and relatively flaccid. As a result, the protective function of the tube is compromised, and retrograde reflux of secretions into the middle ear occurs. During an acute infection, ciliary function is also compromised, further leading to stasis of secretions and persistence of effusion (see next section).

Chronic Otitis Media with Effusion
Two theories have been proposed to account for the persistence of middle ear effusion in the absence of acute infection. As shown by the Boston Collaborative Group, persistent effusion is a natural sequela of acute middle ear infection. 15 Effusion persists for 1 month in 40% of children after an episode of AOM, 2 months in 20%, and 3 or more months in 10%. 15 Because pathogenic bacteria and bacterial DNA have been recovered from “nonacutely infected” fluid in the middle ear, 21, 27, 30 - 31 it seems that Eustachian tube obstruction and retained secretions in these cases are the result of the acute infection, rather than the cause.
Eustachian tube dysfunction may be a primary disorder that causes acute and chronic OME. Primary Eustachian tube dysfunction results in underaeration and poor ventilation of the middle ear space; this leads to negative pressure in the middle ear with resultant transudation of fluid. Negative middle ear pressure also causes hypoxia and hypercapnia of the middle ear mucosa, resulting in goblet cell hyperplasia and hypersecretion. 32, 33 The result is a sterile fluid that becomes secondarily infected. The fluid resolves only after adequate ventilation is restored, either by return of Eustachian tube function or by placement of alternative ventilation, such as a ventilation tube.
According to Gates, 34 the available evidence lends support to the theory that the secretory changes in the middle ear that exist in cases of chronic OME are the histologic sequelae of chronic infection, rather than a separate pathologic disorder. Most cases of chronic OME begin as acute infection of the middle ear; postinflammatory alterations in the mucosa of the middle ear and Eustachian tube lead to persistent effusion. Obstruction of the Eustachian tube is secondary to the infection and not the cause of it. Eustachian tube obstruction prevents clearance of secretions, impedes ventilation and drainage, and perpetuates the inflammatory process.
Allergic rhinitis has been recognized as a risk factor in the development of chronic OME. The actual prevalence of “allergic” chronic OME has been reported in the literature with a very broad range of 10% to 90%. 32
Although it is beyond the scope of this chapter to provide extensive details of the type I hypersensitivity response, we provide a short summary. Atopic disease is initially characterized by antigen exposure and specific sensitization. Subsequent re-exposure results in mast cell degranulation and the release of numerous inflammatory mediators, including histamine, cysteinyl leukotrienes, and cytokines, and the infiltration of eosinophils, mast cells, basophils, and other inflammatory cells. 35 These cells further the release of histamine and cysteinyl leukotrienes, resulting in increased mucosal blood flow, vascular permeability, and mucus production, and continued recruitment of inflammatory cells.
As in the nose, continued allergic inflammation in the middle ear is associated with a marked increase in the number of mucosal mast cells and cell bound IgE. 36 In addition to degranulation, mast cells may also pre-sent antigen to B lymphocytes, dendritic cells, and monocytes, resulting in the further release of proinflammatory 36 cytokines, including tumor necrosis factor, interleukin (IL)-1, and IL-6. 36 IL-4 is released by activated mast cells and circulating basophils, and naïve T cells. IL-4 eventually mediates an isotypic switch from a predominantly T H 1 lymphocytic profile of naïve T cells to the proinflammatory T H 2 cells that are the hallmark of atopic disease. The further release of IL-5, IL-9, and IL-13 by T H 2 lymphocytes results in the recruitment and activation of more basophils, mast cells, and eosinophils, insuring the development of a chronic allergic milieu. 33
The nasal mucosa, middle ear space, nasopharynx, and Eustachian tube, which together comprise the middle ear system, could each potentially serve as the target organ of an allergic reaction resulting in the production of chronic OME. As noted subsequently, not only have allergic effector cells been isolated in each area, but also the intimate anatomic relationships ensure that disruption of the normal functions in one area may have an undesirable effect in another. We now review the evidence of allergic reactivity in each area.

Nose
The nose is the target organ most commonly involved in the allergic reaction, and numerous publications have supported the concept that allergic inflammation resulting in nasal congestion may result in significant Eustachian tube obstruction. 37 - 40 The sensitized mucosa of the nose, adenoid bed, or nasopharynx exposed to allergens releases cytokines, resulting in increased mucus secretion, edema, and inflammation around the torus tubarius. The resulting Eustachian tube obstruction has a negative effect on middle ear ventilation, resulting in the production of chronic OME.

Middle Ear Space
Although it is intuitively tempting to consider the middle ear the most likely target organ of an allergic reaction resulting in the production of chronic OME, there is likely little antigen exposure to the middle ear mucosa. The Eustachian tube is normally closed, unless one is swallowing or yawning, which would make it much less likely than the nose to allow physical contact with inhaled aeroallergens. Supporting this limited role, Bernstein 39 suggested, based on a study determining the local production of IgE in middle ear mucosal biopsy specimens of atopic children undergoing pressure equalization tube insertion, that the middle ear mucosa likely serves as the target organ of an allergic reaction less than 10% of the time. Other authors disagree, however. Eustachian tube dysfunction has been reported from transtympanic challenge on antigen in sensitized animals. 41, 42 Ebert and colleagues 43 showed a similar finding with intratympanic histamine mast cells found to be present in the middle ear effusions and biopsy specimens of children with chronic OME, suggesting local inflammation and reaction. 44 - 47
The middle ear mucosa seems to be capable of being involved directly in an allergic reaction. Authors agree, however, that this direct involvement is likely uncommon. The role of possible local involvement triggered by a food antigen has yet to be defined.

Eustachian Tube
Several mechanisms for Eustachian tube dysfunction have been proposed. First, congestion of the nasal mucosa may produce a retrograde spread of edema and Eustachian tube dysfunction. Second, poor mucociliary function, either innate or resulting from allergic or other inflammatory etiologies, may lead to retention of secretions resulting in obstruction of the Eustachian tube. 48, 49 Third, inhalation of aeroallergens with subsequent direct allergic inflammation within the Eustachian tube may produce venous engorgement and hypersecretion of mucus, with the subsequent obstruction affecting gas exchange in the middle ear space. 50 The resulting negative pressure allows a transudation of fluids into the middle ear space by the interruption of cellular tight junctions. 39, 50 Later, persistent obstruction of the Eustachian tube with mucus results in chronic middle ear inflammation, with resulting mucosal metaplasia and increased glandular activities of goblet cells. 39, 50
Increasingly, physicians who treat allergic patients embrace the concept of one airway, whereby the inflammatory response in one portion of the airway may also lead to inflammatory changes in other portions. The classic example is the recognition of the intimate relationship existing between the upper and lower airways. In a study of atopic subjects, inhaled allergen challenge isolated to the nose produced inflammatory changes in the upper and lower airways. These changes included increased adhesion molecules, increased bronchial hyperreactivity, and eosinophil infiltration. 51 Although it is important that we continue research to define the immunology involved in the subset of patients with chronic OME who have allergy as an underlying etiology, we should keep in mind that allergy does affect the common airway, and that lessening significant allergic inflammation in the entire anatomic area would be beneficial.

DIAGNOSIS


Idiopathic Hemotympanum
Long-standing cases of chronic OME that develop granulomatous deposits in the middle ear and mastoid can lead to idiopathic hemotympanum. Symptoms of idiopathic hemotympanum are those of OME—hearing loss with a plugged or pressure sensation in the ear. Idiopathic hemotympanum is more common in adults. It is characterized by a dark blue–appearing tympanic membrane; fluid at myringotomy is dark brown and syrupy in consistency. Histologically, cholesterol crystals are seen—hence the pathologic term cholesterol granuloma . It is theorized that a small mucosal hemorrhage in the absence of adequate ventilation and drainage results in deposition of hemosiderin, iron, and blood breakdown products into the submucosa. The contents can be walled off, with resultant cyst development. The cyst slowly expands, causing bone thinning and erosion.

TREATMENT AND PATIENT SELECTION


Acute Otitis Media and Recurrent Acute Otitis Media
For a single episode of AOM, antimicrobial therapy targets the most common offending pathogens: S. pneumoniae, H. influenzae, and M. catarrhalis . We recommend a 10-day course of amoxicillin as first-line empirical therapy. Clinical practice guidelines from the Agency for Healthcare Research and Quality (AHRQ) argue for observation without antibiotic therapy in selected patients with AOM ( Table 6-1 ). 7 Studies have shown an increase in the β-lactamase-producing organisms, H. influenzae and M. catarrhalis . 19, 52 β-Lactamase renders the organism that produces it resistant to penicillin (and ampicillin). Persistent or recurrent AOM may be secondary to a β-lactamase-producing organism and requires a broader spectrum antibiotic 53 ; good choices in this setting include cefuroxime, erythromycin-sulfisoxazole, trimethoprim-sulfamethoxazole, amoxicillin-clavulanate, and cefaclor. Antipyretics (but not aspirin) are also indicated for children with AOM.
TABLE 6-1 Criteria for Initial Antibacterial Agent Treatment or Observation in Children with Acute Otitis Media Age Certain Diagnosis Uncertain Diagnosis <6 mo Antibacterial therapy Antibacterial therapy 6 mo–2 yr Antibacterial therapy Antibacterial therapy if severe illness; observation option if nonsevere illness ≥2 yr Antibacterial therapy if severe illness; observation option if nonsevere illness Observation option
From American Academy of Pediatrics Subcommittee on Management of Acute Otitis Media: Diagnosis and management of acute otitis media. Pediatrics 113:1451-1465, 2004.
A child (or adult) with an infectious complication of otitis media requires more aggressive therapy, including intravenous antibiotics and possible surgical intervention. This subject is beyond the scope of this chapter and is discussed in Chapter 19 .
Children with recurrent AOM may exhibit normal middle ear examinations between episodes, or may retain persistent effusions and fall into the category of chronic OME. The goal of any treatment of a patient with recurrent AOM is long-term prevention of further episodes of otitis media.
Placement of tympanostomy tubes is effective treatment in the prevention of recurrent otitis media. Many authorities accept four episodes of AOM in 6 months as a criterion for tympanostomy tube placement. Gebhart 54 was the first to show a reduction in the number of new episodes of AOM after insertion of tympanostomy tubes.
The role of adenoidectomy in the treatment of recurrent AOM is controversial. Although Paradise and coworkers 55 found a significant reduction (28% and 35%) in the incidence of AOM in the first and second years after adenoidectomy, a formal study examining the role of adenoidectomy in the treatment of recurrent AOM has not been done. Results of studies of chronic OME and adenoidectomy may or may not be applicable for patients with recurrent AOM. For patients with recurrent AOM and persistent effusion, adenoidectomy is an appropriate surgical treatment (see the following section on chronic OME).

Chronic Otitis Media with Effusion
As mentioned, 10% of children with AOM have persistent middle ear effusion 3 or more months after resolution of the acute infection. 15 Most children clear their effusion within 1 to 2 months; these patients need no further therapy. The few patients who retain fluid in the middle ear longer than 3 months are at risk for other sequelae, including hearing loss, language delay, vertigo or imbalance, tympanic membrane changes (including atelectasis or retraction pockets or both), further middle ear pathology (including ossicular problems and adhesive otitis), and discomfort with nighttime wakefulness and irritability.
Numerous treatment strategies have been proposed for chronic OME: antimicrobial therapy, antihistamines/decongestants, corticosteroids, tympanostomy tubes with or without adenoidectomy, and mastoidectomy. Updated clinical practice guidelines from the AHRQ do not recommend antibiotics, antihistamines, decongestants, or corticosteroids for the treatment of chronic OME. 8 These modalities and allergic strategies are now reviewed.

Antimicrobial Therapy
More sensitive techniques (e.g., PCR) have shown bacterial DNA in middle ear effusions previously thought to be “sterile” or culture negative. Prolonged antibiotic therapy theoretically eradicates the organism and eliminates the chronic source of effusion. Some studies have shown the efficacy of antibiotics in OME. 21, 56 Despite these studies, theoretical and practical arguments can be made against their use in chronic OME. Clinical experience indicates that the utility of antibiotics is reduced as the number of treatment courses increases. Children receiving four or more courses of antibiotics over a 3 to 4 month period are most likely not going to resolve their effusion with medical management. Other adverse effects of prolonged antimicrobial therapy include development of anaphylaxis and allergic reactions; hematologic disorders; and the emergence of resistant organisms, a serious worldwide problem best shown by the development of resistance to penicillin by S. pneumoniae . Finally, Rosenfeld and Post found through a large meta-analysis of existing studies that the benefit of antimicrobial therapy in chronic OME is slight.

Antihistamines and Decongestant Therapy
Oral antihistamine and decongestant combinations and monotherapy have not been shown to be beneficial in the treatment of chronic OME. 56 The AHRQ clinical practice guideline does not recommend these agents for chronic OME. 8 A possible exception may be in an adult patient with allergen-induced Eustachian tube dysfunction. Stillwagon and colleagues 57 investigated the effects of pharmacotherapy on allergen-induced Eustachian tube dysfunction. In this study, adults with a history of seasonal allergic rhinitis to ragweed pollen received either a combination of antihistamine and decongestants or placebo for 7 days followed by an intranasal challenge with ragweed pollen. Eustachian tube obstruction occurred in fewer patients receiving active treatment than in patients receiving placebo. They concluded that pre-exposure treatment with antihistamines in patients with allergic rhinitis may help decrease the risk of developing Eustachian tube dysfunction. There are no studies to date on a possible role of intranasal antihistamines on treatment of middle ear effusion.

Antileukotrienes
Antileukotrienes have not been well studied for a possible role in the treatment of chronic OME. Combs 58 found a significant decrease, however, in the duration of middle ear effusion in otitis-prone children treated with montelukast after AOM compared with a control group. The reader is advised to take into account the paucity of research and the expense of this relatively safe medication when debating its possible merit in treatment.

Corticosteroid Therapy
Steroid therapy for chronic OME has been controversial. Lambert 59 found no difference in outcomes between the steroid group and the control group with chronic OME. At this time, the AHRQ guideline does not recommend steroid therapy for chronic OME. 8

Treatment for Food Allergy
The younger the child with suspected allergies, the more likely the antigen will be ingested rather than inhaled. Juntti and associates 60 found that 34% of children with allergic rhinitis or asthma who also had cow’s milk allergy had recurrent OME compared with 13% of children who had allergic rhinitis and no diagnosed milk allergy.
Food allergy is usually suspected in a young child with OME or recurrent AOM and a family history of allergy, and the frequent association of rhinitis with or without asthma or eczema or both. Objective confirmation may be obtained by in vitro or skin testing to a panel of food antigens, followed by an oral challenge/elimination diet as needed.

Immunotherapy
Many studies have suggested that more than 70% of children with chronic OME are considered atopic, based on skin tests or in vitro testing. 61 - 64 Immunotherapy for inhalant allergies has been found to be very efficacious in symptom reduction and in lessening the progression of allergic disease. There have been no studies to date of the same rigor on the possible role of immunotherapy for treatment of allergic middle ear disease. The studies that do report a very high (≥75%) rate of resolution of OME with immunotherapy or dietary elimination virtually never have a sufficient (or any) control group, and have varying definitions of allergy and mode of diagnosis, as opposed to studies that have been published on the role of immunotherapy in treatment for allergic rhinitis. 37, 61, 62, 65, 66
Although it is challenging to desensitize young children with injectable immunotherapy, these studies need to be done to define what role this modality should play in evidence-based practices of the future. It is possible that sublingual immunotherapy, currently widely practiced in Europe, but not yet approved for use in the United States, may more easily allow the design of clinical trials involving young atopic children in the future.

Surgical Therapy
Armstrong 67 introduced ventilation tube placement in 1954 as a treatment for OME. The ventilation tube acts as an artificial Eustachian tube, aerating the middle ear and equilibrating middle ear pressure with atmospheric pressure. The pathophysiology of chronic OME involves Eustachian tube dysfunction and reflux of nasopharyngeal organisms. Ventilation tubes are aimed at correcting Eustachian tube dysfunction. Children with tubes in place can still get otitis media; the acute infection is not painful because the infected effusion is allowed to pass through the tube and out of the middle ear. The effusion also is not associated with hearing loss; correction of hearing loss is one of the most important goals of surgical therapy. Tube insertion with or without adenoidectomy has been shown to improve conductive hearing loss secondary to OME, and to decrease the amount of time spent with middle ear effusion. 21 Placement of tubes is often a clinical judgment based on experience and is addressed on a case-by-case basis. Nevertheless, the AHRQ clinical practice guidelines do offer evidence-based recommendations for tympanostomy tube placement (see later). 8

Adenoidectomy
Nasopharyngeal reflux of secretions and microorganisms into the middle ear plays a large role in the pathophysiology of chronic OME. Adenoidectomy is designed to remove the source of the infecting microorganisms. Three landmark studies have shown the efficacy and low morbidity associated with adenoidectomy. 4, 55, 68 Adenoidectomy is effective treatment for chronic OME, and significantly reduces its morbidity. Its effect is independent of adenoid size. It is argued that the small, “smoldering” adenoid chronically harbors bacteria and is a major contributor to OME. The decision for adenoidectomy should be based on the severity and persistence of the middle ear disease, not the size of the adenoid. Nasal obstruction with adenoid hypertrophy stands alone as an indication. Given the increased cost and slightly increased risk to the patient, Paradise and Bluestone 69 have argued for adenoidectomy only in recurrent cases.
Much of the literature published on the role of adenoidectomy in OME has been in children 4 to 8 years old. 8 Nevertheless, adenoidectomy has been shown to be safe in children older than 18 months, 5 and may be effective in younger, high-risk children. In the San Antonio study, the effect of adenoidectomy was greater for younger children. 4 We recommend adenoidectomy for recurrent cases—cases in which the child (>4 years old) needs a second set of tubes.

