Manual of Endoscopic Sinus and Skull Base Surgery [2 ed.] 9783131309723, 3131309725

Table of contents :
Title Page
Copyright
Preface
Acknowledgments
Contributors
Table of Contents
List of Videos
Media Center Information
1 Principles of Practice
2 Pathophysiology of Rhinosinusitis
3 Who Optimizing Diagnosis and Selection of Patients for Surgery
4 When Medical Treatment and Timing of Surgery
5 Preserving and Improving the Sense of Smell
6 Why The Goals of Surgery
7 Applied Anatomy for Endoscopic Sinus and Skull Base Surgery
8 How Operative Procedures A Step-by-Step Safe and Logical Approach
9 An Endoscopic Tour Endoscopic Examination, Anatomical Variations, and Specific Conditions
10 The Place of Radiology
11 Preoperative Checklist
12 Patient Consent and Information
13 Peroperative Aids
14 Hints
15 Preventing and Dealing with Complications
16 Postoperative Management
17 Extended Endoscopic Procedures
18 The Endoscopically Assisted Bimanual Operating Technique
19 Transnasal Endoscopic Approaches to the Skull Base
20 Interdisciplinary Teamwork in Transnasal Endoscopic Skull Base Surgery
21 Transnasal Endoscopic Surgery of Pituitary Tumors
22 Transorbital Surgery of the Skull Base
23 Evidence Base in Rhinosinusitis and Endoscopic Sinus Surgery
Appendix Information for Patients Undergoing Endoscopic Sinus Surgery
Bibliography
Index

Citation preview

Manual of Endoscopic Sinus and Skull Base Surgery Second edition

Daniel Simmen, MD

Professor and Lecturer in Rhinology University of Zurich ENT Center The Hirslanden Clinic Zurich, Switzerland

Nick Jones, MD, BDS, FRCS, FRCS (ORL) Professor Department of Otorhinolaryngology, Head and Neck Surgery Queen’s Medical Centre University Hospital Nottingham, UK

With contributions by Karthik Balakrishnan, Hans Rudolf Briner, Leonardo Lopes Balsalobre Filho, Kris S. Moe, Robert Reisch, Bernhard Schuknecht, Aldo Cassol Stamm

1,442 illustrations

Thieme Stuttgart · New York

Library of Congress Cataloging-in-Publication Data Simmen, D. (Daniel), author. Manual of endoscopic sinus and skull base surgery / Daniel Simmen, Nick Jones. -- Second edition. p. ; cm. Preceded by: Manual of endoscopic sinus surgery and its extended applications / Daniel Simmen, Nick Jones. c2005. Includes bibliographical references and index. ISBN 978-3-13-130972-3 (hardback : alk. paper) I. Jones, Nick, 1953- author. II. Simmen, D. (Daniel). Manual of endoscopic sinus surgery and its extended applications. Preceded by (work): III. Title. [DNLM: 1. Paranasal Sinuses--surgery. 2. Endoscopy-methods. 3. Perioperative Care--methods. 4. Skull Base--surgery. WV 340] RF421 617.5'23--dc23 2013030980

Illustrator: Sandra Schuhmacher

© 2014 Georg Thieme Verlag KG, Rüdigerstrasse 14, 70469 Stuttgart, Germany http://www.thieme.de Thieme Medical Publishers, Inc., 333 Seventh Avenue, New York, NY 10001, USA http://www.thieme.com

Cover design: Thieme Publishing Group Typesetting by Prepress Projects, Perth, UK Printed in China by Everbest Printing Ltd., Hong Kong

ISBN 978-3-13-130972-3 Also available as an e-book: eISBN 978-3-13-173012-1

Important note: Medicine is an ever-changing science undergoing continual development. Research and clinical experience are continually expanding our knowledge, in particular our knowledge of proper treatment and drug therapy. Insofar as this book mentions any dosage or application, readers may rest assured that the authors, editors, and publishers have made every effort to ensure that such references are in accordance with the state of knowledge at the time of production of the book. Nevertheless, this does not involve, imply, or express any guarantee or responsibility on the part of the publishers in respect to any dosage instructions and forms of applications stated in the book. Every user is requested to examine carefully the manufacturers’ leaflets accompanying each drug and to check, if necessary in consultation with a physician or specialist, whether the dosage schedules mentioned therein or the contraindications stated by the manufacturers differ from the statements made in the present book. Such examination is particularly important with drugs that are either rarely used or have been newly released on the market. Every dosage schedule or every form of application used is entirely at the user’s own risk and responsibility. The authors and publishers request every user to report to the publishers any discrepancies or inaccuracies noticed. If errors in this work are found after publication, errata will be posted at www.thieme.com on the product description page.