Mastoidectomy
Rarely, mastoidectomy is required for chronic OME. The continuously draining ear with secretory tissue in the mastoid (serous mastoiditis) benefits most from opening the aditus ad antrum and facial recess to increase aeration of the middle ear/mastoid air cell system. Removal of secretory tissue or granulation tissue also improves symptoms. Because of the rare necessity for mastoidectomy in chronic OME, no systematic study has been undertaken to prove its efficacy. Decision to proceed with mastoid surgery is based on clinical experience and judgment. We have often left a small Penrose drain in the mastoid and carried it out through the postauricular incision. The drain is removed after the drainage has stopped. Mastoidectomy should be reserved for cases with abnormal mucosa or cholesterol granuloma in the mastoid; it is more commonly indicated for idiopathic hemotympanum.

PATIENT COUNSELING
Benefits, limitations, and risks and complications all should be addressed preoperatively with the patient and the parents.

Benefits
Hearing improvement and reduction in the number of subsequent episodes of ear infections are the chief benefits of tympanostomy tube placement. Hearing improvement speeds and sharpens language and developmental maturation. If the child develops otitis media, tympanostomy tubes also eliminate pain because the infected fluid is allowed to drain out of the middle ear space. Studies have also shown improvement in vestibular function after tympanostomy tube placement. 79 - 81 Finally, reducing the number of secondary problems of recurrent ear infections means less time lost from work for the parents, fewer (if any) courses of antibiotics, and reduction in the cost to the parents of multiple courses of antibiotics. Surgery has been shown to be a cost-effective treatment for children in whom medical therapy fails. 1
Benefits of adenoidectomy include improved nasal airway and breathing, and removal of the probable source of the offending pathogens causing middle ear infection. Adenoidectomy is associated with a reduction in the number of new episodes of otitis media. It can also improve sleep, especially in a child with obstructive sleep apnea. As discussed, size of the adenoid has no influence on the incidence of chronic OME; it is theorized that a smaller, chronically infected adenoid may lead to more middle ear problems.

Limitations
Tympanostomy tube placement is only a temporizing measure—the tube ventilates the middle ear, but eventually extrudes. The goal is that the tube serves as an artificial Eustachian tube until the child’s own Eustachian tube matures and functions properly. Some children need second and third sets of tubes before their own Eustachian tube functions well enough to ventilate the middle ear. Some Eustachian tubes never work well, and the child may develop further ear disease. Nevertheless, parents should know that tubes are placed to buy time for their child’s own Eustachian tube to function normally. Tubes can also become obstructed.
Adenoidectomy does not sterilize the nasopharynx, and it does not prevent otitis media. It can improve the nasal airway, but may not cure obstructive sleep apnea.

Risks and Complications
All potential risks and complications, including the risk of anesthesia, should be explained to the parents. Risks of tympanostomy tube insertion include persistent otorrhea, tympanic membrane perforation, and hearing loss. We advise water precautions in children with tubes in place. Eardrum perforation is related to bore of the tube, length of time in place, number of intercurrent infections, and previous history of tubes. Incidence of perforation can be 1% to 15%.
Bleeding occurs in less than 1% of cases of adenoidectomy. It can require a trip back to the operating room. Temporary velopharyngeal insufficiency has been reported in less than 5%; permanent disability is rare in the absence of problems with palatal clefting (must check for submucous cleft palate by palpation and inspection before proceeding with adenoidectomy). Nasopharyngeal stenosis with subsequent nasal airway and speech problems is a rare complication, but should be mentioned preoperatively.

Idiopathic Hemotympanum
We generally recommend tympanostomy tube placement as first-line treatment for idiopathic hemotympanum. This treatment is usually inadequate, however, and the patient requires mastoidectomy. Preoperatively, we order a high-resolution temporal bone computed tomography (CT) scan to examine the air cell pattern, evidence of erosion, and extension of the cholesterol granuloma. Intact canal wall mastoidectomy with removal of diseased mucosa aerates the mastoid and middle ear; aeration is the goal of surgery. The greatest limitation is the risk of recurrence, which is reported to be 50%. Risks of hearing loss, facial nerve injury, and dizziness are low, but are also discussed with the patient.

SURGICAL TECHNIQUE

Preoperative Preparation
The child is kept NPO after midnight the night before surgery. As a consequence, surgery on children should be the first cases when possible. NPO status 4 to 6 hours before the administration of anesthesia is generally adequate. We do not use perioperative antibiotics for tubes or mastoidectomy. We attempt to keep the child with the parent as long as possible, depending on the child’s age, the anesthesiologist, and hospital policy. Anesthesia is delivered via mask induction and maintenance.
A general history and physical examination with screening for anesthetic risks is done for patients needing mastoidectomy. This is done in concert with the anesthesiologist and hospital policy. Mastoidectomy usually requires a general anesthetic.

Surgical Site Preparation and Draping

Tympanostomy Tubes
Sterilization of the external auditory canal is unnecessary; thorough cleaning of the canal is important, however, for visualization of the tympanic membrane and for postoperative care. The child lies in the supine position with the anesthesiologist delivering anesthetic by holding the mask over the face. The head can be turned to gain optimal visualization. A drape is placed over the child’s body, but not over the head. The operating microscope is brought into position directly below (inferior to) the surgeon, next to the patient bed.

Mastoidectomy
The patient is placed in the supine position with the head at the foot end of the table. The table is turned such that the anesthesiologist and equipment are located at the patient’s feet. Long tubing is used to span the distance. The head is turned away from the affected side; a shoulder roll is placed under the child to improve the surgeon’s angle of view. Straps or heavy tape across the chest and pelvis are used to avoid patient sliding as the table is rotated.
The postauricular area is shaved, and clear plastic drapes with sticky edges are applied to the skin edges after the skin is dried and coated with tincture of benzoin. These drapes keep unwanted hair out of the wound, and blood and bone dust out of the hair. An antibacterial soap followed by povidone-iodine is used to scrub the ear, postauricular area, and sticky drapes.
A second layer of sticky blue drapes or blue towels is placed around the postauricular area, followed by a standard ENT split sheet that is placed in such a way as to frame the operative site. A trough is created with the split sheet and clips to catch the irrigant and direct it away from the field and into a floor trash can.

Adenoidectomy
For adenoidectomy, we turn the table 90 degrees from the anesthesiologist. The patient is placed in the Rose position with shoulder roll. The head is brought to the edge of the table. A towel wrap is placed around the head and secured with a towel clip. This wrap leaves the nose and mouth exposed. Care is taken to ensure that the eyes are closed and taped shut properly before the head wrap is placed. A body drape is placed at the level of the shoulders and unfolded down over the body. A single Mayo stand with all necessary instruments is used over the body.

Instruments

Tympanostomy Tubes
A set of metal specula, cerumen curettes, and several sizes of suction cannulas (Baron Nos. 3, 5, and 7) are necessary. The operating microscope is also essential. Sterile myringotomy knives come in various shapes and angles. It is useful to choose a knife with a blade width the size of the tube to aid in making the correct dimensions of the incision. Tubes are placed with a cup or alligator forceps and positioned with a Rosen needle. Placement of long-stemmed T-tubes is facilitated by the use of an inserter in which the tube is positioned with the short arms of the tube folded forward ( Fig. 6-1 B). Care is taken to minimize trauma to the external auditory canal, drum, or ossicles.

FIGURE 6-1 A, Incision in tympanic membrane. B, Placement of T-tube within the inserter. C, Proper position of the tube.
FIGURE 6-2. A, Technique of adenoidectomy using the curette. It is important to keep the handle in the sagittal or parasagittal plane to prevent injury to the torus tubarius. B, Use of the suction cautery with mirror for hemostasis.
The tremendous variety of tube shapes and sizes is testament to the success of the operation. Choice of tube is dictated by surgeon preference on a case-by-case basis. The following basic principles guide tube choice:
1. Short, wide-bore tubes offer little resistance to water entry into the middle ear compared with the longer shaft tubes.
2. Longer shaft tubes can be more easily removed in the office; removal of short tubes with rigid flanges may require an anesthetic.
3. For longer middle ear intubation, long-stemmed T-tubes are preferred.
4. The Richards T-tube with flanges that rest against the middle ear side of the tympanic membrane stay in longest and can be permanent.
5. Risk of perforation increases with increasing duration of intubation, increasing number of infections, and increasing size of the tube.
For short-term intubation, short grommets are the best choice—they can last several months to 2 years. For long-term intubation, T-tubes are preferred.

Adenoidectomy
Any of the available mouth gags/retractors are adequate with proper technique. Adenoid curettes are available in several sizes and configurations. Angled instruments are easier to use than straight ones. Red rubber catheters placed through the nares and brought out the mouth are used to retract the soft palate. Laryngeal mirrors are useful to inspect the adenoid pad, any residual adenoid tissue, bleeding sites, and final operative site. Tonsil packs are used to pack the nasopharynx for hemostasis. A malleable suction cautery can also be helpful for hemostasis; we urge caution using this device, however, because it can lead to nasopharyngeal stenosis. A bulb irrigator and suction are also used to flush the nose and nasopharynx.

Mastoidectomy
The ideal operating room table has motorized controls for adjustment of height and side-to-side rotation. The surgeon’s stool has casters, easy height adjustment, and a flexible back support that permits the surgeon to lean backward as necessary while still receiving full back support. The operating microscope should be adjusted to the surgeon’s refraction and interpupillary distance. A standard set of ear instruments is necessary, including Rosen needle, annulus elevator, round knives, flat knives, and right angle dissectors. Bovie electrocautery can be used in the subcutaneous tissue of the postauricular incision, but it is not recommended around the middle or inner ear. Drill systems (e.g., Ototome, Midas Rex, Med-Next, Anspach) with various sizes of cutting and diamond burrs and suction irrigators are also necessary. Finally, facial nerve monitoring may be necessary. Several facial nerve monitors are available; the device should have the capacity for continuous monitoring and for stimulating the nerve for localization during the case.

Technical Details

Tympanostomy Tube Insertion
The ear canal is gently cleaned of all wax and debris. Contact with the anterior bony canal wall is avoided because of risk of bleeding. The tympanic membrane is inspected, and the short process of the malleus is identified. This is a constant landmark and may be the only one available in cases of acute infection. The tympanic membrane is incised anteroinferiorly by using an incision that parallels the fibrous annulus (see Fig. 6-1 ). Use of a radial incision is satisfactory, but may be limited by an overhanging anterior canal wall. Posterior incisions should be avoided because they place the ossicles at risk. The incision is gently spread open. Care is taken to avoid any major vessel in the tympanic membrane to prevent hemorrhage into the layers of the eardrum. This bleeding into the drum is thought to predispose to tympanosclerosis.
The middle ear should be evacuated by using a small-diameter (5 Fr) suction cannula. Occasionally, gluey material is too viscous to pass through the cannula. We do not recommend using anything larger than the 5 Fr cannula. In these cases, the middle ear and ear canal can be irrigated with warm sterile saline. This usually breaks the viscous material up enough to pass through the cannula. Not all of the effusion needs to be evacuated; as long as the middle ear has a near-normal airspace to place the tube, the remainder of the effusion is carried into the Eustachian tube or drains out the tube. Culture of the effusion rarely is done.
It is important to position the tube such that the lumen is in line with the surgeon’s line of sight, facilitating postoperative examination of the middle ear mucosa in the office and cleaning of the tube should it become plugged later on. When using T-tubes, the surgeon should ensure that the short arms of the tube are completely unfolded. Ototopical drops are placed if there is an acute infection. A small cotton ball is placed in the meatus.

Laser Myringotomy
The laser has become a useful, albeit expensive, tool in the management of chronic OME. Advantages of the laser include office-based application, ease of use, and the ability to place a controlled perforation in the tympanic membrane that stays open for a medium length of time (2 to 6 weeks). Using the CO 2 laser at 12 W with a single 100 ms pulse through a 200 mm objective, Goode 73 reliably placed 1.5 to 2 mm perforations in the tympanic membranes of 10 subjects. Ten of the 11 ears healed within 6 weeks. Tube placement was avoided.
Marchant and Bisschop 74 performed 20 consecutive CO 2 laser myringotomies on ears with chronic OME. All myringotomies closed within 4 weeks, with an average closing time of 17 days; 60% of cases of chronic OME were cured after 3 months. CO 2 laser myringotomy has application in clinical situations when middle ear ventilation is needed for a medium length of time (weeks) without having to place a ventilation tube. Disadvantages include cost, need for extra machinery that can be bulky, required maintenance, instruction on use and technique, and office space. Local anesthesia (iontophoresis or topical phenol application) is still required. Most otologists prefer simple cold-steel myringotomy with or without tube placement, but CO 2 myringotomy is an alternative; only time and experience will tell whether this technique will have widespread application and use.

Adenoidectomy
For an adenoidectomy, the patient is given a general anesthetic, and the airway is secured via endotracheal intubation. The patient is placed in the Rose position with the neck extended over a shoulder roll and draped, as described earlier. The mouth gag is inserted and suspended from the Mayo stand located over the body of the patient. The soft palate is retracted with red rubber catheters. The hard and soft palates are palpated for the presence of a submucous cleft palate. The adenoid pad is inspected with the curved laryngeal mirror.
The adenoid is excised with curved curettes of various sizes ( Fig. 6-2 A). The curette is seated high in the nasopharynx, and the adenoid pad is resected with a down-sweeping motion on the curette. Care must be taken to avoid injury to the prevertebral fascia and muscles, which may cause excessive bleeding. The nasopharynx is palpated for residual adenoid tissue; a second or third pass may be necessary. Curved biting forceps are useful to remove tissue inaccessible by the curette. The mirror is again used to inspect the site. Curettage of the tissue in the fossa of Rosenmüller is not done because it may lead to scar tissue formation and contracture that might result in stenosis or Eustachian tube reflux or both. Direct injury to the Eustachian tube also is avoided. The goal of surgery is the complete removal of the midline adenoid pad to achieve smooth re-epithelialization of the nasopharynx.
Bleeding usually stops quickly; tonsil sponges are used to pack the nasopharynx for hemostasis. The nasal cavities and nasopharynx are irrigated with warm saline. A malleable suction cautery can be used for precise coagulation, but its use is cautioned because of the risk of stenosis (see Fig. 6-2 B).

Mastoidectomy
The ear canal and postauricular areas are initially injected with 1% lidocaine with 1:100,000 concentration of epinephrine. Vascular strip incisions are started medially at the fibrous annulus and carried laterally along the tympanomastoid and tympanosquamous suture lines (approximately 12 and 8 o’clock positions for a right ear and 12 and 4 o’clock positions for a left ear). The incisions should come over the bony-cartilaginous junction laterally. The incisions are connected medially around the annulus with the round knife, and the vascular strip is elevated from medial to lateral. A cotton ball soaked in 1:100,000 epinephrine solution (with or without lidocaine) is placed in the canal, and attention is turned to the postauricular area.
The postauricular incision is based about 1 fingerbreadth behind the postauricular crease, roughly paralleling the free margin of the helix ( Fig. 6-3 ). The further posterior the incision, the greater the ease of inspecting the middle ear and Eustachian tube through the facial recess. The incision is carried slightly anterior in its inferior dimension to allow the ear to be retracted forward easily. In a child, care is taken not to extend the incision beyond the mastoid tip, which is more superior than in an adult. Carrying the incision more inferior or anterior puts the facial nerve at risk. Superiorly, the temporalis fascia is identified, and a piece of fascia is harvested if needed. The fascia identifies the plane of dissection. The ear is held forward with a self-retaining retractor. The linea temporalis is palpated, and an incision is made down to the bone along this line from anterior to posterior. A second incision is made perpendicular to the first in a curvilinear fashion down to the mastoid tip. The Lempert elevator is used to elevate the periosteum to identify the cribriform area and posterior canal wall. A small elevator is next used to elevate the vascular strip out of the canal. The vascular strip is held forward with the ear under the self-retaining retractor. The tympanic membrane is carefully elevated, and the middle ear is inspected.

FIGURE 6-3 Skin incision and the second incision for the Palva flap.
FIGURE 6-4. Mastoidectomy in progress. The sigmoid plate is skeletonized, and the bulge of the lateral semicircular canal in the antrum is visible. Note the positioning of the large retractor and dural hooks to keep the Palva flap rotated forward.
FIGURE 6-5. Completed mastoidectomy in the right ear with the facial recess opened. The dimensions of the facial recess are exaggerated by the artist to display the middle ear structures that may be seen by the surgeon after multiple repositionings of the viewing angle of the microscope.
A large cutting burr and continuous suction-irrigation are used to remove the lateral mastoid cortex. Important landmarks to identify include the posterior bony canal wall anteriorly, the tegmen mastoideum superiorly, the sigmoid sinus posteriorly, and the digastric ridge inferiorly. Care is taken not to expose the dura of the middle cranial fossa or the sigmoid sinus. When these lateral landmarks have been identified, the dissection is continued medially under the microscope. Körner’s septum is opened medially, and the mastoid antrum is identified. This dissection is carried anteriorly to open the aditus ad antrum and attic. The fossa incudis and short process of incus are carefully uncovered. The short process of the incus should be seen refracted through water. The short process marks the level of the facial recess. All air cells of the mastoid cortex should be taken down to reduce the surface area of the system. The bony plates over the posterior and middle fossa dura are skeletonized to form a smooth surface ( Fig. 6-4 ). Care is taken to avoid exposing dura. The mucosa regenerates into a single large cavity.
The descending segment of the facial nerve is identified (using a diamond burr and copious suction-irrigation) by gentle dissection from superior to inferior using the fossa incudis, lateral semicircular canal, and digastric ridge as essential landmarks. The nerve and blood vessels on the nerve can be seen through bone. Care is taken not to expose the nerve.
The facial recess is opened into the middle ear by the use of progressively smaller diamond burrs. The plane of the short process of the incus leads to the facial recess ( Fig. 6-5 ). When the fallopian canal and chorda tympani nerve are identified, the dissection is carried between them medially to open into the middle ear. Coupled with the tympanotomy, all parts of the mesotympanum can be inspected. The ossicular chain is palpated, and any hyperplastic mucosa, granulation tissue, or secretory tissue is removed. If bone of the middle ear/promontory is exposed, a piece of absorbable gelatin film (Gelfilm) is placed through the facial recess and across the promontory toward the Eustachian tube at the end of the procedure to prevent adhesions and to keep the recess open.
When all hyperplastic mucosa has been removed, the tympanic membrane is folded down back over the bony annulus and grafted if necessary. Cortisporin-soaked absorbable gelatin sponge (Gelfoam) packing is placed in the medial canal. The vascular strip is returned to the posterior canal wall, and the periosteal flap is resutured to the native periosteum with 2-0 chromic suture. The vascular strip is inspected transcanal and carefully placed back so that no edges are rolled under. The remainder of the canal is packed with Cortisporin-soaked Gelfoam. The postauricular incision is closed meticulously with 3-0 undyed (Vicryl) in the subcutaneous layer, avoiding the need for skin sutures. A small Penrose drain can be placed in the mastoid and carried out through the inferior aspect of the incision if the mastoid is very weepy. The drain is removed when the mastoid no longer drains. A cotton ball is placed in the meatus, Steri-Strips are applied to the postauricular incision, and a sterile dressing consisting of Telfa, gauze, fluffs, and a mastoid (or cup) wrap is placed.

POSTOPERATIVE CARE AND FOLLOW-UP

Tympanostomy Tubes
A cotton ball is inserted into the ear canal to absorb any drainage. Parents are asked to change the cotton ball once or twice daily for a couple of days, until the drainage stops. If the ear was acutely infected at the time of surgery, a topical antibiotic/steroid suspension is used twice a day for 5 days. The first follow-up visit is at 10 to 14 days to ensure tube placement and resolution of infection. Children are seen every 6 months for tube check thereafter. Water precautions are instituted. Parents are instructed to treat any new otorrhea with the antibiotic/steroid suspension. If the drops do not clear the infection in 2 to 3 days, an oral antibiotic is prescribed. Should this fail, the child is seen in the office for aural hygiene and cleaning, and possibly intravenous antibiotics if the infection fails to resolve. Occasionally, the tube elicits an allergic reaction with granulation tissue; removal of the tube often resolves the reaction. Tubes generally extrude within 1 to 2 years.

Adenoidectomy
Otalgia is common after adenoidectomy, and the parents should be counseled as such. Acetaminophen is usually adequate. The child should be started on a liquid diet initially, and if tolerated, advanced. Transient nasal speech may occur in a small percentage of cases, but regurgitation of liquids through the nose is rare. Palatal and pharyngeal wall compensation occurs quickly. If the child is old enough, chewing gum may speed the process and strengthen the pharyngeal and palatal musculature. Children return to the office 10 to 14 days after surgery for a checkup.

Mastoidectomy
Mastoidectomy is generally well tolerated. Patients receive pain medication; antibiotics are given in cases of acute infection. If a drain was placed, it is removed when the drainage has ceased—usually on the first or second postoperative day. Most patients do not require drains and are discharged the evening after surgery. Some require overnight observation for prolonged recovery from general anesthesia. We advise patients not to lift anything heavier than 5 to 10 lbs and not to blow their nose. The postauricular area should be kept dry. Patients return to the office 7 to 10 days after surgery for wound and canal-packing inspection. Drops are started 1–2 weeks after surgery to dissolve the packing; patients return again 8 weeks after surgery to check and clean the canal and for a postoperative audiogram. Drops can be started earlier if drainage or infection develops.

SURGICAL PITFALLS

Tympanostomy Tubes
Great care should be taken to avoid trauma to the external auditory canal during tube insertion. The resultant bleeding, although minor in amount, leads to a clot that is difficult to remove and obscures visibility in the office. Irrigation with saline and application of a topical vasoconstrictor such as phenylephrine or oxymetazoline usually bring this bleeding under control.
Bleeding within the tympanic membrane is commonly seen when a vessel is included in the incision. Such bleeding dissects between the layers of the drum and may result in the formation of a tympanosclerotic plaque. Careful placement of the incision avoids this potential problem.
Dislodgment of the tube into the middle ear may be a problem with a large myringotomy incision and small tube, or too small a myringotomy where the tube is pushed through. Tubes usually fall toward the Eustachian tube orifice; widening a small myringotomy allows the surgeon to retrieve the tube. Early extrusion of the tube usually occurs because the incision is too large or the tube is only partially inserted. Placement of a tube in an atelectatic ear can be difficult. The best area to place the tube is around the Eustachian tube orifice (anterior) because this area usually contains the most aeration and allows tube placement. Ossicular injury is rare if the incision is kept anterior, and tube manipulation is gentle.

Adenoidectomy
The chief surgical pitfalls to avoid during adenoidectomy are trauma to the torus tubarius, which protects the opening of the Eustachian tube, and deep removal of the posterior wall of the nasopharynx, which leads to excessive bleeding. Palpation and careful inspection of the nasopharynx with a mirror avoid inadequate removal of adenoid tissue. Bleeding usually can be controlled with packing of the nasopharynx and saline irrigation. Bleeding is usually from residual adenoid tissue; mirror examination can be helpful to identify the source and apply precise suction cautery or to remove adenoid remnants. Before placing a patient with Down syndrome in the Rose position with the neck extended, the cervical spine should be cleared.

Mastoidectomy
The chief pitfall of mastoidectomy is injury to the facial nerve when opening the facial recess. This trauma is rare in experienced hands, especially with continuous monitoring of the nerve during the procedure. Dural exposure in the tegmen mastoideum should be avoided because of the risk of later encephalocele. Care also should be taken around the sigmoid sinus; opening of the sinus can usually be controlled with precise packing with absorbable cellulose packing (Surgicel).
Contact of the drill with the incus may result in mild to moderate high-frequency sensorineural hearing loss owing to vibratory energy transmitted to the cochlea. Drill contact should also be minimized on labyrinthine bone. Blue lining or opening a semicircular canal should be addressed immediately by gently closing the opening with bone wax. A blue-lined canal should be recognized and avoided. Wound infection is uncommon; copious irrigation during and after the procedure aids in removal of unwanted debris or bone dust that might serve as a nidus for infection.

RESULTS
Goals of surgery include hearing improvement, reducing the time spent with middle ear effusion, and reducing the number of recurrences of middle ear effusion. Tube insertion with and without adenoidectomy has been shown to improve conductive hearing loss secondary to chronic OME and to decrease the amount of time spent with effusion. 21
Gates and colleagues 4 assigned 491 children, 4 to 9 years old with OME persisting 60 days or more after repeated medical therapy, to various combinations of myringotomy, tympanostomy tube insertion, and adenoidectomy for chronic OME. They found that time with recurrent middle ear effusion was decreased by 29% in the tympanostomy tubes–only group, by 38% in the adenoidectomy-plus-myringotomy group, and by 47% in the adenoidectomy-plus-tympanostomy tubes group. Hearing was equivalent in all groups except the myringotomy-alone group; hearing in this group was significantly worse. Surgical retreatments were necessary more often in children initially treated with myringotomy alone (36%) or tympanostomy tubes alone (20%) than in children treated by adenoidectomy and myringotomy (10%) or adenoidectomy plus tympanostomy tubes (10%). The number of repeat operations in the two adenoidectomy groups was significantly less than in the two groups without adenoidectomy ( P < .001). 4
Paradise and associates 55 randomly assigned patients who had previously undergone tympanostomy tube placement and had recurrent middle ear disease into either an adenoidectomy or control group. During the first and second years of follow-up, the adenoidectomy group had 47% and 37% less time with otitis media than the control patients.
Although most cases of idiopathic hemotympanum resolve satisfactorily, surgical management (tube placement or mastoidectomy or both) is generally successful. Often it takes months for the ear to aerate and for satisfactory hearing to return. Nonetheless, persistence and patience are often rewarded.

COMPLICATIONS AND MANAGEMENT

Tympanostomy Tubes

Otorrhea
The most common sequela of tympanostomy tubes is purulent otorrhea. In the Gates study, 4 otorrhea occurred one or more times in 22% of the myringotomy-alone group, 29% of the tympanostomy tubes group, 11% of the adenoidectomy-myringotomy group, and 24% of the adenoidectomy-tympanostomy tubes group. Some cases of otorrhea are due to water contamination; others are the result of AOM. Some cases also involve an inflammatory reaction to the tube itself. Treatment is the same: a topical polymicrobial-steroid suspension with or without an oral antibiotic, along with aural hygiene in the office. Most cases clear quickly. In recalcitrant cases, the tube is removed, and cultures are done. Failure to clear persistent otorrhea after maximal medical therapy is an indication for tympanoplasty with mastoidectomy.

Persistent Perforation
Tympanostomy tubes extrude within 1 to 2 years of insertion. Depending on the tube, 1% to 15% of cases result in a persistent perforation. Older children may be able to tolerate attempts to close the perforation in the office with freshening of the edges and placement of a paper patch. Other children are good candidates for a fat plug myringoplasty 75 or more formal myringoplasty/tympanoplasty under anesthesia.

Adenoidectomy

Bleeding
The most common complication of adenoidectomy is postoperative bleeding. The incidence is low, however: of 250 cases done by 13 surgeons, only 1 child required operative treatment for bleeding, and none needed transfusion. 4 Helmus and colleagues 85 noted that only 4 patients in 1000 (0.4%) bled after outpatient adenoidectomy; all instances occurred in the first 6 postoperative hours and were managed without transfusion. Return trip to the operating room for bleeding involves the same positioning as for routine adenoidectomy. Irrigation with suction cautery generally controls bleeding.

Velopharyngeal Insufficiency
Other, less common complications include nasopharyngeal stenosis and velopharyngeal insufficiency. Stenosis results from excessive tissue destruction, including excessive use of cautery, excessive curettage of the fossa of Rosenmüller, and removal of the lateral pharyngeal bands. Stenosis can require reoperation for scar tissue removal or pharyngeal flap reconstruction. The best treatment is prevention.
Transient velopharyngeal insufficiency may occur after removal of a large adenoid, but resolves quickly in most cases. If the child is old enough, gum chewing strengthens and reconditions the injured pharyngeal musculature. Persistent velopharyngeal insufficiency is the most feared complication because it requires either a prosthesis or a secondary procedure (pharyngeal flap) for reconstruction. Most cases are due to an undetected submucous cleft palate. Preoperative palpation and inspection (note bifid uvula) identify patients at risk.

Mastoidectomy

Facial Paralysis
Complications after mastoidectomy are rare. Facial paresis occurs rarely in experienced hands. Intraoperative facial nerve monitoring has decreased this complication further. Heat injury should not occur if continuous irrigation is used. Intimate knowledge of the anatomy and anatomic relationships is the best prevention of facial nerve injury. Injury, if it involves more than 25% of the nerve, has historically been repaired with direct anastomosis after mild decompression and freshening of the edges. Review of our results reveals that recovery to a maximum House-Brackmann grade III was similar for primary anastomosis and cable graft. 86

Hearing Loss
High-frequency sensorineural hearing loss may be caused by drill trauma around the ossicles, especially the incus. Careful inspection of the aditus through water identifies the incus and minimizes drill trauma. Drilling on labyrinthine bone should be kept to a minimum. Inadvertent opening of a semicircular canal should be sealed with bone wax with no suctioning around the fistula.

Recurrent Hemotympanum
Recurrent idiopathic hemotympanum is common. Treatment should be with a large-bore tympanostomy tube. Occasionally, a second-look mastoid operation is indicated. Hearing amplification helps with hearing loss.

ALTERNATIVE TECHNIQUES
Children with persistent effusion for whom medical and surgical treatment have failed should be evaluated for auditory trainer, hearing aid use, or other form of hearing rehabilitation, especially when the child is in school. Preferential seating in class is strongly encouraged.

ALLERGY TREATMENT
Children with symptomatic food or inhalant allergy deserve therapy whether they have OME or not. Because most patients with OME have had prior nasal infection, and children with nasal allergy have a higher prevalence of infection, allergy evaluation is appropriate for children with OME who also have nasal symptoms. Gates and colleagues 4 found a lower incidence of allergy in their subjects with OME, however, than in the general population. Although a cause-and-effect relationship between nasal allergy and OME has not been shown, the surgeon should inquire about allergic symptoms to provide proper therapy to patients with dual problems.

BIOFILMS
It has been known for more than a decade that culture-negative OME is not sterile, or bacteria negative. 87-89 Sophisticated techniques including in situ hybridization, PCR, and blotting techniques have shown bacterial DNA, RNA, and proteins in “culture-negative” middle ear fluid. 81
A logical explanation for this phenomenon is bacterial biofilm formation. Ninety-nine percent of bacteria in nature live in complex aggregates or communities called biofilms. Biofilm formation begins with the adhesion of bacteria in an aqueous environment to any organic or inorganic surface. Irreversible adsorption of the bacteria to the surface is followed by bacterial colony formation. The colony forms a complex polysaccharide coating, an extracellular polysaccharide matrix that protects the colony from outside stresses. The colony enlarges and forms water channels through which the bacteria gain nutrients and excrete waste. The community is extremely complex, where some bacteria are responsible for waste excretion, other bacteria are responsible for detecting changes in the outside environment, and other bacteria are responsible for producing the extracellular matrix. The bacteria within this complex community communicate, a process called quorum sensing, through various mechanisms, including differential gene expression and release of local cytokines. The biofilm has a characteristic appearance on scanning electron microscopy. The final step in the biofilm life cycle is the breaking off of pieces of the community to travel “downstream” to set up a new biofilm community.
Biofilms are implicated in chronic infections of indwelling catheters, including line sepsis. The treatment is removal of the foreign body. In otolaryngology, biofilms have been proposed to cause chronic adenoiditis/tonsillitis, chronic rhinosinusitis, and chronic OME. 82
Tympanostomy tube otorrhea has been directly linked to biofilm formation on the tube. 83 After the demonstration that biofilms form in the middle ear in an animal model of OME, 84 biofilm formation has more recently been shown in the middle ear mucosa of children with chronic OME. 85 Resistant to antibiotics, biofilms are a proposed mechanism for chronic OME.
Biofilms are very difficult to eradicate because the extracellular polysaccharide matrix makes the biofilm impervious to white blood cells and antibodies. Not only is the biofilm resistant to cellular and humoral immunity, but it also blocks antibiotic penetration. Strategies to eradicate biofilm formation include tympanostomy tubes coated with antibiotic to prevent adhesion of bacteria, detergents to dissolve the polysaccharide matrix, probiotics (replacing bad with good bacteria), and disruption of quorum sensing. Macrolide and quinolone antibiotics seem to be the most effective agents against biofilms. Further research into biofilms may uncover the pathophysiology of chronic OME and elucidate new strategies to prevent biofilm formation and to eradicate biofilms to reduce the impact and sequelae of OME.

GUIDELINES FOR THE MANAGEMENT OF ACUTE OTITIS MEDIA AND OTITIS MEDIA WITH EFFUSION
In 2004, AHRQ and the American Academies of Pediatrics, Family Medicine, and Otolaryngology–Head and Neck Surgery published clinical practice guidelines for the management of AOM and chronic OME. The guidelines for the management of AOM recommend judicious use of antibiotics and promote observation as a viable management strategy (see Table 6-1 ). 7
The AHRQ and Academies of Pediatrics, Family Medicine, and Otolaryngology–Head and Neck Surgery also published clinical practice guidelines for the management of children 2 months through 12 years with OME. 8 These guidelines stress the importance of distinguishing OME from AOM; the role of pneumatic otoscopy in the diagnosis of OME; and the importance of documenting laterality, duration, and presence and severity of associated symptoms at each assessment of a child with OME.
The guidelines recommend that clinicians should distinguish the child with OME who is at risk for speech, language, or learning problems from other children and recognize their need for more prompt intervention. Children not at risk can be managed with watchful waiting for 3 months from the onset of effusion; antihistamines, decongestants, antimicrobials, and steroids do not have long-term efficacy, and are not recommended for the routine treatment of OME. Hearing and language testing are recommended for children with OME that persists longer than 3 months, or at anytime a significant hearing loss or language delay is suspected. 8
Children with persistent OME should be observed at 3 to 6 month intervals until the effusion clears, significant hearing loss (>30 dB hearing level in the better hearing ear) is identified, or structural abnormalities of the eardrum or middle ear are suspected. When a child becomes a surgical candidate, tympanostomy tube insertion is the preferred initial procedure. Repeat surgery should include adenoidectomy with myringotomy, with or without tube insertion. No recommendations were made with regard to alternative medicine or allergy management. 8 These evidence-based evaluations and recommendations are expected to sharpen the focus on managing AOM and OME, and are likely to result in more careful use of antimicrobial therapy with less bacterial resistance and better patient outcomes.

Acknowledgments
We would like to thank George A. Gates, M.D., author of this chapter in the previous edition. We would also like to thank Liz Gnerre for her assistance on this chapter.

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Chapter 7 Diagnosis and Management of the Patulous Eustachian Tube

Dennis S. Poe, Ophir Handzel
Videos corresponding to this chapter are available online at www.expertconsult.com .
A patient with a patulous or abnormally patent eustachian tube (ET) can experience symptoms that lead him or her to seek medical advice and possibly undergo surgery. This condition can be overlooked or mistakenly thought of as not having sufficient bearing on a patient’s quality of life to warrant efforts for its identification and correction. The ET has a pivotal role in the maintenance of proper volume and pressure homeostasis of the middle ear cleft, in expelling middle ear secretions, and in protecting the middle ear from reflux of sound and material from the pharynx. 1 Dysfunction of the ET may be divided into two groups: dilatory dysfunction with failure to open the valve of the ET adequately, and patulous dysfunction with failure to close the valve adequately. This chapter addresses the diagnosis and treatment of an excessively open ET.