Some of the product names, patents, and registered designs referred to in this book are in fact registered trademarks or proprietary names even though specific reference to this fact is not always made in the text. Therefore, the appearance of a name without designation as proprietary is not to be construed as a representation by the publisher that it is in the public domain. This book, including all parts thereof, is legally protected by copyright. Any use, exploitation, or commercialization outside the narrow limits set by copyright legislation, without the publisher’s consent, is illegal and liable to prosecution. This applies in particular to photostat reproduction, copying, mimeographing, preparation of microfilms, and electronic data processing and storage.

Preface If you go to the mountain often enough, you will meet the tiger. Ancient Chinese proverb This book not only represents our individual experience, but it is also the result of what we have each learnt from one another working together. We hope that it is of practical use as it is a distillation of our clinical practice.

We have become more and more convinced that patient selection is one of the main keys to successful surgery, and we have tried to explain how we go about this. Much of the book focuses on how to improve the surgical approach, but we have also placed emphasis on what matters to the patient. The final chapters of the book involve advanced techniques and reflect the current direction in endoscopic sinus and skull base surgery. Daniel Simmen, Zurich, Switzerland Nick Jones, Nottingham, UK

Acknowledgments To Dr. Hans Rudolf Briner, Lecturer in Rhinology, ORLZentrum – Center for Rhinology and Skull Base Surgery, The Hirslanden Clinic, Zurich, Switzerland. To Dr. Kris S. Moe and Dr. Karthik Balakrishnan, Facial Plastic and Skull Base Surgery, University of Washington School of Medicine, Seattle, Washington, USA. To Professor Dr. Robert Reisch, Center for Minimal Invasive Endoscopic Neurosurgery, The Hirslanden Clinic, Zurich, Switzerland. To Professor Dr. Bernhard Schuknecht, Diagnostic and Vascular Interventional Neuroradiology, Medical Radiological Institutes, MRI Zurich, Switzerland.

To Dr. Aldo Cassol Stamm and Dr. Leonardo Lopes Balsalobre Filho, Federal University of São Paulo and Hospital Edmundo Vasconcelos, São Paulo, Brazil. To Dr. Jean Shaw for her comments on the manuscript. To Professor Jan Ullrich, Director of the Department of Anatomy, Institute of Anatomy, University of Zurich, and Dr. med. M. Vich and Dr. M. Manestar, also of the Department of Anatomy, for their help in supporting our courses and in preparing the anatomical specimens. To Sandra Schuhmacher for all illustrations used in this edition. Finally, we are grateful to our teachers, colleagues, and trainees who have all helped to educate us.

V

Contributors Karthik Balakrishnan, MD, MPh Department of Otorhinolaryngology, Head and Neck Surgery University of Washington Seattle, Washington, USA

Kris S. Moe, MD, FACS Chief, Division of Facial Plastic and Reconstructive Surgery Department of Otolaryngology, Head and Neck Surgery University of Washington Seattle, Washington, USA

Hans Rudolf Briner, MD ENT Center The Hirslanden Clinic Zurich, Switzerland

Robert Reisch, MD ENT Center The Hirslanden Clinic Zurich, Switzerland

Nick Jones, MD, BDS, FRCS, FRCS (ORL) Professor Department of Otorhinolaryngology, Head and Neck Surgery Queen’s Medical Centre University Hospital Nottingham, UK

Bernhard Schuknecht, MD Professor Medical Radiological Institute Bethanian Clinic Zurich, Switzerland

Leonardo Lopes Balsalobre Filho, MD Fellow Federal University of São Paolo and Hospital Edmundo Vasconcelos São Paolo, Brazil

VI

Daniel Simmen, MD Professor and Lecturer in Rhinology University of Zurich ENT Center The Hirslanden Clinic Zurich, Switzerland Aldo Cassol Stamm, MD Affiliated Professor Federal University of São Paulo Director, Hospital Edmundo Vasconcelos São Paolo, Brazil

Table of Contents 1  Principles of Practice Accurate Diagnosis Is the Key to Success  . . . . . . Focus on the Patient’s Main Complaint  . . . . . . . Dealing with the Patient’s Expectations  . . . . . . Some Psychological Aspects of Nasal Symptoms  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Optimize Medical Treatment  . . . . . . . . . . . . . . . . .

1 1 1 1 6 7

Tailor the Surgery to Fit the Extent of the Problem  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Minimize Surgical Morbidity  . . . . . . . . . . . . . . . . How Can This Be Achieved?  . . . . . . . . . . . . . . . . . . Sense of Smell Should Be Preserved at All Costs  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . The Importance of Postoperative Treatment  . . .

2  Pathophysiology of Rhinosinusitis Chronic Rhinosinusitis  . . . . . . . . . . . . . . . . . . . . . . Definition of CRS   . . . . . . . . . . . . . . . . . . . . . . . . . . . . Limited Evidence Associated with Anatomical Factors  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Comments on Specific Conditions  . . . . . . . . . . . . Allergic Rhinosinusitis  . . . . . . . . . . . . . . . . . . . . . . .