ANATOMY AND PATHOPHYSIOLOGY OF THE PATULOUS EUSTACHIAN TUBE
The ET is an organ composed of a skeleton made of cartilage and bone and associated muscles, fat, connective and lymphoid tissues, nerves, and blood supply. 2 The normal ET is maintained at a closed resting position, and opens by voluntary and nonvoluntary maneuvers, such as swallowing; yawning; and deliberate manipulations of the palate, pharynx, muscles of mastication, and mandible. The tube may also open passively by changes in ambient air pressure or by forcing passage of air, such as with a Politzer maneuver.
As mentioned, tubal opening can be a by-product of movements initiated for other purposes (e.g., swallowing), but it can also be triggered by direct reflex stimuli. Gas is exchanged between the middle ear space, surrounding mucosa, and blood vessels. There is a net absorption of gas into the circulation; when the ET is closed, this causes an increasingly negative pressure beyond that of the normal resting pressure of the middle ear. The absorption rates of the constituents of air differ with nitrogen being the predominant gas, but having relatively slow absorption compared with oxygen and carbon dioxide. Therefore, the gas composition varies over time after each dilation of the ET. It is thought that deviation from the set-points of pressure and gas composition may be detected by a combination of baroreceptors and chemoreceptors that initiate the opening of the ET to convey air into the middle ear and re-establish homeostasis. 3
Active opening of the ET usually lasts about 400 ms. It is the result of a coordinated effort of four muscles, the most important of which is the tensor veli palatini (TVP), laterally dilating the anterolateral membranous wall. 1, 4, 5 Although the opening mechanism of the ET has been studied extensively, closing of the ET has received less attention. The part of the ET that is normally closed at rest and open on dilation is referred to as the valve. The valve constitutes the approximately 5 mm long segment of apposing mucosal surfaces within the middle of the cartilaginous portion of the ET. 6 Closure of the ET is thought to be the result of the following factors: recoiling memory properties of the cartilaginous ET, relaxing bulk of the TVP muscle, and pressure of neighboring paraluminal tissue. The closed lumen is likely maintained by all of these factors, and aided by the surface tension of the apposed wet mucosal surfaces.
Transnasal endoscopy and surgery of patulous ETs has revealed that the underlying pathology is a longitudinal concave defect in the anterolateral wall of the valve ( Fig. 7-1 ). This wall normally has a convex bulge into the lumen of the ET in the relaxed position. The defect represents a lack of tissue volume that can be a deficiency of the lateral cartilaginous lamina, Ostmann’s fat, TVP muscle bulk, submucosa, or mucosa. Examples of these deficiencies, either isolated or in combination, are seen in clinical cases. Temporary or permanent obliteration of the defect, even with some mucus, immediately relieves patients’ symptoms.

FIGURE 7-1 Tympanometry tracing shows superimposition of a sawtooth pattern of tympanic membrane excursions resulting from breathing while the eustachian tube (ET) is patulous. Tympanometry shows an abnormality only while the patient is actively symptomatic.
The cartilaginous canal is anchored to the basisphenoid bone in its lateral side. The medial cartilaginous lamina is mobile, principally by action of the levator veli palatini muscle. Superiorly, the medial and much smaller lateral cartilaginous laminae come together to form a junction rich in elastin fibers that contributes to the springlike quality of the cartilage. The recoiling qualities of the cartilaginous canal play an important role in ET closure.
Because the cartilaginous backbone of the ET is open in its medial-anterior aspect, the lumen patency also depends on the pressure of the abutting soft tissues. The relaxed paratubal muscles (mainly the TVP) and Ostmann’s fat pad contribute to lumen closure. Glandular tissue and the size of Ostmann’s fat pad were found to be smaller in patients with a patulous ET compared with normal controls as measured by computed tomography (CT) scans. 7 The mucosal and submucosal tissue layers increase in thickness as they are relieved of tension with muscle relaxation, and are in themselves a factor in closure of the valve. A report of fluctuating patulous symptoms in hemodialysis patients describing relief of symptoms during fluid retention and exacerbation after excretion showed the close connection between periluminal mass and symptoms of patulous ET. 8

ETIOLOGY AND CLINICAL PRESENTATION
An overly patent ET allows for the free passage of air and the sound it carries from the nasopharynx to the middle ear, creating a pathologic acoustic and pressure environment. The most prominent symptoms of a patulous ET are aural fullness and autophony of a patient’s own breathing noises and voice. Symptoms are mostly related to free passage of air and sound, but not reflux of material. Symptoms compatible with patulous ET have been described since the second half of the 19th century. The constellation of symptoms compatible with those seen in patients with patulous ET was reported by Jago in 1858, 9 who later described his personal experience with the condition. Schwartze recognized the connection between the patulous ET and excursions of the tympanic membrane with respiration. Zollner and Shaumbaugh emphasized the important symptom of autophony in a series of patients with patulous tubes (as reported by Bluestone and Magit 10 ).
Autophony is described by patients as hearing their own voice and breathing noises. A patient’s own voice sounds to them as if they are talking very loudly into a barrel, typically prominent on pronunciation of “M” and “N.” Clinicians can simulate the symptoms by talking and breathing into the diaphragm of their stethoscopes. Because the auditory feedback can be disturbingly loud, there is a wide range of cognitive and emotional responses ranging from asymptomatic to suicidal ideation. Autophony can be disturbing to the extent of leading to depression and the need for psychiatric medication or intervention. The perception of pressure changes in the middle ear with breathing can be loud windlike noise, constant ear blockage or pressure, and the sense of the medial and lateral excursions of the tympanic membrane. When patients forcibly blow their nose, there can be pain from the increased middle ear pressure on the tympanic membrane.
Aural fullness and the sensation of ear blockage can be misdiagnosed as dilatory dysfunction of the ET, especially because the patient usually describes the ear as “blocked.” The differential diagnosis for aural fullness also includes temporomandibular joint or related musculoskeletal dysfunction, Minor’s syndrome of semicircular canal dehiscence, and endolymphatic hydrops (see Fig. 7-3 ). Because of the typical complaint of “ear blockage,” many patients are initially treated with medications directed against dilatory dysfunction, such as nasal decongestants, steroid topical sprays, and topical or systemic antihistamines, all of which fail to help or even aggravate the symptoms.
Symptoms are mitigated by maneuvers and conditions that support tubal closure by increasing venous congestion in tubal tissues, causing inflammation of the tissues, or restoring some hydration or mucus onto the luminal surfaces. Placing the head in a dependent position (supine or between the legs), pressure on the ipsilateral internal jugular vein, upper respiratory tract infections and allergies, and sniffing inward to “lock” the ET closed by creating negative middle ear pressure all are capable of generating temporary symptom relief in most patients. Symptoms are typically relieved overnight and may start sometime after arising in the morning. They are often initiated by exercise, possibly because of dehydration or epinephrine-like hormones causing nasal decongestion, or by prolonged speaking and singing, possibly from desiccation of the mucosa from air movement.
The etiology for the loss of tissue creating a patulous ET is uncertain. Possibly associated factors such as weight loss and tissue atrophy from chronic disease account for only two thirds of the patients. 11 Loss of tissue volume from within the tubal lumen is cited as the most common pathogenesis and most commonly reported with weight loss. 12 Shea (personal communication, 2007) noted that one third of patients have a significant weight loss, and one third have some sort of rheumatologic condition. The authors’ experience has been similar.
Simonton 13 grouped etiologies according to positive and negative contributing factors. Positive factors were defined as factors actively reducing tissue volume, such as with scarring from previous procedures, inflammation, and radiation. 14, 15 Negative factors were due to a passive loss of tissue around the pharyngeal orifice, loss of tonic action of the TVP muscle, and conceivably reduced coiling properties of the ET. Hormonal factors include pregnancy, 16 high-dose oral contraceptives, and estrogen treatment for prostate cancer. Estrogen can reduce the viscosity of tubal secretions, reduce the elastic properties of the tubal cartilage, and elevate the level of surfactant via a change of prostaglandin levels. All these factors would support opening of the ET. Reflux of gastric contents and allergy were reported to be the cause in 3 of 11 patients in one series. 17 Other contributors reported include abuse of nasal decongestants and cocaine, poliomyositis, multiple sclerosis and other neuromuscular disorders, cerebrovascular accidents, craniofacial abnormalities, temporomandibular joint malfunction, and malocclusion. Occasional association between patulous ET and palatal myoclonus has been reported. 18 The habit of sniffing or Valsalva’s maneuver can be acquired in patients attempting to aerate their middle ears at times of otitis media, but may ultimately result in a patulous tube.

DIAGNOSIS
The diagnosis is certain when medial and lateral excursion of the tympanic membrane with breathing is observed. Otoscopy should be done with an otoscope or microscope and the patient seated. If the patient does not have autophony at the time of the examination, it may be induced by physical activity. Excursions of the tympanic membrane can be enhanced by closure of the contralateral nostril during nasal breathing.
The improved inspection and manipulation of the nasopharynx brought about with the introduction of endoscopic sinus surgery tools greatly improved the ability to diagnose and correct patulous ET. High-quality endoscopy allows for direct and detailed examination of the ET valve. Done with either a rigid or a flexible endoscope, it may show a concave defect in the anterolateral part of the valve, instead of the normal convexity. 19 The defect prevents normal closure of the orifice in the resting position, leaving a slitlike opening in the lumen of the orifice.
Ancillary tests may be of some assistance in the diagnosis of patulous ET. Impedance tympanometry while the patient experiences autophony may reveal fluctuation in tracing in line with tympanic membrane excursion ( Fig. 7-2 ). Tympanometry can also record middle ear negative pressure or hypermobility of the tympanic membrane. Sonotubometry can directly measure ET patency. 20, 21 During the examination, a sound is emitted in the nasal cavity and is recorded by a microphone located in the external auditory canal of the examined ear. As the ET opens, the sound recorded in the external auditory canal intensifies, and an increase of 5 dB or more is considered to reflect opening of the ET reliably. 22 Severity of subjective autophony was found to be correlated with objective measurements of ET function by sonotubometry. 23 This test is not available routinely in the clinical setting. It has been suggested more recently to make use of this principle in performing audiometry masked by a nasally presented noise. In subjects with patulous tubes, thresholds of low tones were significantly elevated more than in normal controls because sound presented in the ear was masked by the noise escaping the nasal cavity to the middle ear through the patent ET. The thresholds normalized in most patients after corrective measures were taken. 24

FIGURE 7-2 Diagnostic algorithm for the evaluation of aural fullness.
Imaging is not routinely used for the diagnosis of patulous ET. Until more recently, CT scanners required a recumbent examinee, a position that commonly results in closure of the patulous tube. The availability of scanners allowing examinations in the seated position has allowed researchers to record patency of the ET in resting and under Valsalva maneuver. 25 Imaging-based measurements of a group of patients with patulous ETs were statistically significant compared with normal controls.
To date, the diagnosis of patulous ET is mainly a clinical one and is based on history and physical examination. Patulous excursions of the tympanic membrane during nasal breathing are pathognomonic for the condition, but this is generally seen only while symptoms are active. Patients may be asked to run up and down stairs for several minutes in an attempt to generate the symptoms when not initially present. Patulous symptoms and signs (e.g., tympanic membrane excursions) are present only while the ET valve is stuck in the open position. If patients complain that they actively have their fullness and autophony symptoms, but there are no patulous tympanic membrane excursions and no visible ET valve defect at that moment, another cause for the symptoms must be sought. Ancillary tests may be important to distinguish this pathology from others sharing similar symptoms.
The other causes for aural fullness or ear blockage should be systematically considered ( Fig. 7-3 ). ET dilatory dysfunction causes negative pressure in the middle ear or effusion that should be visible on otologic examination and tympanometry. Endoscopic examination reveals evidence of an obstructive problem with mucosal swelling or inflammation, or a dynamic disorder with failure of muscular dilation. 19

FIGURE 7-3
The diagnosis of semicircular canal dehiscence syndrome, or Minor’s syndrome, must be considered before making a final diagnosis of patulous ET (of which most are dehiscences of the tegmen into the superior semicircular canal). 26 These two very different pathologies can manifest with similar symptoms of autophony of the voice, but autophony of breathing sounds is much more pronounced in patulous ET. 17 Differential diagnosis is made more difficult by the fact that superior semicircular dehiscence (SSCD) may manifest without vestibular symptoms. 27 Older series of patients assumed to have a patulous ET most likely included patients who had Minor’s syndrome.
Almost 20 years before the first description of SSCD syndrome by Minor and associates, 28 O’Connor and Shea 14 described some patients thought to have patulous ET who experienced vertigo accompanied by nystagmus induced by a sharp increase in nasopharyngeal and intratympanic pressure. They attributed symptoms and signs to stapedial or round window membrane movement, although in retrospect, it is highly likely that the patients had Minor’s syndrome. Of the senior author’s series of patients with SSCD, 94% complained of autophony of their voice, and half of them found relief by placing their head in a dependent position. 17 Relief of autophony while lying supine has long been thought to be pathognomonic for patulous ET, but changes with intracranial or intralabyrinthine pressure with the head dependent probably also influence the impedances of the dehiscences that cause Minor’s syndrome. Patients with Minor’s syndrome tend to have unremitting autophony when it becomes present, as opposed to symptoms of patulous ET, which are generally intermittent. Vertigo and nystagmus induced by sound or pressure, supranormal bone conduction, and conductive hearing loss with intact stapedial reflexes all should raise the suspicion of SSCD. The diagnosis is confirmed by demonstration of the bone dehiscence with high-resolution temporal bone scan reconstructed in the Poschel and Stenvers planes, and by lower than normal thresholds in Vestibular Evoked Myogenic Potential.
Patients with aural fullness complaints but normal tympanic membrane findings should be asked about and evaluated for temporomandibular joint and musculoskeletal disorders. Aural fullness with otalgia is especially suggestive of these problems. The joint capsule is examined with the patient opening the mouth as widely as comfortable; the space between the condyle and the glenoid fossa is palpated deeply looking for any tenderness. The mouth is moved side to side during a portion of the examination, again palpating for areas of tenderness, especially superiorly and posteriorly to the condyle. Deep palpation is made in the temporalis and masseter muscles surrounding the temporomandibular joint, examining for spasms and tenderness. Bimanual examination of the lateral pterygoid muscle is done to look for spasms and tenderness. If a patient does not have active symptoms during the office visit, it is likely that no findings will be elicited, so the patient is instructed in how to do a self-examination during episodes of future symptoms, especially if there is aural pain. Inner ear conditions such as Meniere’s disease can cause aural fullness. Patients would characteristically have a fluctuating sensorineural hearing loss and vertigo. Appropriate studies would be indicated if Meniere’s disease is suspected.