13 13 15 15 15

18 18 18 18 21 23 25 25 26 26 27 27 33 33 34 34 35 35 36 36 36 36 36

10 10

12 Entopy or Local Allergy  . . . . . . . . . . . . . . . . . . . . . . . Nonallergic Rhinitis  . . . . . . . . . . . . . . . . . . . . . . . . . . A Note on the Term “Nasal Polyposis”  . . . . . . . . . Chronic Rhinosinusitis Without Nasal Polyps  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Practical Comments  . . . . . . . . . . . . . . . . . . . . . . . . .

3  Who? Optimizing Diagnosis and Selection of Patients for Surgery Symptom-oriented Patient Selection  . . . . . . . . . Which are the Cardinal Symptoms? What Criteria in the History are Best to Focus on?  . . . . History—Interpreting Nasal Symptoms  . . . . . . . Nasal Obstruction  . . . . . . . . . . . . . . . . . . . . . . . . . . . . Disorders of Smell  . . . . . . . . . . . . . . . . . . . . . . . . . . . Rhinorrhea  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Catarrh and Postnasal Drip  . . . . . . . . . . . . . . . . . . . Postnasal Drip Syndrome   . . . . . . . . . . . . . . . . . . . . Chronic Cough  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Sneezing  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Crusting  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Facial Pain and Pressure  . . . . . . . . . . . . . . . . . . . . . . Relevant Medical History  . . . . . . . . . . . . . . . . . . . . . Clinical Examination  . . . . . . . . . . . . . . . . . . . . . . . . Investigations  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Skin Prick Tests  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Total or Specific Immunoglobulin E Tests  . . . . . . Immunity Testing  . . . . . . . . . . . . . . . . . . . . . . . . . . . . Other Hematologic Tests  . . . . . . . . . . . . . . . . . . . . . Ciliary Motility/Structural Studies  . . . . . . . . . . . . Sweat Sodium Concentration  . . . . . . . . . . . . . . . . . Serum Biochemistry  . . . . . . . . . . . . . . . . . . . . . . . . . Culture  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

7 8 10

Radiology  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Histology  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Who Will Most Likely Benefit from Surgery?  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Disease-oriented Patient Selection  . . . . . . . . . . . Chronic Infective Rhinosinusitis  . . . . . . . . . . . . . . Aspergillosis/Fungal Disease  . . . . . . . . . . . . . . . . . . Mycetoma/Saprophytic Fungal Disease  . . . . . . . . Allergic Aspergillosis  . . . . . . . . . . . . . . . . . . . . . . . . . Chronic Invasive Fungal Sinusitis  . . . . . . . . . . . . . . Fulminant Aspergillosis  . . . . . . . . . . . . . . . . . . . . . . Maxillary Sinusitis Secondary to Dental Disease  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Antrochoanal Polyp  . . . . . . . . . . . . . . . . . . . . . . . . . . Inverted Papilloma  . . . . . . . . . . . . . . . . . . . . . . . . . . . Unilateral Nasal Polyps Associated with Neoplasia  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Benign and Malignant Tumors  . . . . . . . . . . . . . . . . Pediatric Rhinosinusitis  . . . . . . . . . . . . . . . . . . . . . . Endoscopic Sinus Surgery in Children  . . . . . . . . Summary  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Who Not to Select for Surgery  . . . . . . . . . . . . . . . . Patient Expectations  . . . . . . . . . . . . . . . . . . . . . . . . .

15 16 16 16 17

18 36 37 37 37 37 37 37 38 39 39 40 40 40 42 42 42 46 47 47 48

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4  When? Medical Treatment and Timing of Surgery Optimizing Medical Treatment Before Surgery  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . The Management of Chronic Rhinosinusitis with Polyposis  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . The Management of Chronic Rhinosinusitis without Polyposis  . . . . . . . . . . . . . . . . . . . . . . . . . . . The Management of Infective Rhinosinusitis  . . .

49 49 53 55

The Management of Fungal Rhinosinusitis  . . . . . Optimizing the Timing of Surgery  . . . . . . . . . . . . Preoperative Counseling  . . . . . . . . . . . . . . . . . . . . . Expectations  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Explanation  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Preparation for Surgery  . . . . . . . . . . . . . . . . . . . . . . Patient Communication  . . . . . . . . . . . . . . . . . . . . .