TREATMENT
Treatment should be designed in a stepwise fashion. In some patients, the specific etiology can be determined, and treatment can be initiated. Often a correctable etiology cannot be found. For most patients, reassurance suffices. Others find relief by swallowing, yawning, or positioning their heads in a dependent position. Patients are advised to discontinue decongestants and nasal steroids, observe good hydration, and use nasal saline drops, which are more effective than sprays. For the subset of patients experiencing unwarranted weight loss, appropriate evaluation is recommended.
When indicated, treatment is directed toward augmenting the periluminal tissue, specifically filling the defect in the valve. This can be done by adding bulk to the native tissue by inducing congestion or by introducing mass from other sources (autografts, allografts, xenografts, or synthetic implants). Numerous agents affecting the mucosal lining of the valve can be used with good, albeit temporary, results. In an off-label use, a conjugated estrogen preparation (Premarin) can be administered as a nasal solution resulting in mucosal edema. 29 A dose of 25 mg of intravenous Premarin is diluted in 30 mL of isotonic sodium chloride to be taken as nasal drops three times a day. Side effects include epistaxis and nasal irritation. Saturated solution of potassium iodide (SSKI), an expectorant designed to enhance viscosity of the mucus, is taken three times a day as 8 to 10 drops diluted in water or juice. Powder of boric and salicylic acid (4:1 ratio) insufflated to the nasopharynx or instilled with a catheter causes local irritation and edema offering temporary relief. 12 Insufflation of mucosal irritants can also be used as a diagnostic test or temporary treatment for patulous ET. Some local irritants reported have included the application of silver nitrate, nitrate acid, and phenol. 11, 29 These irritants can also scar the mucosa and restrict the opening of the ET. Although many of these treatments brought about improvements in patients’ symptoms, the improvements were transient.
Surgical intervention is reserved for the few patients with symptoms significantly affecting their quality of life, when less intrusive methods of treatment fail. Myringotomy with the placement of ventilation tubes is probably the most common surgical intervention, reported to aid approximately 50% of patients. 30 Ventilation tubes alleviate mostly symptoms related to middle ear pressure changes and tympanic membrane movements, but less so reflux of sound—autophony. 17
Various materials have been injected in an effort to fill the orifice defect responsible for creation of patulous ET. In 1937, Zollner 31 proposed infiltrating paraffin anterior to the ET orifice, in an attempt to recreate the missing mass abutting the orifice. Pulec 12 reported only 1 patient out of 26 not helped by injecting polytef (Teflon) to the anterior part of the orifice; 19 patients had complete relief from symptoms after one injection of 0.75 to 1.5 cm 3 of Teflon paste. None of the patients had otitis media after the procedure. The same material was used by O’Connor and Shea, 14 who injected Teflon anterior to the orifice. Use of Teflon for this indication was discontinued because of complications, including cerebral thrombosis and death, possibly as a result of injection of Teflon into the immediately adjacent internal carotid artery. Ogawa and colleagues 32 reported their successful, albeit short-lived, experience with injection of absorbable gelatin sponge (Gelfoam) mixed with glycerin to the lumen of the ET.
Brookner and Pulec 33 studied a dog model and pointed to the anterior wall of the pharyngeal orifice of the ET as the correct location for augmentation. Injection of Teflon paste into this area resulted in an increased resistance in airflow through the ET without initiating otitis media. Injecting the posteromedial wall of the posterior cushion (torus tubarius) resulted in elevated resistance of the tube as well, but three of four injected dogs developed serous otitis media. Impediment of lymphatic flow was thought to be the likely cause of this side effect.
Complete blockage of the ET cures patients from symptoms of patulous ET, but usually results in the need for long-term or permanent ventilation tubes. Simonton 13 reported partial success in three cases using conization of the ET cartilage and suturing the mucosa closed. Doherty and Slattery 11 used circumferential electric coagulation and application of a fat graft to seal the tube successfully with symptomatic improvement in two patients.
A different approach to obstruct the patent ET is by placing an intraluminal catheter. Plugging the ET with a catheter sealed with bone wax that was introduced through a tympanotomy or myringotomy approach resulted in long-term resolution of symptoms. 34 An anteriorly based tympanomeatal flap was raised, and if required the bony annulus would be drilled to facilitate exposure of and approach to the ET orifice. An intravenous catheter filled with bone wax was introduced into the lumen of the ET through the middle ear. Nine patients, who failed previous medical and surgical interventions, were treated by insertion of an intraluminal catheter through the tympanotomy approach and placement of tympanostomy tubes, and were followed for 2 to 15 years. Six patients had marked improvement in symptoms. Two patients extruded their catheter and tympanostomy tubes, but still obtained relief of symptoms. Two patients extruded the tympanostomy tubes, and although the catheters were in place did not experience middle ear effusion, probably because of sufficient leak of air around the catheter. 10
Intraoperative manometric measurement was employed by Bluestone 1 with a tympanometer noting that opening pressure of the ET had been increased to 500 to 700 mm ( Figs. 7-4 through 7-7 ). Shea Jr. and associates at the Shea clinic offer a similar transtympanic procedure: introducting of one or more Teflon catheters of various appropriate sizes. According to information available from the Shea clinic’s website www.sheaclinic.com , of 40 patients operated on, 90% were improved, and 5% were made worse; in 5%, the symptoms were unchanged.
Release of the TVP muscle by transposing it medially to the hamulus relieved symptoms for at least 6 months in 9 of 10 patients undergoing this procedure. 35 The incidence of postoperative otitis media was not reported. Virtanen and Palva 15 published their experience with pterygoid hamulotomy. Release of the tendon of the TVP was supplemented at times with cutting its tendon if deemed necessary. Clinical relief was achieved in 11 of 16 of the operated patients, although sonotubometry recording normalized in only 9 patients.

TECHNIQUE OF TRANSNASAL AND TRANSORAL OCCLUSION OF THE PATULOUS EUSTACHIAN TUBE DEFECT
Repair of the patulous defect can be done less invasively through the nasopharyngeal orifice without tympanotomy ( Figs. 7-8 through 7-14 ). An intravenous catheter can be inserted into the tubal lumen wedged into the isthmus, the narrowest segment of the ET for long-lasting relief of patulous symptoms while generally maintaining the patency of the tube when it dilates normally to the open position. The physiologic function of the ET can be preserved in most cases, while repairing the patulous defect in the valve.

FIGURE 7-8 Patulous eustachian tube reconstruction with cartilage grafts. Thick cartilage is harvested from the nasal septum or inferomedial aspect of the conchal cartilage. It is cut into wedges 1 mm wide at the apex, 3 mm wide at the base, and 3 to 4 mm long.

FIGURE 7-9 Superior semicircular incision is made on the leading edge of the eustachian tube nasopharyngeal orifice from 9 to 3 o’clock.

FIGURE 7-10 Sharp and blunt dissection is done to create an intraluminal submucoperichondrial pocket. Great care is taken to avoid tears in the flap. A suction dissector is particularly helpful in developing this flap well into the eustachian tube valve area inferior/distal to the bony-cartilaginous isthmus.

FIGURE 7-11 Cartilage grafts are wedged, apex first, into the pocket, creating a convexity to the anterolateral wall and depressing the superior wall inferiorly. Wedges are inserted and rotated to make them stable in position. Delayed extrusion may occur if the grafts are held in place under tension against the suture closure. ET, eustachian tube.

FIGURE 7-12 A, Technique of suture closure using needle driver to engage the medial mucosal edge. B, Suture is grasped just behind the needle’s swedge to allow the needle to be toggled into position for insertion into the lateral mucosal edge. C, Olive-tipped maxillary antral suction is used as a knot pusher.

FIGURE 7-13 Nasopharyngeal eustachian tube catheter insertion. A, Eustachian tube insertion tool is loaded with a precut angiocatheter prefilled with bone wax that is held within the insertion tool by a small plug of bone wax against the internal piston. Catheter is smoothly inserted, with some resistance noted as it engages the isthmus. B, Catheter is inserted within the orifice just past the posterior cushion to avoid contact with the cushion or palate during swallowing and speaking. It is pushed into place with a curved empty laser catheter guide or a frontal sinus ball-tipped probe.

FIGURE 7-14 A, Preoperative patulous eustachian tube. B, Postoperative eustachian tube after patulous eustachian tube reconstruction.
The ipsilateral nasal cavity is sprayed with pseudoephedrine-containing nasal drops. The mandible is retracted with a tonsillectomy mouth gag. A soft red rubber catheter is passed through the contralateral nasal passage and used to retract the soft palate. The nasopharynx is seen with a 45 degree rigid telescope introduced through the ipsilateral naris. An intravenous catheter, 14 or 16 gauge (2.1 or 1.7 mm diameter), is prepared, cutting it to 35 to 38 mm length, preserving the tapered tip; the lumen is obliterated full length with bone wax by pouring it melted into the lumen before cutting the catheter to size. The length is determined by the size of a patient’s head and by CT scan. The CT scan is inspected for any dehiscence of the internal carotid artery into the ET. The catheter is loaded into a custom-made piston within a tube introducer (see Fig. 7-13 ). 17 The catheter is held in place by a small piece of bone wax having been initially placed into the introducer and against the mobile piston. The introducer with the catheter is passed through the oral cavity and oropharynx, and is brought to the proximity to the nasopharyngeal orifice of the ET under view with the endoscope. The catheter is pushed into the lumen of the ET with the piston-like movement of the introducer; engagement of the catheter into the isthmus is felt as heightened resistance.
Care is taken to ensure smooth intraluminal placement without any mucosal injury. Creation of a false passage into the soft tissues could risk inadvertent penetration of the internal carotid artery. Otoscopy at the end of the procedure with a microscope or a 0 degree endoscope is done to ascertain that the catheter is not visible within the middle ear. If it is seen within the middle ear, it is withdrawn further into the nasopharynx, and the ear is reinspected to ensure it is no longer visible. The catheter should protrude slightly from the nasopharyngeal orifice, but not so long as to protrude into the palate when it elevates with speaking and swallowing. The catheter should not protrude into the nasopharynx beyond the inferior edge of the anterior cushion, the free end of the anterolateral wall.
Alternatively, the defect in the ET valve can be augmented. Knowledge of the exact area of the defect is the key to good results. Correction of this defect can restore the competence of the tubal valve, avoiding overcorrection and otitis media with effusion.
The patulous defect has been identified as a loss of bulk in the valve within the anterolateral wall, superiorly. The senior author has injected various materials (e.g., fat, collagen, hydroxyapatite) into this location in patients. Introduction of 0.3 cm 3 resulted in immediate alleviation of symptoms in all patients, but most results tend to be temporary with return of symptoms 2 weeks to several months later in most patients. 17
Because hydroxyapatite is radiopaque, CT scans of patients injected with this material have illuminated the fate of injectable materials. When injected into the anterolateral defect of the valve, hydroxyapatite gained access to the musculofascial plane superficial to the TVP, and spread superiorly and inferiorly up to the basisphenoid and down to the parapharyngeal space. This finding offered explanations for the usual transient relief experienced by injected patients. Injecting the posteromedial part of the orifice (posterior cushion), the hydroxyapatite remained in place. Correcting the defect of the orifice with this type of injection is difficult, however, requiring a larger volume of material than the submucosal tissue is likely to hold. Additionally, inadvertent passage of the needle through the medial cartilaginous lamina within the posterior cushion brings the injected material to the internal carotid artery.
In search of a material that can be safely used to fill the valve’s defect with stable long-term results, the senior author used acellular dermal matrix (AlloDerm) and cartilage grafts to augment the defect in a patulous ET reconstruction (PETR) procedure. 17 AlloDerm is typically resorbed by about 65% and is no longer used because of a higher long-term failure rate than cartilage grafts. The graft is placed into a luminal, submucoperichondrial pocket made in the superior half of the ET orifice. The procedure is done using transoral and endoscopic transnasal approaches, with the patient supine and under general anesthesia. The nose is decongested by topical application of phenylephrine solution, and a mixture of lidocaine 1% and epinephrine 1:100,000 is injected by an angled needle into the nasopharyngeal orifice of the ET. The cartilage graft can be taken from the tragus (with the posterior perichondrium attached), concha, or nasal septum (without perichondrium). The mouth is opened with a mouth gag, and the soft palate retracted with a soft rubber catheter, introduced through the contralateral nose. The nasopharynx is viewed with a 45 degree rigid endoscope with a camera. The endoscope is attached to a gag-mounted endoscope holder. All instruments other than the endoscope are passed through the oral cavity.
The incision in the mucosa is made with an otologic diode pumped KTP laser (Iridex Corporation, Mountain View, CA) set at 2500 mW/1000 mS. Standard otologic fiberoptic laser probes (200 μ diameter) are used with the probe gently curved to reach the ET orifice through the mouth. The incision is made into the mucosa of the anterior cushion extending superiorly from 9 to 3 o’clock. The incision is carried down until the superior cartilage is encountered. A submucoperichondrial plane is developed superiorly and carried deeply into the valve, avoiding tearing the flap. The plane is followed superiorly and distally into the level of the tubal valve. The flap may include a segment of the ET cartilage, which for this purpose is separated from the basisphenoid bone and from the lateral and medial cartilaginous laminae. If the cartilage is excessively thick, it is thinned with a sharp knife or laser dissection. The cartilage grafts are cut into wedges approximately 1 mm wide at the apex and 3 to 4 mm wide at the base and 5 to 8 mm long. The grafts are firmly packed deeply into the pocket, usually using two to four grafts. There should be sufficient mucosal coverage of the grafts to allow the edges to be sutured together.
The incision is closed with two or three 4-0 polyglactin 910 (Vicryl) sutures on a TF needle shaped into a J toward the tip to allow for easy passage through the lateral mucosal edge after first traversing the medial edge. At least one suture is passed through one of the cartilage grafts. The suture is tied through the oral cavity, passing one limb of the suture into a curved olive-tipped maxillary antral suction while the vacuum is engaged. The suction tubing is removed, and the threaded suture limb is maintained on tension as the suction catheter is advanced to serve as a knot pusher. If the patient is to fly within 6 weeks of the procedure, a ventilation tube may be placed in the drum. Initially taking about 3.5 hours, operative time was later reduced to 1.5 to 2 hours (see Figs. 7-8 through 7-14 ).
The results of PETR performed in 14 ETs of 11 patients have been published. 17 All patients had long-standing (1 to 38 years) patulous ET that failed previous therapies. Eight patients had a trial of myringotomy and placement of tubes, and two had undergone previous ET procedures at other centers. The most common and most disturbing symptom was autophony. All patients experienced immediate and complete relief after the operation. Follow-up duration ranged from 3 to 30 months (average 15.8 months). Symptoms were completely relieved in one patient, significantly improved to satisfaction in five patients, and significantly improved but with patient’s dissatisfaction in seven patients; in only one patient were symptoms unchanged. No complications were experienced. One patient required a supplementary hydroxyapatite injection, following which complete relief of autophony persisted for another 22 months.
Presently, we offer the minimally invasive catheter insertion procedure as the primary procedure (see Fig. 7-14 ). In the event of failure, we may offer insertion of a larger or a second catheter or a cartilage PETR. The catheter approach can also be used after failure of the PETR. Ultimately, obliteration of the ET and long-term tympanostomy tube can be done for repeated failures; we prefer an endoscopic method for occlusion similar to that described by Doherty and Slattery, 11 but we also suture the lumen closed over the fat graft. This technique may prove to be effective for control of cerebrospinal fluid leakage after skull base operations.

CONCLUSION
Patulous ET can cause autophony of one’s own voice and breathing sounds and aural fullness. When a cause can be identified, correction of patulous ET can relieve the symptoms. A concave defect in the anterior wall of the nasopharyngeal orifice of the ET can be seen in these patients. The lack of tissue in this area prevents normal closure of the ET valve in its resting position. Most patients do not need further treatment other than reassurance. A small subset of patients find their symptoms debilitating to such an extent that they seek medical and surgical attention. Before issuing such interventions, SSCD, inner ear hydrops, or temporomandibular joint dysfunction must be ruled out. Various materials have been injected in the defect to allow for tubal closure, but success is not uniform and is temporary. Complete closure of the ET lumen solves the problem of patulous ET, but patients may need permanent middle ear ventilation via tubes.
PETR with a subocclusive catheter relieves most patients of their symptoms with very mild and temporary side effects. If the catheters fail, PETR with cartilage graft can be placed under a submucoperichondrial flap with generally excellent long-term benefits. Some patients require additional adjunctive procedures over time, suggesting loss of graft volume or ongoing loss of ET valve tissue.

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19. Poe S.D., Pyykko I., Valtonen H., Silvola J. Analysis of eustachian tube function by video endoscopy. Am J Otol . 2000;21:602-607.
20. van der Avoort S.J.C., van Heerbeek N., Zielhuis G.A., Cremers C.W.R.J. Sonotubometry: eustachian tube ventilatory function test: State-of-the-art review. Otol Neurotol . 2005;26:538-543.
21. van der Avoort S.J.C., van Heerbeek N., Zielhuis G.A., Cremers C.W.R.J. Validation of sonotubometry in healthy adults. J Laryngol Otol . 2006;120:853-856.
22. Di Martino E.F.N., Thaden R., Antweiler C., et al. Evaluation of eustachian tube function by sonotubometry: Results and reliability of 8 kHz signals in normal subject. Eur Arch Otorhinolaryngol . 2007;264:231-236.
23. Hori Y., Kawase T., Oshima T., et al. Objective measurements of autophony in patients with patulous eustachian tube. Eur Arch Otorhinolaryngol . 2007;264:1387-1391.
24. Hori Y., Kawase T., Hasegawa J., et al. Audiometry with nasally presented masking noise: Novel diagnostic methods of patulous eustachian tube. Otol Neurotol . 2006;26:596-599.
25. Kikuci T., Oshima T., Ogura M., et al. Three-dimensional computer tomography imaging of the sitting position for the diagnosis of patulous eustachian tube. Otol Neurotol . 2007;28:199-203.
26. Zhou G., Gopen Q., Poe S.D. Clinical and diagnostic characterization of canal dehiscence syndrome: A great otologic mimicker. Otol Neurotol . 2007;28:920-926.
27. Mikulec A.A., McKenna M.J., Ramsey M.J., et al. Superior semicircular canal dehiscence presenting as conductive hearing loss without vertigo. Otol Neurotol . 2004;25:121-129.
28. Minor L.B., Solomon D., Zeinreich J.S., Zee D.S. Sound-and/or pressure-induced vertigo due to bone dehiscence of the superior semicircular canal. Arch Otolaryngol Head Neck Surg . 1998;24:249-258.
29. Dyer R.K., McElveen J.T. The patulous eustachian tube: Management options. Otolaryngol Head Neck Surg . 1991;105:832-835.
30. Luxford W.M., Sheehy J.L. Myringotomy and ventilation tubes: A report of 1,568 ears. Laryngoscope . 1982;92:1293-1297.
31. Zollner F. Die Klaffende ohrtompete, storungen dadurch und vorschlage zu ihrer behebung. Z Hals Nasen Ohr . 1937;42:287-298.
32. Ogawa S., Satoh I., Tanaka H. Patulous eustachian tube. Arch Otolaryngol . 1976;102:276-280.
33. Brookner K.H., Pulec J.L. Auditory tube patency after injection of Teflon paste. Arch Otolaryngol . 1969;90:60-64.
34. Bluestone C.D., Cantekin E.I. Management of the patulous eustachian tube. Laryngoscope . 1981;91:149-152.
35. Stroud M.H., Spector G.J., Maisel R.H. The patulous eustachian tube syndrome. Arch Otolaryngol . 1974;99:419-421.
Chapter 8 Office Management of Tympanic Membrane Perforation and the Draining Ear

Peter S. Roland, Brandon B. Isaacson, Joe W. Kutz
Otorrhea can arise from many causes: acute and chronic external otitis, acute and chronic otitis media, chronic myringitis, and secondary to a cerebrospinal fluid (CSF) fistula.