5  Preserving and Improving the Sense of Smell Why Should We Focus on the Sense of Smell?  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 60 Preoperative Assessment  . . . . . . . . . . . . . . . . . . . . 61 Surgical Strategy to Preserve and Improve Olfaction  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 64

67 68 68 68 68 68 69 69 73

Mucoceles  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Antrochoanal Polyp  . . . . . . . . . . . . . . . . . . . . . . . . . . Inverted Papilloma  . . . . . . . . . . . . . . . . . . . . . . . . . . . Malignant Tumors  . . . . . . . . . . . . . . . . . . . . . . . . . . . Repair of Dural and Skull Base Defects  . . . . . . . . . Pituitary Surgery  . . . . . . . . . . . . . . . . . . . . . . . . . . . . Decompression of the Orbit  . . . . . . . . . . . . . . . . . . . Decompression of the Optic Nerve  . . . . . . . . . . . . Penetrating Injuries of the Skull Base  . . . . . . . . . . Quality of Life  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

80 80 83 83 84

Frontal Sinus  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Pterygopalatine Fossa  . . . . . . . . . . . . . . . . . . . . . . . Cavernous Sinus  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Pituitary Gland  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Cribriform Plate  . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

8  How? Operative Procedures: A Step-by-Step Safe and Logical Approach Infundibulotomy (Uncinectomy) ± Maxillary Sinusotomy (I, II, III)  . . . . . . . . . . . . . . . . . . . . . . . . . 91 Terminology and Classification  . . . . . . . . . . . . . . . 91

VIII

60

67

7  Applied Anatomy for Endoscopic Sinus and Skull Base Surgery Ethmoidal Infundibulum  . . . . . . . . . . . . . . . . . . . . Maxillary Sinus  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Anterior Ethmoid  . . . . . . . . . . . . . . . . . . . . . . . . . . . Posterior Ethmoid  . . . . . . . . . . . . . . . . . . . . . . . . . . . Sphenoidal Sinus  . . . . . . . . . . . . . . . . . . . . . . . . . . . .

55 57 58 58 59 59 59

Concept of the “Controlled Moderate Lateralization of the Middle Turbinate”  . . . . . . . . 64 How to Prevent Loss of Olfaction  . . . . . . . . . . . . . . 65 Hints  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 65

6  Why? The Goals of Surgery Why Surgery Can Help the Diseased Mucosa  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Rationale and Goals of Surgery in Specific Conditions  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Periorbital Abscess  . . . . . . . . . . . . . . . . . . . . . . . . . . . Barotrauma  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Choanal Atresia  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Epistaxis  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Distal Nasolacrimal Duct Obstruction  . . . . . . . . . Unknown Pathology/Biopsy  . . . . . . . . . . . . . . . . . . Benign Tumors  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

49

74 75 75 76 76 76 76 77 77 79

80 85 87 88 89 90

91

Indications for Infundibulotomy and Maxillary Sinusotomy  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 92 Anatomy  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 94 Surgical Technique  . . . . . . . . . . . . . . . . . . . . . . . . . . . 96

Table of Contents Alternative Surgical Techniques  . . . . . . . . . . . . . . . Useful Instruments  . . . . . . . . . . . . . . . . . . . . . . . . . . Endoscopic Transnasal Anterior Approach to the Maxillary Sinus Ostium  . . . . . . . . . . . . . . . . . . . Partial Anterior Ethmoidectomy  . . . . . . . . . . . . . Terminology and Classification  . . . . . . . . . . . . . . . Indications  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Anatomy  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Surgical Technique  . . . . . . . . . . . . . . . . . . . . . . . . . . . Alternative Surgical Techniques  . . . . . . . . . . . . . . . Frontoethmoidectomy ± Frontal Sinusotomy (I, II, III)  . . . . . . . . . . . . . . . . . Terminology and Classfication  . . . . . . . . . . . . . . . . Indications  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Anatomy  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Surgical Technique  . . . . . . . . . . . . . . . . . . . . . . . . . . . Alternative Surgical Techniques  . . . . . . . . . . . . . . . Useful Instruments  . . . . . . . . . . . . . . . . . . . . . . . . . . Sphenoethmoidectomy ± Sphenoidal Sinusotomy (I, II, III)  . . . . . . . . . . . . . Terminology and Classfication  . . . . . . . . . . . . . . . . Indications  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Anatomy  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Surgical Technique  . . . . . . . . . . . . . . . . . . . . . . . . . . .

101 104 107 110 110 110 110 111 114 114 114 115 118 126 137 138 138 138 139 139 139

Alternative Surgical Techniques  . . . . . . . . . . . . . . . Useful Instruments  . . . . . . . . . . . . . . . . . . . . . . . . . . Frontosphenoethmoidectomy ± Frontal Sinusotomy (I, II, III) ± Maxillary Sinusotomy (I, II, III) ± Sphenoidal Sinusotomy (I, II, III)  . . . . . . . . . . . . . Terminology and Classification  . . . . . . . . . . . . . . . Indications  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Sphenoidal Sinusotomy (I, II, III)  . . . . . . . . . . . . . Terminology and Classification  . . . . . . . . . . . . . . . Indications  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Anatomy  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Surgical Technique  . . . . . . . . . . . . . . . . . . . . . . . . . . . A Comment on the Management of the Middle and Superior Turbinates  . . . . . . . . . . . . . . Surgical Technique  . . . . . . . . . . . . . . . . . . . . . . . . . . . Alternative Surgical Techniques  . . . . . . . . . . . . . . . A Comment on the Management of the Inferior Turbinate  . . . . . . . . . . . . . . . . . . . . . . . . . . . Terminology  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Indications  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Anatomy  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Surgical Technique  . . . . . . . . . . . . . . . . . . . . . . . . . . . Comments  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