OTORRHEA FROM CEREBROSPINAL FLUID FISTULA
CSF is a rare cause of persistent or intermittent otorrhea. CSF otorrhea may be classified as spontaneous or acquired. Temporal bone trauma is the most common cause of acquired CSF otorrhea, but it may also arise secondary to neoplasms, infections, and iatrogenic causes.
Brodie and Thompson 1 observed that CSF otorrhea resulting from temporal bone fractures resolved within 1 week of onset in 95 of 122 subjects (77.8%). They also showed that leaks persisting beyond 7 days had a much higher incidence of meningitis (23% versus 3%). Iatrogenic CSF otorrhea may occur immediately after surgery or may be delayed for days or years.
Spontaneous CSF otorrhea may result from congenital temporal bone abnormalities, or can arise in the setting of normal temporal bone morphology as a consequence of arachnoid granulations, or increased intracranial pressure. 2, 3 More recent studies have shown that subjects with spontaneous CSF otorrhea are often morbidly obese and often have empty or partially empty sella on radiographic examination. 3, 4
Patients who are eventually diagnosed with CSF otorrhea are often initially identified during an evaluation of persistent unilateral middle ear effusion. The diagnosis is often confirmed when persistent watery drainage follows myringotomy. A careful history may elicit symptoms of intermittent positional nasal drainage. The diagnosis is usually established by history and physical examination, but may be confirmed with β 2 -transferrin if enough fluid can be collected. High-resolution temporal bone computed tomography (CT) and magnetic resonance imaging (MRI) with cisternogram, FIESTA, or CISS images are complementary studies often obtained in evaluating patients with CSF otorrhea.
Traumatic CSF otorrhea is often managed conservatively with stool softeners, head of bed elevation, serial lumbar punctures, or lumbar drainage. Occasionally, patients require operative management if conservative measures fail. The surgical approach is dictated by the fracture location, and hearing status in patients with temporal bone trauma. Patients with little or no residual hearing can be managed with a transmastoid or translabyrinthine approach, whereas patients with residual hearing can be managed with a middle fossa approach.
Spontaneous CSF otorrhea requires surgical repair of cases caused by fistula between the subarachnoid space and temporal bone air cell system. The middle fossa approach is often used because these patients commonly have multiple tegmen defects. A transmastoid approach may be used if the defect is solitary and is sufficiently lateral in the temporal bone, or if the patient has significant medical comorbidities. CSF otorrhea resulting from congenital inner ear anomalies may be managed via a transcanal or transmastoid approach. Autologous (e.g., bone, cartilage, fascia) and nonautologous (e.g., acellular dermal matrix [AlloDerm], bone cement) materials have been used to repair these defects. Bone defects with communication into the posterior fossa are usually repaired with a transmastoid approach.

CHRONIC SUPPURATIVE OTITIS MEDIA

Definition
There is no widely agreed on definition of chronic suppurative otitis media (CSOM). Nonetheless, most practicing otologists would agree that the following elements should be present:
1. The drainage must be purulent, mucoid, or mucopurulent.
2. The otorrhea must arise from the middle ear space through a tympanic membrane perforation or tympanostomy tube.
3. Drainage must persist beyond 3 weeks despite appropriate medical management. 5, 6
Although some otologists refer to an infected cholesteatoma as a form of CSOM, others prefer to limit the term only to ears without cholesteatoma. Although many of the management principles discussed in this chapter may be applicable to individuals with an infected cholesteatoma, surgery, and not office management, is the mainstay of treatment when cholesteatoma is present. Consequently, ears with cholesteatomas are not a focus in this discussion.

Etiology
Many, perhaps most, cases of CSOM arise from acute infections that have not resolved. Whether or not all cases of CSOM have an infectious etiology is unclear. Antonelli and colleagues 5, 6 have suggested that some cases may be due simply to “bacterial colonization and overgrowth in an ear that remains moist because of tubal pathology.” Many authors believe that allergy alone can result in chronic drainage through tympanic membrane perforation, at least occasionally.
Although tympanic membrane perforations are invariably present (by definition), the etiologic role of membrane perforations in the development of CSOM is also unclear. Sometimes the tympanic membrane perforation is simply a result of the initial middle ear infection that never resolves. Alternatively, there are some cases in which a long-standing, dry perforation becomes infected, and the infection persists either because of lack of treatment or inadequate or inappropriate treatment. Most tympanic membrane perforations do not result in infected middle ears, however, and, when they do, most such infections, during the acute phase, respond briskly to appropriate treatment.
As noted by Bluestone and others, 7, 8 a nonintact tympanic membrane (perforation or tympanostomy tube or both) eliminates the “middle ear cushion” and facilitates eustachian tube reflux. By eliminating the middle ear cushion, a tympanostomy tube or tympanic membrane perforation allows air to escape from the middle ear space, which eases the retrograde reflux of nasopharyngeal secretions into the middle ear. Eustachian tube reflux may be an especially important etiologic factor in populations who are otherwise prone to it (e.g., aboriginal North Americans).
Many cases of CSOM arise from inadequately or incompletely treated cases of acute otitis media (AOM). Gibney and coworkers 9 showed that aggressive treatment of AOM in aboriginal children in Australia reduces the incidence of CSOM. It is usually unclear why an acute infection fails to resolve and becomes chronic. We do know that AOM causes mucosal sloughing, causes impairment of ciliary clearance, and exposes microbial binding sites. 5.6 Even so, only a few episodes of AOM evolve into CSOM.
The onset of CSOM is characterized initially by increased vascularity of the mucosa and submucosa. As CSOM persists, the proportion of chronic inflammatory cells increases. This increase in cells leads to osteitis and mucosal edema with ulceration, and two important pathophysiologic events follow: (1) capillary proliferation, which results in formation of granulation tissue and polyps, and (2) a rarifying osteitis, which ultimately produces new bone formation and fibrosis. Osteitis is present in virtually 100% of CSOM patients, a finding that distinguishes CSOM from more transient pathologic alterations in the middle ear cleft. 10

Bacteriology
CSOM is predominantly a gram-negative infection, although staphylococcal species occur with sufficient frequency that they must be taken into consideration when any microbial therapy is considered. Pseudomonas aeruginosa is generally the most common gram-negative organism, but other gram-negative organisms are commonly encountered, especially species of Enterobacteriaceae. 11 The extent to which anaerobic organisms or fungi or both are pathogenically involved is controversial. Anaerobic organisms are often present, but whether or not they are cultured depends on how rigorously they are sought. 12, 13 The contributions of anaerobes to pathophysiology remain unclear. Fungi are commonly recovered, but the extent to which they are pathogens as opposed to saprophytes is unresolved, and probably variable.

Pathophysiology
Granulation tissue is almost an invariant accompaniment of CSOM. It can develop quickly in a draining ear, and is already present in many infections of less than 6 weeks’ duration. The presence of granulation tissue, especially when it is abundant, may be a factor that contributes to treatment failure of acute infections, and the evolution of AOM into CSOM. The formation of granulation tissue in the middle ear begins with a break in the basement membrane of the surface epithelial cells. Inflammatory cells in the underlying lamina propria traverse through the broken basement membrane and enter the lumen of the middle ear space. The rupture of the basement membrane and epithelial lining cell is caused by bacterial toxins, inflammatory mediators produced by ruptured liposomes, and the accumulation of subepithelial fluid and vacuoles, all of which exert pressure on the surface epithelium. 14
The next step in the formulation of granulation tissue occurs when a small piece of the herniated lamina propria extrudes through the ruptured area between epithelial cells. Initially, the extruded lamina propria pushes into the middle ear without any epithelial covering. Angiogenic growth factors incite capillary budding, vascular hyperpermeability, and fibroblast recruitment—that is, granulation tissues form. If the growth of granulation tissue is vigorous and aggressive, polyps develop. 15 Meyerhoff and colleagues 10 evaluated temporal bone from subjects with CSOM and reported that granulation tissue develops in 90% of all CSOM, and in 100% of cases of CSOM that develop intracranial complications.

ACUTE OTITIS MEDIA WITH AN OPEN TYMPANIC MEMBRANE
Inadequately treated AOM with a nonintact tympanic membrane is a frequently cited cause of CSOM. 16 Acute infections in an ear with a nonintact tympanic membrane are frequently inadequately or inappropriately treated (especially in children) because it is not universally recognized that in many ways an acute infection occurring in an open middle ear cavity is significantly different from classic AOM. Most importantly, the microbiology is significantly different. Although some cases of acute infection in an open middle ear arise from the typical AOM pathogens— Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis —most, especially in patients older than 2 years, are caused by species of Staphylococcus, Pseudomonas, or other gram-negative organisms. 17 Yeasts ( Candida spp.) are occasionally encountered when the eardrum is not intact, but rarely when the middle ear space is closed. 17 The oral antibiotics usually prescribed for AOM are poorly active against Staphylococcus and completely inactive against gram-negative organisms. Individuals treated with these systemic antibiotics consequently are often treated inappropriately or inadequately. Aggressive, appropriate treatment of acute middle ear infections in individuals with a nonintact tympanic membrane is an important way of preventing the development of CSOM.
Another meaningful difference between AOM with an intact tympanic membrane and AOM in an open middle ear is that the natural history of these two infections seem to be different. It is well established that 80% or more of untreated children with AOM and intact eardrums recover spontaneously, and that suppurative complications are unlikely. Ruohola and associates 18, 19 found that AOM in children with tympanostomy tubes is significantly different in this respect: at the end of their study, 60% of nontreated children still had infection and drainage.

MANAGEMENT OF OTORRHEA
There are three principal components to effective management of the draining ear:
1. Effective aural toilet
2. Use of an appropriate antimicrobial agent
3. Management of granulation tissue

Aural Toilet
Effective aural toilet mechanically decreases the bacterial burden, eliminates debris that nurtures bacterial growth, and removes obstacles to the effective delivery of antimicrobial agents. The most effective aural toilet is achieved using an operating microscope and microinstrumentation. When microscopic débridement cannot be performed, the use of irrigation solutions to remove debris and mucopurulent exudate is a reasonable alternative. Irrigation of the external auditory canal can be performed at home using a small bulb syringe. When used in combination with antimicrobial drops, irrigation should precede the instillation of drops by 20 to 30 minutes, allowing time for the instilled irrigation solution to drain out of the ear completely.
Various solutions have been advocated for this purpose, including 3% hydrogen peroxide, vinegar, and isopropyl alcohol. Many otologists dilute these solutions 50:50 with sterile water. Water alone should not be used. The use of water alone increases the ambient humidity; may alkalize the ear canal or middle ear space or both; and, if not sterile, can introduce pathogenic organisms. Isopropyl alcohol is not recommended because it can be painful on instillation and is potentially ototoxic.
“Dry mopping” refers to the use of twisted pieces of cotton or tissue pushed into the external auditory canal to “mop up” and remove any secretions within the canal. Its effectiveness is unknown, but it may be better than nothing, especially if the principal component to be removed is liquid and not desquamated epithelial debris or inspissated mucopus.

Antimicrobial Therapies
Elimination of infection is crucial to the successful management of a draining ear. Consequently, appropriate antimicrobial treatment is pivotal. Infection that is limited to the external auditory canal or an open mastoid cavity can sometimes be managed with the use of antiseptics or acidifying agents, or both, alone. When effective, these agents have several advantages: they are inexpensive, are easy to procure, do not promote bacterial resistance, and are generally effective against bacteria and fungi. The relative merits of one of these preparations versus another is generally unknown, although Tom 20 showed that Cresylate is more effective in vitro than other antiseptics against fungal organisms.
The acidifying agents and antiseptics are unattractive agents when the middle ear is open. Almost all have been shown to be potentially ototoxic. Most of these preparations are acidic (ototoxic in itself) and may be quite painful when they come in contact with the middle ear mucosa, which is of neutral pH.
When antibiotics are used, topical delivery in the form of otic drops is more effective and safer than the use of systemic antibiotics, either orally or parenterally. 21 - 25 27 By using a topical agent, the physician can deliver a concentration of medication that is several orders of magnitude higher in affected tissues than the concentration that can be achieved by using a systemic agent. A 3 to 5 drop dose of a 0.3% solution of antibiotic contains only 90 to 150 mg of medication, but its concentration is 3000 μg/mL, which exceeds the minimum inhibitory concentration of any known relevant pathogen. In contrast, consider the typical drug levels in middle ear fluid that can be achieved by three systemic antibiotics:
Cefuroxime 1 to 2 μg/mL
Amoxicillin 8 to 10 μg/mL
Ceftriaxone 25 to 30 μg/mL
Because the concentration of medicine delivered to infected tissue is so much higher than can be achieved with systemic antibiotics, antibiotic sensitivities as determined by clinical laboratories are irrelevant. These sensitivity determinations made by clinical laboratories are based on what are believed to be realistically achievable tissue levels after systemic administration of a drug. An organism with a minimal inhibitory concentration (MIC) of 4 to ciprofloxacin would generally be considered to be a “resistant” organism because it is unlikely that a tissue level of 4 μg/mL of ciprofloxacin could be achieved by oral or parenteral administration of ciprofloxacin. If otic drops with a concentration of 3000 μg/mL (a concentration available in commercial preparations) is delivered, however, the organism would succumb. Consequently, sensitivity determinations made in clinical laboratories can be safely ignored when topical therapy is used.
A second important consequence of such high concentrations is that the risk of the emergence of resistant organisms is minimized. Neither resistant clones already present nor newly emerging resistant mutants would survive in such very high concentrations of antibiotic. Despite the very high concentration of antibiotic in topical ear drops, the risk of systemic side effects or adverse reactions is very low because the total dose administered (approximately 1 mg per dose) is low, and systemic absorption is limited.
Skepticism has been voiced that topical drops would not provide sustained levels of antibiotic inside the middle ear space, especially if the perforation is small or delivery is through a tympanostomy tube. Ohyama and associates 26 documented that topical antibiotic drops can be, and often are, effectively delivered into the middle ear space and have long dwell times. These investigators measured the persistence of a single dose of topically applied 0.3% ofloxacin in otorrhea fluid, serum, and middle ear mucosa at various time intervals after administration. They found a very high level of antibiotic in the otorrhea fluid several hours later. Perhaps the most surprising finding was the high concentration of drug in biopsy specimens of middle ear mucosa approximately 1 hour after the administration of ear drops. As expected, drug concentrations in serum were very low or nondetectable.
The superior efficacy of topically applied antibiotics is well documented in the literature. Esposito and colleagues 28 studied 60 subjects with CSOM who were randomly assigned to receive one of three treatment regimens: one group received oral ciprofloxacin twice a day, another received three drops of ciprofloxacin solution twice a day, and a third group received oral and topical ciprofloxacin doses twice a day. The topical group had a clinical response rate of 100% and a bacteriologic cure rate of 95%, and the topical/oral group had response rates of 95% and 85%. By contrast, the group that received oral antibiotics alone had a clinical response rate of 65% and a rate of bacterial eradication of only 40%. These differences were statistically significant. 28 Two years later, Esposito and colleagues 29 published the results of their comparison of topical ciprofloxacin versus intramuscular gentamicin in 60 adults. All patients had CSOM, and 40 of them had previously undergone systemic therapy. Half of the group received four drops of ciprofloxacin solutions twice a day, and the other half received twice-daily injections of 80 mg of gentamicin. Favorable clinical responses were seen in 87% of the topically treated patients and only 67% of patients who received systemic gentamicin. Only 43% of the patients receiving systemic gentamicin achieved microbiologic eradication compared with 83% of the group receiving topical drops.
Two studies have compared the relative efficacy of topical drop regimens with the use of systemic antibiotics with amoxicillin/clavulanic acid. 30, 31 Both studies showed enhanced efficacy with the topical treatment regimen. These studies were performed in children with acute otorrhea after insertion of a tympanostomy tube. Because Pseudomonas and Staphylococcus aureus are more prominent pathogens in CSOM, the superiority of a topical regimen over amoxicillin/clavulanic acid should be even greater because S. aureus is a more frequent pathogen in CSOM than an acute otitis media with a tympanostomy tube (AMOT).
In 1994, Yuen and coworkers 32 published results of a prospective trial comparing 0.3% ofloxacin otic drops with oral amoxicillin/clavulanic acid in 56 patients. One week after completion of treatment, 76% of the ofloxacin group had dry ears compared with only 26% of the other group. de Miguel-Martinez and associates 33 divided 125 patients into five treatment arms. The participants received one of the following treatments:
1. Oral ciprofloxacin, 500 mg every 12 hours
2. Topical ciprofloxacin/hydrocortisone, 3 drops every 8 hours
3. Topical 0.2% ciprofloxacin 3 drops every 8 hours
4. Combination of oral and topical ciprofloxacin
5. Topical neomycin/polymyxin B
The best outcomes were achieved in the group that received 0.2% ciprofloxacin.
In 2000, the Cochrane database published a review by Acuin and coworkers. 24 The review concluded that topical antibiotics are superior to systemic antibiotics for the treatment of CSOM, and that a combination of systemic plus topical antibiotic offers no therapeutic advantage. Fluoroquinolone topical antibiotics were seen to be more effective than other types of topical antibiotic drops. The systemic review emphasized the superior microbiologic eradication rates achieved with topical therapy, and emphasized the importance of bacterial eradication.
The addition of a steroid to a topical antibiotic was compared with the ototopical antibiotic alone in three studies by Roland and colleagues. 15, 34, 35 Both studies showed that the steroids hastened the resolution of otorrhea, and in one study the final cure rate was higher in the group treated with a topical antibiotic that included a steroid. The efficacy of combination ototopical drops that contain an antibiotic and a steroid has not been specifically studied in the treatment of CSOM. The improved effectiveness of steroid-containing drops in the treatment of post-tympanostomy tube otorrhea and the management of granulation tissues has led many clinicians, however, to adopt them as the topical treatment of choice in individuals with CSOM.
Combination powders are widely used by experienced clinicians in the treatment of CSOM and in the management of draining mastoid cavities. Powders dry moist surfaces and stick to moist tissue tenaciously. They consequently have long dwell times after a single application. Various preparations are available. Most contain a combination of an antibiotic, antifungal agent, and steroid. Although none of these preparations has been systematically evaluated in controlled clinical trials, and although none is approved by the U.S. Food and Drug Administration (FDA), many experienced clinicians rely on them and is convinced they are more efficacious than otic drops.
Despite the superior efficacy of topically delivered medications, topical delivery does have some disadvantages, as follows:
1. Topical application can be uncomfortable. The mucosa of the middle ear space is much more sensitive than the skin of the external auditory canal. When very acidic drops (e.g., neomycin/polymyxin B/hydrocortisone preparations, whose pH may range between 3 and 3.5) are placed in the middle ear cavity, they can cause intense burning pain. Likewise, alcohol-containing drops sting and burn intensely, and their use should be avoided if they would enter the middle ear space. Discomfort can be caused simply because the drops are cold, especially in children. Children may have difficulty distinguishing between pain and the unpleasant sensation of cold medication. When possible, medication should be delivered close to body temperature. It is recommended that otic drops be warmed before instillation.
2. Topical medications can have direct inflammatory effects. Some antibiotics have inflammatory properties, and excipients mixed with antibiotics in topical antibiotic solutions (e.g., propylene glycol) can be irritating. It is believed that the steroid component present in some commercial preparations may minimize the inherent irritating properties of other ingredients.
3. The aminoglycoside antibiotics and polymyxin B are devastatingly ototoxic in animals. A single dose of neomycin/polymyxin B/hydrocortisone instilled into the external auditory canal of a chinchilla passes easily through tympanostomy tube and produces a significant loss of hair cells in the basal turn of the cochlea. Although the extent to which these animal data can be extrapolated to humans is arguable, researchers at the University of Toronto have shown that vestibular toxicity may be a significant risk when aminoglycoside drops are used. In contrast, animal data indicate that fluoroquinolones are not ototoxic. Although antibiotic drops other than quinolones are available, all are potentially ototoxic, and none is FDA approved for use in the middle ear space. A Consensus Panel of the American Academy of Otolaryngology–Head and Neck Surgery has advised against the use of potentially ototoxic drops when the middle ear is open on the grounds that because they convey no apparent benefit (other than low cost), the additional risk is unwarranted. 36
4. Aminoglycosides, and especially neomycin, have a propensity to cause topical sensitization. Although severe hypersensitivity reactions are usually easy to recognize, hypersensitivity may take a more subtle form. Often, the only manifestations of hypersensitivity are persistent erythema, edema, and otorrhea. When sensitization assumes this more subtle form, it may be impossible to distinguish between hypersensitivity reactions and clinical treatment failures. 37, 38
5. The biggest liability associated with topical therapy is that drops must come into direct contact with infected tissues if they are to be effective. Failure of delivery may arise from various causes (see later).
If the infection fails to resolve after 1 week to 10 days of topical therapy, it is not unreasonable to consider a course of systemic therapy. In contrast to topical therapy, systemic therapy should be based on the sensitivity of the infecting organism to available antibiotics. Oral therapy is preferred, unless the appropriate antibiotic is available only in a parenteral form, or is significantly more effective when delivered parenterally. Oral quinolones achieve the same blood and tissue levels when administered orally as when administered parenterally. Theoretically, systemic antibiotics should be effective only in cases in which effective delivery of topical drops cannot be achieved.