9 An Endoscopic Tour: Endoscopic Examination, Anatomical Variations, and Specific Conditions Outpatient Examination  . . . . . . . . . . . . . . . . . . . . . The Endoscopic Tour  . . . . . . . . . . . . . . . . . . . . . . . . Endoscopic Evidence of Mucosal Disease  . . . . . Anatomical Variations  . . . . . . . . . . . . . . . . . . . . . . . Agger Nasi Air Cells  . . . . . . . . . . . . . . . . . . . . . . . . . . Concha Bullosa  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . A Paradoxical Middle Turbinate  . . . . . . . . . . . . . . . A Bifid Middle Turbinate  . . . . . . . . . . . . . . . . . . . . . . A Polypoid Anterior End of the Middle Turbinate  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . A Paradoxical Uncinate Process  . . . . . . . . . . . . . . . Pneumatized Uncinate Process  . . . . . . . . . . . . . . . .

166 167 169 171 171 171 172 172 173 174 174

Accessory Ostia of the Maxillary Sinus Posterior to the Uncinate Process  . . . . . . . . . . . . . Defect in the Uncinate Process  . . . . . . . . . . . . . . . . An Atlas of Specific Conditions To Help Recognize Variations in Anatomy and Different Pathologic Conditions  . . . . . . . . . . . . . . Allergy  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Infection  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Inflammatory Diseases  . . . . . . . . . . . . . . . . . . . . . . . Benign Tumors  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Malignant Tumors  . . . . . . . . . . . . . . . . . . . . . . . . . . . Miscellaneous  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

10  The Place of Radiology The Role of Radiology  . . . . . . . . . . . . . . . . . . . . . . . Conventional Radiology  . . . . . . . . . . . . . . . . . . . . . . Cross-sectional CT and Cone-beam CT  . . . . . . . . . The Role of Computed Tomography  . . . . . . . . . . When to Request CT in the Management of Rhinosinusitis  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

148 149

149 149 150 154 154 154 154 154 155 156 160 160 160 160 161 161 162

166 175 175

176 176 176 178 178 180 180

181 181 181 181 184 185

When Should MRI be Requested?  . . . . . . . . . . . . Magnetic Resonance Angiography  . . . . . . . . . . . . Digital Subtraction Angiography and Embolization  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Interdisciplinary Cooperation  . . . . . . . . . . . . . . . .

186 191 191 195

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11  Preoperative Checklist Confirm the Diagnosis  . . . . . . . . . . . . . . . . . . . . . . . Reviewing the Effect of Maximum Medical Treatment Helps in Determining Prognosis  . . . Optimize the Immediate Preoperative Condition  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Check That Relevant Investigations Have Been Done  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Allergy Tests  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Immune Status  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

196 196 197 197 198 198 198

Hematological Parameters  . . . . . . . . . . . . . . . . . . . . Olfaction  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Vision  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Review the Relevant Medical History  . . . . . . . . . Preoperative CT Checklist  . . . . . . . . . . . . . . . . . . . . Planning and Staging the Procedure  . . . . . . . . . . Informed Consent  . . . . . . . . . . . . . . . . . . . . . . . . . . . Review Medication That May Affect Anesthesia or Surgery  . . . . . . . . . . . . . . . . . . . . . . . .

12  Patient Consent and Information How to Communicate the Benefits and Risks of Surgery to the Patient  . . . . . . . . . . . . . . . . . . . . . 212 Time Off Work and Advice About Flying  . . . . . . 214 Complications  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 214

X

210

212 Specific Surgical Complications  . . . . . . . . . . . . . . . 215 Shortfall in Doctor–Patient Communication  . . . . 216 Psychology and the Surgeon  . . . . . . . . . . . . . . . . . . 216

13  Peroperative Aids Anesthesia  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Local Anesthesia  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . General Anesthesia  . . . . . . . . . . . . . . . . . . . . . . . . . . Operating Room Setup  . . . . . . . . . . . . . . . . . . . . . . . Operating Table  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Surgeon’s Seat  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Position of the Anesthesiologist  . . . . . . . . . . . . . . . Setup for One Surgeon  . . . . . . . . . . . . . . . . . . . . . . . Setup for Two Surgeons  . . . . . . . . . . . . . . . . . . . . . . Video Stack/Cameras  . . . . . . . . . . . . . . . . . . . . . . . . . Cables  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Lighting  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Radiograph Screen  . . . . . . . . . . . . . . . . . . . . . . . . . . . Ancillary Staff  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Instruments  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Endoscopes  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Camera Systems  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Suckers  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Curved Olive-ended Suckers  . . . . . . . . . . . . . . . . . . Ball Probes  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Curettes  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Blakesley Forceps  . . . . . . . . . . . . . . . . . . . . . . . . . . . . Through-cutting Instruments (Rhinoforce Blakesley/Mackay–Grunewald Forceps)  . . . . . . . . Rhinoforce Stammberger Antrum Punch (“Back-biters”)  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Hajek–Kofler Punch and Kerrison Punches  . . . . . Stammberger Cutting Mushroom Punch  . . . . . . . Freer Elevator  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

199 199 199 200 201 208 209

217 217 217 218 219 219 219 219 219 219 220 220 220 220 220 221 221 223 224 224 225 225 226 226 226 227 227 228

Sickle Knife  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Belluci and Zurich Microscissors  . . . . . . . . . . . . . . Stammberger Side-biting Punch Forceps  . . . . . . . Heuwieser Antrum Grasping Forceps  . . . . . . . . . . Giraffe Forceps (Kuhn–Bolger)  . . . . . . . . . . . . . . . . Frontal Sinus Punch: Curved Modified Hajek Punches for the Frontal Sinus (Bachert, Hosemann)  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Powered Instruments  . . . . . . . . . . . . . . . . . . . . . . . . Computer-aided Surgery—Navigation Technology  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Advantages  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Disadvantages  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Preoperative Work-up  . . . . . . . . . . . . . . . . . . . . . . . Modeling  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Positioning of the Patient, Surgeon, and Equipment  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Registration  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Methods of Localization  . . . . . . . . . . . . . . . . . . . . . . Display of Images  . . . . . . . . . . . . . . . . . . . . . . . . . . . . Accuracy  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Operating Time  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Economic Factors  . . . . . . . . . . . . . . . . . . . . . . . . . . . . Teaching  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Real-time Computer-aided Surgery  . . . . . . . . . . . Laser  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Balloon  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Future Perspectives  . . . . . . . . . . . . . . . . . . . . . . . . . Imaging  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

228 229 229 229 230

230 230 232 233 233 233 233 233 233 234 235 235 235 235 236 236 236 237 237 237

Table of Contents

14 Hints In the Operating Room  . . . . . . . . . . . . . . . . . . . . . . Before Starting the Operation  . . . . . . . . . . . . . . . . . Anesthesiologist’s Goals  . . . . . . . . . . . . . . . . . . . . . Hints to Reduce Bleeding  . . . . . . . . . . . . . . . . . . . . .

239 239 239 239 239

Preparation  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 240 Surgical Hints  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 240 Objectives of the Operation  . . . . . . . . . . . . . . . . . . 241

15  Preventing and Dealing with Complications Peroperative Complications  . . . . . . . . . . . . . . . . . . Bleeding  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Fat Herniation and Violation of the Orbit  . . . . . . Cerebrospinal Fluid Leak  . . . . . . . . . . . . . . . . . . . . . Retro-orbital Hemorrhage  . . . . . . . . . . . . . . . . . . . . Medial Rectus Damage  . . . . . . . . . . . . . . . . . . . . . . . Optic Nerve Lesion  . . . . . . . . . . . . . . . . . . . . . . . . . . . Postoperative Complications  . . . . . . . . . . . . . . . . . Bleeding  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

242 242 245 250 252 254 255 255 255

Adhesions  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Epiphora  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Periorbital Emphysema  . . . . . . . . . . . . . . . . . . . . . . Anosmia  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Frontal Recess Stenosis  . . . . . . . . . . . . . . . . . . . . . . . Crusting  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Infection  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Osteitis  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Neuropathic Pain  . . . . . . . . . . . . . . . . . . . . . . . . . . . .

16  Postoperative Management

256 256 256 256 257 258 258 258 258

260

Patient Communication  . . . . . . . . . . . . . . . . . . . . . 260 Patients Vary  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 260 The Postoperative Course  . . . . . . . . . . . . . . . . . . . . 261

In the Hospital  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 262 Outpatient Visit at One Week  . . . . . . . . . . . . . . . . . 263 Postoperative Problems  . . . . . . . . . . . . . . . . . . . . . . 264

17  Extended Endoscopic Procedures Dacryocystorhinostomy and Surgery of the Nasolacrimal System  . . . . . . . . . . . . . . . . . . . . . . . . Terminology and Classification  . . . . . . . . . . . . . . . Indications  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Surgical Anatomy  . . . . . . . . . . . . . . . . . . . . . . . . . . . . Assessment  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Surgical Technique  . . . . . . . . . . . . . . . . . . . . . . . . . . . Principles of Surgical Technique in DCR  . . . . . . . . Alternative Surgical Techniques  . . . . . . . . . . . . . . . Revision DCR  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Stents  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Useful Instruments  . . . . . . . . . . . . . . . . . . . . . . . . . . The Treatment of Common Canalicular Pathology  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Management of the Sphenopalatine Artery  . . . Terminology and Classification  . . . . . . . . . . . . . . . Indications  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Anatomy  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Surgical Technique  . . . . . . . . . . . . . . . . . . . . . . . . . . . Alternative Surgical Techniques  . . . . . . . . . . . . . . . Useful Instruments  . . . . . . . . . . . . . . . . . . . . . . . . . .