Granulation Tissue
Granulation tissue is an important component of the pathophysiology of CSOM. There are four components to the successful management of granulation tissue: aural toilet, appropriate antibiotic therapy, use of steroids, and débridement. Aural toilet and antibiotic therapy have been discussed previously.
Otolaryngologists have long held as an article of faith that steroids are important in suppressing, eliminating, and preventing granulation tissue. Several animal studies have found that steroids are effective in controlling keloids and hypertrophic scarring, and reducing angiogenesis with subsequent formation of granulation tissue. 39 - 43 More recently, evidence has shown that steroids are effective in humans as well. A randomized, controlled, double-blind drug comparison study of 599 children with patent tympanostomy tubes and AOM with otorrhea of 3 weeks or less duration provides such evidence. Children with granulation tissue associated with tympanostomy tubes were treated with either a quinolone plus a steroid or a quinolone alone. Not only did the combination product prove to be significantly more effective in establishing clinical and microbiologic cure in all patients, but also it was significantly more effective in eliminating granulation tissue. 15, 44 A more potent steroid seems to be more effective than a less potent steroid.
Office débridement of granulation tissue can be performed using the microscope and microinstrumentation, but it is most commonly performed using chemical cautery. Silver nitrate is the agent most commonly used, although trichloroacetic acid is used by some clinicians. Chemical cautery is, in effect, a chemical burn, and control over the depth and severity of that burn is limited. 45 If care is not exercised, vital structures (i.e., facial nerve) can be permanently injured. Mechanical removal should be done sharply, with clear visualization of exactly what tissues are being incised. Avulsion of aural polyps is not usually recommended because when the polyp is removed, the otolaryngologist might find that the stapes is attached to it. Using sharp techniques under direct visualization avoids inadvertent injury to important structures. Tympanomastoid surgery for chronic otitis media is an aggressive form of débridement and is often very effective.

Preventing Bacterial Resistance
The FDA and major infectious disease societies of the United States have urged clinicians to use treatment regimens that minimize the opportunity for the development of bacterial resistance. Acquired resistance refers to a change in the susceptibility of an organism to a particular antibiotic. Topical therapy is less likely to result in emergence of resistant strains for two reasons:
1. The very high concentration of antibiotic delivered to infected tissues when a topical therapy is used
2. The relatively shorter duration of therapy recommended when a topical treatment or regimens are used
Applying the term resistant to a bacterial species is based on two determinations:
1. The MIC for a given organism to a given antibiotic
2. The amount of antibiotic that can reasonably be expected to reach the site of infection after systemic administration (intramuscular, intravenous, or oral).
The MIC is an inherent biologic characteristic of an individual bacterial strain. The organism is resistant to an antibiotic, however, if, and only if, the amount of antibiotic that can be delivered to the site of infection does not exceed the particular MIC of that organism to the antibiotic used. Consequently, although MIC is a biologic characteristic of the organism, the designation of either sensitive or resistant is relative.
As a practical matter, increases in bacterial resistance to a specific antibiotic are manifest by increasing MICs for that particular antibiotic. An analysis of clinical failures from several large clinical trials verified that changes in MIC have not occurred as a result of treatment using topical antibiotic drops. 35

Causes of Failed Therapy
Although the principal virtue of a topical antibiotic therapy is the very high concentrations of drugs that can be delivered, the weakness of topical therapy is that efficacy depends on effective delivery. When one considers the MICs of infective organisms (virtually never >250 μg/mL) and the concentration of antibiotic in topical drops (3000 μg/mL), it becomes apparent that a cure would be achieved if the medication is effectively delivered to infected tissues. Virtually all failures of topical therapy are failures of delivery . There are many reasons why successful delivery may not be achieved, including the following:
1. Noncompliance
2. Poor delivery technique
3. Voluminous drainage
4. Mucosal edema
5. Granulation tissue
Noncompliance can take several forms. The medicine may never be purchased, and the treatment regimen never begun. The potential efficacy and potency of topical antibiotic therapy is not widely recognized by the public. The medicine may never be purchased because it is too costly. Inquiries into whether or not the patient can afford medication are important, especially if more expensive brand-name products are chosen. More typically, noncompliance takes the form of inconsistent, erratic dosing or early termination of treatment or both.
Proper technique requires that the drops are delivered into the internal auditory canal, which is often difficult with a squirming child. “Tragal” pumping (rhythmic pressure just anterior to the tragal cartilage) is important in ensuring that drops penetrate through a tympanostomy tube or tympanic membrane perforation into the middle ear space. 46 Issues related to management of granulation tissue have been discussed previously. Occasionally, mucosal edema is sufficient to prevent adequate delivery of antibiotics into and through the middle ear space. When this is the case, patience is required. The use of a steroid-containing antibiotic drop generally results in progressively increasing middle ear mucosal edema over several days. Voluminous drainage is managed as mentioned earlier by effective aural toilet.
Occasionally, therapy fails because there is a sequestered nidus of infection in a portion of the middle ear or mastoid, inaccessible to topical drops. Sometimes such a nidus is focused around a small area of devascularized or dead bone. When this is the case, topical therapy may never be effective. Such cases occasionally respond to systemic antibiotics, however. Consequently, a treatment regimen of systemic antibiotic therapy in individuals who failed topical therapy is logical and occasionally effective, even though, as noted earlier, topical treatment regimens are generally more effective than systemic treatment. Appropriate imaging studies occasionally can identify such areas. A fine cut CT scan of the temporal bone may provide useful information if systemic therapy is contemplated or necessary.
An occult cholesteatoma is a common source of persistent drainage that does not respond to topical therapy. Cholesteatomas can be extremely difficult to visualize in an infected, purulent ear. Effective resolution of otorrhea can often be achieved with topical therapy even if a cholesteatoma is present. When topical therapy is effective, and when granulation tissue, edema, and purulence are eliminated, physical examination often allows easy identification of the cholesteatomatous process. It may be impossible to eliminate infection, however, when this source is an infected cholesteatoma. Imaging studies are often capable of identifying a cholesteatomatous process even in the face of significant infection. An experienced radiologist can often detect the pattern typical for cholesteatoma, and differentiate a cholesteatoma-driven from a purely infectious process.
When drainage cannot be resolved, the patient should be evaluated for disease in remote locations. Most specifically, in children, the tonsils, adenoids, and sinuses need to be considered. Chronic, unremitting rhinosinusitis can produce constant reseeding of the middle ear space, especially in young children with eustachian tube reflux. Infected adenoids can be another ongoing source for persistent infection. Whether or not infected tonsils can repeatedly reseed the middle ear space has not been clearly shown or refuted.
Occasional patients have persistent middle ear and mastoid infection because of depressed or diminished immune capacity. Topical antibiotic therapy is almost certain to be insufficient treatment for individuals who have diseases at remote sites or compromised immune systems.
Biofilms have been shown not only on tympanostomy tubes, but also in the middle ear and mastoid with suppurative otitis media. The biofilms seen in patients with CSOM resemble those found on the surface of the middle ear mucosa of chinchillas after inoculation with nontypable Haemophilus influenzae . Although the role of biofilms in the pathogenesis of culture-negative otitis media with effusion is outside the scope of this chapter, the presence of biofilms in individuals with persistent/recurrent otologic infections does suggest a possible pathogenic role for biofilms. 47, 48 It is widely recognized that patients who fail combined topical/systemic therapy often resolve the infection after the removal of a tympanostomy tube.
Effective treatment of biofilms depends on restoration of the normal physiology of the middle ear combined with supratherapeutic doses of antibiotics. Whether or not sufficiently high doses of antibiotic therapy can be achieved with topical regimens remains unclear.
The draining mastoid cavity is a problem occasionally seen in patients who have undergone open cavity techniques, usually for the management of cholesteatoma. Drainage persists in such cavities for several reasons. The most common cause of unremitting drainage is either persistent infection in a sequestered air cell or a small area of osteitis. In such cases, the cavity as a whole heals up well except for a small area that remains covered with granulation tissue. Occasionally, aggressive, nonsurgical management of the small area of granulation tissue permits brief episodes of epithelial coverage, but the epithelium breaks down again as infection wells up beneath it from the area of osteitis. When this is the case, the only solution is the removal of the involved area.
Sometimes this removal can be done with the patient under local anesthesia in the clinic using small curettes to scrape away the involved area. More frequently, it requires a brief return to the operating room, where surgical drills can be used to eliminate infected bone. If the area of the osteitis is large, and postoperative otorrhea has persisted for months or years, consideration should be given to skin grafting. Skin grafts are occasionally used in cavities that have developed mucosal as opposed to squamous epithelial linings on one or more occasions. Sometimes persistent or recurrent drainage is caused by residual cholesteatoma. The only viable solution for recurrent cholesteatoma is reoperation with removal of residual disease.
Sometimes persistent or recurrent drainage is caused by persistent otitis media as a result of eustachian tube obstruction or reflux. Generally, infection is clearly limited to the middle ear, and the patient has a draining perforation. The mastoid cavity may seem healthy, or may be repeatedly contaminated by mucopurulent exudate flowing out of the middle ear, which can result in persistent mastoid infection or granulation tissue or both. Therapy should be directed toward resolving the persistent infection of otitis media. Revision surgery can eliminate foci of persistent infection in the middle ear space and successfully close recurrent tympanic membrane perforations leading to a clean, dry, healed ear.
Pharmacologic management of the draining cavity follows the same principles as for other chronic middle ear and mastoid infections. Topical therapy is the treatment of choice—in the setting of a draining cavity, powders are particularly useful. If the middle ear space is closed (i.e., the tympanic membrane graft has healed), the antiseptics are more attractive because issues relating to ototoxicity are irrelevant.

OFFICE TECHNIQUES FOR CLOSURE OF TYMPANIC MEMBRANE PERFORATIONS
Two techniques are used for closure of tympanic membrane perforations in the outpatient office setting: a fat graft tympanoplasty and paper patch tympanoplasty. Paper patching is used much more commonly in the outpatient setting than fat graft tympanoplasty.

Cauterization and Paper Patching
The use of paper patches, placed in an outpatient setting (a general anesthetic may be necessary for children), has been widespread for many decades. Paper patches are designed to promote healing of perforated tympanic membranes, while avoiding a formal surgical procedure. The technique is based on the recognition that one cause of failure to heal is epithelialization of the margin of a perforation. Removing the healed epithelial edge transforms the perforation into an open wound, and allows the regenerative process to begin anew.
Rose and Politzer were among the first to use silver nitrate cauterization of the margins of a perforation to promote healing. 49 Dunlap and Schuknecht reported that closure generally requires repeated application of cautery with removal of dried exudates every 2 weeks; closure was complete, on average, only after 6 to 12 months. 49 Jeurs and Wright reported success in closing perforations by marginal stimulation in 80% to 90% of cases; multiple treatment episodes were required. 50 Derlacki 51, 52 was able to close 75% of 131 perforations he treated, with an average of 14 treatments required. Although Derlacki 51, 52 had some success in larger perforations, most successes are reported for small to medium-sized perforations. Repeated cauterizations are always necessary.
Trichloroacetic acid has become the agent of choice for removal of the old epithelial margin. It is applied to the margins of the perforation using a very small cotton swab (Calgiswab or handmade). Effective chemical cauterization turns the edge of the perforation white about 1 or 2 mm from the rim. A small paper patch can be applied to act as a scaffolding for the regenerating epithelium. Paper patches are often made from either cigarette or filter paper. A commercially available “hole punch” creates a patch of ideal size. The patient needs to be seen at weekly intervals for recauterization and patch refreshing until the perforation is closed. There is a general consensus that cauterization and patching techniques are impractical when perforations exceed 25% to 50% of the tympanic membrane, and are contraindicated in the presence of frank or suspected cholesteatoma, chronic drainage, and ossicular disruption.
Some otologists believe that traumatic tympanic membrane perforations must be managed acutely. They believe the best results are achieved when torn areas of drum are immediately reapproximated, often over absorbable gelatin sponge (Gelfoam) placed through the perforation into the middle ear to support the reapproximated portions of drum ( Figs. 8-1 through 8-6 ). Special emphasis is often placed on elevating segments of drum that are folded back on themselves after an implosion-type injury. Accurate reapproximation of drum fragments requires microinstrumentation and a microscope. Some authors recommend combining fragment reapproximation with paper patching.

FIGURE 8-1

Fat Graft Tympanoplasty
The technique of fat graft tympanoplasty was first described by Ringenberg in 1962, 53 but differed substantially from the technique currently recommended in two respects: (1) Ringenberg turned a tympanomeatal flap and explored the middle ear as part of the procedure, and (2) the fat graft was placed lateral to (and not through) the perforation. Donor fat is generally harvested from the earlobe. Ringenberg 53 evaluated fat from several anatomic sites, and determined that earlobe fat was more compact and contained more connective tissue than fat harvested from the abdomen or the buttocks. Other advantages include the ease with which lobule fat from the lobe can be obtained, and that enough donor fat can be taken from a single lobule to graft more than one tympanic membrane perforation. 54
The technique as currently described is quite simple ( Figs. 8-7 and 8-8 ). The epithelial margin of the perforation is removed so that the edges of the perforation are fresh and open. This is sometimes referred to as “rimming” the perforation. A globule of fat slightly larger than the perforation is pushed through the perforation so that a portion of the inserted fat is medial to the tympanic membrane, and a portion is lateral.

FIGURE 8-7
Histologically, the graft seems to epithelialize over 2 to 3 weeks. The graft atrophies in the first couple of weeks, but at 3 to 4 weeks a significant volume of fat can still be seen within the epithelialized medial and lateral surface. This fat atrophies almost completely in the following 3 to 6 weeks. Very little of the fat remains within the middle layer of the now healed tympanic membrane 6 to 8 weeks after grafting. 53, 55 It is widely agreed that the technique is most suitable for small perforations involving no more than 25% to 30% of the tympanic membrane. 54, 56 - 59 The technique should be limited to individuals whose hearing is normal or close to normal, and in whom there is little or no possibility of associated ossicular abnormality. 54, 56, 57, 60, 61
Because this technique is most frequently used in pediatric patients for small perforations that persisted after extrusion of tympanostomy tubes, most cases have been done in a day surgery setting. The technique is suitable for office outpatient use, however, and can be performed with local anesthesia. Because the middle ear space is not entered, it is reasonable to perform the procedure bilaterally. 54, 57 Closure rates have been reported as 76% to 92% of cases. 54, 56 - 62 In a small series of 15 tympanostomy tubes removed for persistent unremitting otorrhea, Liew and associates 63 reported a success rate of 100%.