242

266 266 266 268 268 268 274 274 274 274 275 275 276 276 277 277 277 280 282

266 Management of the Anterior Ethmoidal Artery  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Terminology and Classification  . . . . . . . . . . . . . . . Indications  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Surgical Anatomy  . . . . . . . . . . . . . . . . . . . . . . . . . . . . Surgical Technique  . . . . . . . . . . . . . . . . . . . . . . . . . . . Alternative Surgical Techniques  . . . . . . . . . . . . . . . Useful Instruments  . . . . . . . . . . . . . . . . . . . . . . . . . . Median Frontal Sinus Drainage Procedure  . . . . Terminology and Classification  . . . . . . . . . . . . . . . Indications  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Contraindications  . . . . . . . . . . . . . . . . . . . . . . . . . . . . Surgical Anatomy  . . . . . . . . . . . . . . . . . . . . . . . . . . . . Surgical Technique  . . . . . . . . . . . . . . . . . . . . . . . . . . . Modifications  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Alternative Surgical Techniques  . . . . . . . . . . . . . . . Useful Instruments  . . . . . . . . . . . . . . . . . . . . . . . . . . Orbital Decompression  . . . . . . . . . . . . . . . . . . . . . . Terminology and Classification  . . . . . . . . . . . . . . . Indications  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Surgical Anatomy  . . . . . . . . . . . . . . . . . . . . . . . . . . . .

282 282 282 282 284 285 285 285 285 288 288 291 291 299 301 304 304 304 306 306

XI

Table of Contents Surgical Technique  . . . . . . . . . . . . . . . . . . . . . . . . . . . Useful Instruments  . . . . . . . . . . . . . . . . . . . . . . . . . . Optic Nerve Decompression  . . . . . . . . . . . . . . . . . . Terminology and Classification  . . . . . . . . . . . . . . . Indications  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Surgical Anatomy  . . . . . . . . . . . . . . . . . . . . . . . . . . . . Surgical Technique  . . . . . . . . . . . . . . . . . . . . . . . . . . . Useful Instruments  . . . . . . . . . . . . . . . . . . . . . . . . . . Choanal Atresia Surgery  . . . . . . . . . . . . . . . . . . . . . Terminology and Classification  . . . . . . . . . . . . . . . Indications  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Surgical Anatomy  . . . . . . . . . . . . . . . . . . . . . . . . . . . . Surgical Technique  . . . . . . . . . . . . . . . . . . . . . . . . . . . Alternative Surgical Techniques  . . . . . . . . . . . . . . . Useful Instruments  . . . . . . . . . . . . . . . . . . . . . . . . . . Medial Maxillectomy  . . . . . . . . . . . . . . . . . . . . . . . . Terminology and Classification  . . . . . . . . . . . . . . . Indications  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Surgical Anatomy  . . . . . . . . . . . . . . . . . . . . . . . . . . . . Surgical Technique  . . . . . . . . . . . . . . . . . . . . . . . . . . . Alternative Techniques  . . . . . . . . . . . . . . . . . . . . . . . Useful Instruments  . . . . . . . . . . . . . . . . . . . . . . . . . . Management of Cerebrospinal Fluid Leaks   . . . Terminology and Classification  . . . . . . . . . . . . . . . Indications  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Surgical Anatomy  . . . . . . . . . . . . . . . . . . . . . . . . . . . . Diagnosis  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Surgical Technique  . . . . . . . . . . . . . . . . . . . . . . . . . . . Comment  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Modifications and Alternatives  . . . . . . . . . . . . . . . . Management of Encephaloceles  . . . . . . . . . . . . . . Terminology and Classification  . . . . . . . . . . . . . . . Indications  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Surgical Anatomy  . . . . . . . . . . . . . . . . . . . . . . . . . . . . Surgical Technique  . . . . . . . . . . . . . . . . . . . . . . . . . . . Alternative Surgical Techniques  . . . . . . . . . . . . . . . General Principles  . . . . . . . . . . . . . . . . . . . . . . . . . . . Specific Conditions  . . . . . . . . . . . . . . . . . . . . . . . . . .