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53. Ringenberg J.C. Fat graft tympanoplasty. Laryngoscope . 1962;72:188-192.
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63. Liew L., Daudia A., Narula A.A. Synchronous fat plug myringoplasty and tympanostomy tube removal in the management of refractory otorrhoea in younger patients. Int J Pediatr Otorhinolaryngol . 2002;66:291-296.
Chapter 9 Tympanoplasty—Outer Surface Grafting Technique

Jose N. Fayad, James L. Sheehy
Videos corresponding to this chapter are available online at www.expertconsult.com .
The aims of tympanoplasty are elimination of disease and restoration of function. Restoration of function requires a tympanic membrane; an air-containing, mucosal-lined middle ear (so that the membrane vibrates); and a secure connection between the tympanic membrane and the inner ear fluids. This chapter presents one of the three major techniques of tympanic membrane grafting: the outer surface, or onlay, procedure. This technique is used with rare exceptions by physicians of the House Clinic. Before describing the surgical procedure, the evolution of tympanic membrane grafting techniques, patient selection, and evaluation and counseling before surgery are discussed.

HISTORICAL ASPECTS
Systematic reconstruction of the tympanic membrane, the sine qua non of the modern era of reconstructive ear surgery, had its beginning with reports by Wullstein 1 and Zollner. 2 Split-thickness or full-thickness skin was placed over the de-epithelialized tympanic membrane remnant. The initial results were very encouraging, but graft eczema, inflammation, and perforation were common.
As a result of these experiences, most surgeons had begun changing to undersurface (underlay) connective tissue grafts by the late 1950s (see Chapters 11 and 12 ). The House Clinic physicians continued using an onlay technique, but changed to “canal skin,” 3, 4 which actually was periosteum graft covered by canal skin. This change was made in 1958, and resulted in an immediate improvement in results. Draining ears and total perforations continued to have a failure rate reaching 40%.
In 1961, Storrs 5 published the results of a small series of cases in which temporalis fascia had been used as an outer surface graft. Changing to this technique resulted in a dramatic improvement in results over the next 3 years: greater than 90% graft take. 6 - 8

PATIENT SELECTION AND EVALUATION
A patient with chronic otitis media may consult a physician because of a hearing impairment or because of discharge from the ear. Occasionally, the patient may have symptoms of more advanced chronic ear pathology, such as pain, vertigo, or facial nerve paralysis. Careful evaluation of the symptoms and findings allows the otologist to determine the need for surgery, its urgency, and the anticipated result. Only by completing the evaluation can the patient be advised properly. A good surgical result should not be a disappointment to the patient if there is proper counseling.
Let us assume, for purposes of this chapter, that the patient has a dry central perforation. The ear may drain briefly with upper respiratory infections or if water is allowed to get into the ear. This discharge responds promptly to local medication. The preoperative treatment of the draining ear is discussed in depth in Chapter 16 . When one is dealing with a dry central perforation, or inactive disease, surgery is elective, and the patient (or family) should be so informed. Assuming that the problem is unilateral, with only a mild hearing impairment, the only indication for surgery is to avoid further episodes of otorrhea.
In children, it is best (from a psychological standpoint) to avoid elective surgery of any type between the ages of 4 and 7 years. In ear surgery, it is wise to wait until after age 7 so as not to lay the groundwork for serous otitis media. If the problem is bilateral, there is a hearing problem, and the ears do not drain often, fitting with hearing aids in each ear may be preferable for children younger than 8 years; however, the parents have to make the decision. At age 8 and thereafter, the patient (and child) should be allowed to make the decision.
When contemplating tympanoplasty, the House Clinic physicians do not usually test to determine the status of the eustachian tube. 9 The philosophy has been that tubal malfunction per se is not a contraindication to tympanoplasty, but that the operation would not be successful unless tubal function is re-established. Many patients showing no tubal function by various available tests used in the past have been operated on to eliminate a chronic drainage problem. When the ear heals, the drum is usually mobile. Re-exploration in some of these patients has shown normal mucosa in the tubotympanum, where before surgery the mucosa was of a very poor quality. It would seem that the surgery, in eliminating infection and sealing the ear, is in itself the best treatment for the obstructed tube.

PATIENT COUNSELING
What is the outlook with surgery, and what are the risks and complications? A surgeon must relate his or her own experience. House Clinic physicians explain that the likelihood of obtaining a permanently healed, dry ear, which may be treated normally, is better than 90%. “The only complication that happens with any degree of regularity, and is serious, is a total loss of hearing in the operated ear. That likelihood is no more than 1%. All of the other things listed here are either very remote or are temporary.” (“Listed here” refers to the Risk and Complications section of a patient Discussion Booklet. The Risk and Complications Sheet is given to the patient at the time the surgery is scheduled, which allows the patient to review the sheet leisurely. Appendix 1 is the Risk and Complications Sheet.)

PREOPERATIVE PREPARATION
If the patient is a child, the preoperative visit occurs the day before surgery. Surgery is done under general anesthesia the following morning. The child is released to the parents’ care in the afternoon.
For adults, the preoperative visit is sometimes the morning of surgery. The patient goes to the hospital for afternoon surgery, which is done under local or general anesthesia. The patient may be kept in the hospital overnight, depending on many circumstances.

PREPARATION IN THE OPERATING ROOM
The smoothness with which the operation proceeds depends not only on the ability of the surgeon, but also on the organization of the team (anesthesiologist and surgical nurse) and arrangements in the operating room. The patient’s hair is shaved 3 cm above and behind the ear. The skin is cleansed with an iodine-based soap and rinsed with water. A sterile plastic adhesive drape is placed after applying tincture of benzoin. The mattress of the operating table is taped securely to the table to prevent it from slipping when the table is tipped from side to side or into the Trendelenburg position. The patient is placed on the table with his or her head at the foot of the table, which allows the circulating nurse or anesthesiologist free access to the table controls, which are at the feet of the patient. The patient’s head and shoulders should be as near to the surgeon’s side of the table as possible. A pillow is placed under the patient’s knees. The Bovie plate goes under the patient’s buttocks.

Anesthesia
Ear surgery can be performed with the patient under local anesthesia in many cases. The decision depends on the age of the patient and other factors. Lidocaine with 1:100,000 epinephrine is used for postauricular and meatal incisions. Some of the injection material should find its way under the skin of the posterior superior wall of the canal (the vascular strip) and into the middle ear. General anesthesia is used in children, in most mastoid surgery, and in procedures that require more than 1.5 hours of operating time. The anesthesiologist should be at the feet of the patient (which is actually the head of the table) to allow the surgeon and scrub nurse complete freedom at the patient’s head.
A few useful suggestions for the anesthesiologist are as follows:
1. Have extra-long tubing for the gas machine to allow seating at the foot of the patient.
2. Start the intravenous infusion in the forearm, and extend the tubing to the foot of the table.
3. Place the blood pressure cuff on the arm opposite the ear to be operated on.
4. Be certain that the patient is secured to the table with wide adhesive tape. The eyes should be taped shut.

Arrangement and Instrumentation
Particular attention should be paid to operating room arrangement ( Fig. 9-1 ). The anesthesiologist is at the patient’s feet, far removed from the operating field, and the scrub nurse is directly across from the surgeon, where the nurse may be of the most assistance. The same arrangement, minus the anesthesiologist, is used for procedures done with the patient under local anesthesia.

FIGURE 9-1
It is important for the comfort of the surgeon that the patient is in a satisfactory position. The table is usually placed in a few degrees of Trendelenburg position and rolled slightly toward the surgeon. The patient’s head is adjusted as necessary, usually flexed slightly onto the opposite shoulder. The surgeon should be comfortably seated on a chair with a back support. The surgeon should use the back support and be in a comfortable position so that all back and arm muscles are relaxed.

SURGICAL TECHNIQUE
The lateral surface grafting technique involves eight steps: (1) transmeatal canal incisions, and elevations of the vascular strip; (2) postauricular exposure, and removal and dehydration of the temporalis fascia; (3) removal of canal skin; (4) enlargement of the ear canal by removal of the anterior (and inferior) canal bulge; (5) de-epithelialization of the tympanic membrane remnant; (6) placement of the rehydrated fascia on the outer surface of the remnant, but under the manubrium; (7) replacement of canal skin; and (8) closure of the postauricular incision and replacement of the vascular strip transmeatally. 10

Transmeatal Incisions
Incisions are made along the tympanomastoid and tympanosquamous suture lines, demarcating the vascular strip with a No. 1 (sickle) knife ( Fig. 9-2 ). The vascular strip is the area of the canal skin that covers the superior and posterior portions of the ear canal between these two suture lines. It is easily demarcated from the skin of the remainder of the ear canal because of its thickness, and the fact that it balloons up when local anesthesia is injected into the area. The vascular strip is elevated from the bone, from within outward using a round knife ( Fig. 9-3 ).
A semilunar incision is made in the outer third of the ear canal, using a Beaver knife with a No. 64 blade, connecting the two incisions already made along the border of the vascular strip ( Fig. 9-4 ). The knife blade is angled toward the bone to thin the 1 or 2 mm section of the membranous canal included.

Postauricular Exposure and Removal of Fascia
The skin incision must provide adequate exposure for the operative field. It should extend far enough forward superiorly and inferiorly to allow adequate exposure of the bony meatus when the ear is retracted forward. Failure to do this may result in difficulty seeing structures in the posterior part of the middle ear. The superior portion of the incision begins at the most anterior extent of, and 1 cm above, the postauricular fold. It is continued into the postauricular fold at the level of the lower border of the muscle and extends inferiorly under the lobule of the ear.
Exposure of the temporalis fascia is facilitated if ample local anesthetic has been injected to balloon the area. A retractor is inserted to retract the skin margins in this area and to obtain hemostasis. By lifting up on the retractor, one may pull the areolar tissue away from the fascia, facilitating the dissection and ensuring that all loose areolar tissue is lifted off the fascia before the fascia’s removal.
Local anesthesia is injected under the fascia to elevate it slightly from the underlying muscle. A 2 × 2 cm piece of fascia is removed. The fascia is spread on a polytef (Teflon) block, undersurface upward, and any adherent muscle is removed. The fascia is placed on a fascia press, absorbable gelatin sponge (Gelfoam) is placed on the fascia, and the press is closed. The press is opened after 5 minutes, and the Gelfoam is removed; the fascia, now smooth and partially dehydrated, is left attached to the press. The press, with the attached fascia, is placed under an electric lamp to complete the dehydration process.
An incision is made through the soft tissue above the meatus, from the root of the zygoma, horizontally, along the linea temporalis. This horizontal incision is extended posteriorly to the level of the skin incision. The incision is extended inferiorly, below the linea temporalis, following the postauricular incision, incising the periosteum until the incision curves forward, down to the level of the floor of the ear canal. The periosteum is elevated superiorly (under the temporalis muscle), posteriorly and anteriorly, using a Lempert elevator, to obtain adequate exposure of the mastoid cortex. A self-retaining retractor is inserted to retract the auricle and vascular strip forward, exposing the ear canal.

Removal of the Canal Skin
The periosteum and canal skin are elevated from the bone as far as the annular ligament ( Fig. 9-5 ). Care should be taken not to elevate the ligament and the remnant of the middle fibrous layer. The dissection is superficial to the fibrous layer of the remnant in such a way that the remnant is de-epithelialized in continuity with the canal skin, if possible. It is often easier to begin the final removal and de-epithelialization by starting anterosuperiorly, using a cup forceps ( Fig. 9-6 ). Removal of the canal skin and de-epithelialization are continued inferiorly and posteriorly. The periosteum and canal skin are removed from the ear and kept moist in Tis-U-Sol irrigating solution.

FIGURE 9-5
In elevating the periosteum and the canal skin, one works perpendicular to the annular ligament and remnant, keeping the instrument on the bone at all times, until the dissection is completed to the level of the remnant. The dissection is continued parallel to the annular ligament to avoid elevating it and the remnant ( Fig. 9-7 ).

Enlargement of the Ear Canal
Through the use of a drill and continuous suction-irrigation, the ear canal is enlarged by removal of the anterior and inferior canal bulges ( Fig. 9-8 ). The importance of this step in the lateral surface grafting technique cannot be overemphasized. Removal of this bone enlarges the field of surgery. The anterior and inferior sulci are thoroughly exposed to allow de-epithelialization and satisfactory graft placement. The acute angle that exists anteriorly is opened, helping to prevent postoperative blunting. There is no area hidden from postoperative observation. Enlarging the ear canal is routine in all lateral surface grafting procedures, and is the main reason for removal of canal skin.

De-epithelialization of the Tympanic Membrane Remnant
The lateral surface grafting technique demands a complete de-epithelialization of the remnant. Although the graft may take without all the skin having been removed, postoperative epithelial cysts may develop. Attention is directed first to the ear canal bone immediately adjacent to the bony annulus. Particular attention is paid to the anteroinferior bone 1 mm lateral to the annulus, where a small vessel and nerve perforate the bone, and where there is a particularly tight attachment to the skin. Next, the tympanic membrane remnant is checked carefully for skin. If there is a question about whether de-epithelialization has been thorough, a portion of the remnant is removed to be certain. The size of the perforation is of no consequence in regard to graft take in the lateral surface technique.

Preparation of Packing
The surgical nurse should have begun preparing Gelfoam packing before or shortly after the beginning of the operation. Uncompressed Gelfoam is cut into an ample number of various-sized pieces and soaked in antibiotic-cortisone solution. Pieces of Gelfoam are removed from the solution and compressed (on a tongue blade or a paper Gelfoam packet) until most of the solution has been removed. The Gelfoam is put aside and allowed to dry more until needed by the surgeon.

Placement of Fascia
When the perforation is large, or the fascia is unusually thin, it is helpful to fill the middle ear with Gelfoam packing before placing the graft. The Gelfoam serves as an artificial remnant and facilitates graft placement. The fascia is placed under the malleus handle. When the manubrium is surrounded by remnant (small perforation), the remnant is separated from the malleus handle to allow proper placement of the fascia.
The dehydrated fascia is trimmed to an oval shape measuring approximately 1.3 × 1.5 cm. A slit is cut in the fascia to allow placement under the manubrium ( Fig. 9-9 ). The two cut ends are grasped with the forceps, and the fascia is immersed for a few seconds in Tis-U-Sol irrigating solution to hydrate it.
The fascia is placed over the perforation and immediately slipped under the manubrium ( Fig. 9-10 ). One ensures that the apex of the slit in the fascia comes into contact with the tensor tendon. The fascia is adjusted to the remnant anteriorly and inferiorly, with care being taken that it does not extend onto the bony wall anteriorly, unless there is no remnant at all, then it should extend only for 1 mm at the most. The anterior flap is turned back over the exposed manubrium, resulting in a better appearance of the membrane when healed ( Fig. 9-11 ).
When the malleus is absent, and there is only a small remnant present, it is necessary to insert the fascia in a different way to result in the stabilized graft ( Fig. 9-12 ). The fascia is cut twice, creating a flap that can be tucked under the lateral wall of the epitympanum. The anterosuperior edge of the fascia is swung posteriorly to overlap the upper edge of the graft and secure the seal of the middle ear ( Fig. 9-13 ).

Replacement of Canal Skin
The canal skin is replaced to cover the bone from which it was removed. It is positioned only slightly more medially, allowing it to overlap the fascia by 1 mm ( Fig. 9-14 ), which helps promote rapid epithelialization. Epithelialization is particularly important in preventing blunting in the anterosuperior sulcus. There must be no edges of epithelium turned under, or small epithelial cysts may develop on the surface of the fascia during healing.

FIGURE 9-14
The first piece of packing is a small, dry, rolled-up (cigar-shaped), tightly compressed piece of absorbable Gelfoam, which is placed in the sulcus anteriorly. The canal is packed tightly with pledgets of slightly moist Gelfoam, leaving room posterosuperiorly for the vascular strip.

Closure and Replacement of the Vascular Strip
The retractors are released, and the vascular strip is pushed anteriorly to lie over the packing. One suture is placed subcutaneously postauricularly to stabilize the auricle. Transmeatally, the vascular strip is replaced in the ear canal in the exact position from which it came ( Fig. 9-15 ). Gelfoam packing in the canal is completed, and a plug of cotton is placed in the outer meatus. The postauricular incision is closed with subcutaneous sutures, and a mastoid dressing is applied.

POSTOPERATIVE CARE
The mastoid dressing is removed the day after surgery. The patient is given a postoperative instruction card ( Appendix 2 ) just before entering the hospital. It is important to review some aspects of this information with the patient. The patient should be reminded not to blow the nose and not to get water in the ear. An antibiotic is prescribed and should be taken as directed on the prescription label. There will be discomfort for a few days, and the patient should take aspirin or acetaminophen four times a day regularly for the first few days to keep the pain under control. Nothing need be done with the cotton in the ear, but it may be changed if it becomes soiled.
The patient is asked to touch the edge of the auricle; the physician points out that the ear is numb, and that it is going to take a few months for the numbness to fade. There is also tenderness on the incision behind the ear. This tenderness diminishes rapidly, but it may be 6 months before it is totally gone. Finally, the patient should be reminded of the first postoperative appointment, which should be scheduled 7 to 10 days later in the physician’s office.
At the first postoperative visit, the cotton plug in the ear canal is removed, and the ear is inspected. The Gelfoam should appear firm. A piece of Gelfoam should be removed to show to the patient so that the patient understands that it will eventually turn to a liquid and will run out of the ear. The patient is instructed to begin using ear drops (of one type or another) 3 weeks after the date of surgery, twice daily. The drops may be started sooner if the ear begins to drain, an indication of liquefaction of the Gelfoam. The second postoperative visit is scheduled for 6 to 8 weeks after the date of surgery. At this point, 80% to 90% of the ear should be totally healed.

PROS AND CONS OF OUTER SURFACE TECHNIQUE
One of the problems faced by a novice surgeon is that there are many techniques and prostheses recommended as “the best—always works well.

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