308 310 310 310 310 311 311 312 312 312 312 312 312 314 314 315 315 315 317 317 323 327 327 327 328 328 330 333 339 339 340 340 340 341 341 342 344 344

Mucoceles  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Inverted Papilloma  . . . . . . . . . . . . . . . . . . . . . . . . . . . Osteoma  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Hemangioma  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Angiofibroma  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Schwannoma  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Chordoma  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Chondroma  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Langerhans Cell Histiocytosis  . . . . . . . . . . . . . . . . . Pleomorphic Adenoma  . . . . . . . . . . . . . . . . . . . . . . . Other Benign Pathological Lesions  . . . . . . . . . . . . Lesions of the Cribriform Plate and Fovea Ethmoidalis  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Frontal Sinus  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Ethmoidal Complex, Lateral Nasal Wall, and Orbit  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Maxillary Sinus  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Pterygopalatine Fossa  . . . . . . . . . . . . . . . . . . . . . . . Sphenoidal Sinus, Clivus, and Cavernous Sinus  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Access for Biopsies  . . . . . . . . . . . . . . . . . . . . . . . . . . . Postoperative Monitoring  . . . . . . . . . . . . . . . . . . . . Surgical Technique  . . . . . . . . . . . . . . . . . . . . . . . . . . Endoscopic Resection of Malignant Anterior Skull Base Tumors  . . . . . . . . . . . . . . . . . . . . . . . . . . . Alternative Techniques  . . . . . . . . . . . . . . . . . . . . . . Combined Craniofacial and Endoscopic Resection  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Olfactory Neuroblastoma  . . . . . . . . . . . . . . . . . . . . Malignant Melanoma  . . . . . . . . . . . . . . . . . . . . . . . . Plasmacytoma  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Recurrent or Residual Malignant Disease  . . . . . . Epistaxis  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Preoperative Embolization  . . . . . . . . . . . . . . . . . . . Juvenile Nasopharyngeal Angiofibroma  . . . . . . . . Tumor Hemorrhage  . . . . . . . . . . . . . . . . . . . . . . . . . Postfunctional Endoscopic Sinus Surgery  . . . . . Complications of Embolization  . . . . . . . . . . . . . . .

18  The Endoscopically Assisted Bimanual Operating Technique From Basic Endoscopic Sinus Surgery to More Extended and Advanced Skull Base Surgery  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Advantages of the Endoscopically Assisted Bimanual Operating Technique  . . . . . . . . . . . . . . Operating with Both Hands  . . . . . . . . . . . . . . . . . . . Suction Tip Stays in the Operative Field: Fewer Instrument Changes  . . . . . . . . . . . . . . . . . . . Optimum Exposure  . . . . . . . . . . . . . . . . . . . . . . . . . . Holding and Cutting  . . . . . . . . . . . . . . . . . . . . . . . . . Teamwork  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

XII

378 380 380 380 381 381 381

Training  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Theater Setup and Technical Aspects  . . . . . . . . . Operating Theater Setup  . . . . . . . . . . . . . . . . . . . . . Practical Hints  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Ergonomic Handling of the Endoscope  . . . . . . . . Stabilizing the Endoscope in the Nasal Vestibule  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Cleaning the Endoscope  . . . . . . . . . . . . . . . . . . . . . . Holding and Cutting  . . . . . . . . . . . . . . . . . . . . . . . . . Retraction of Structures and Tissue  . . . . . . . . . . . Drilling and Suction  . . . . . . . . . . . . . . . . . . . . . . . . . .

344 346 348 348 350 355 355 356 356 356 356 361 361 361 362 362 363 364 364 366 366 372 372 372 374 374 375 375 376 376 376 377 377

378 382 382 382 383 383 384 384 384 384 385

Table of Contents Coagulation and Suction  . . . . . . . . . . . . . . . . . . . . . 385 Navigation and Drilling  . . . . . . . . . . . . . . . . . . . . . . . 385

Modifications of the Standard “One-nostril Approach”  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 386

19  Transnasal Endoscopic Approaches to the Skull Base Surgical Anatomy  . . . . . . . . . . . . . . . . . . . . . . . . . . . Anterior Cranial Fossa  . . . . . . . . . . . . . . . . . . . . . . . . Clivus  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Pterygopalatine Fossa  . . . . . . . . . . . . . . . . . . . . . . . . Operative Technique  . . . . . . . . . . . . . . . . . . . . . . . . . Instrumentation  . . . . . . . . . . . . . . . . . . . . . . . . . . . . Transnasal Surgical Approaches to the Skull Base  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

388 388 388 389 389 389 390

Transseptal/Transnasal (Bi-nostril Approach) for the Sphenoidal Sinus  . . . . . . . . . . . . . . . . . . . . . . Transsphenoidal  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Transcribriform  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Transmaxillary/Transpterygoid/ Infratemporal  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Approaches to the Cavernous Sinus  . . . . . . . . . .

20  Interdisciplinary Teamwork in Transnasal Endoscopic Skull Base Surgery Preoperative Planning  . . . . . . . . . . . . . . . . . . . . . . . 401 Operating Theater and Patient Preparation  . . . 401 The Role of Navigation and Intraoperative Imaging  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 403

409 409 409 415

425 425 427 427

396 399

400

409

Removal of Pituitary Tumors—General Hints  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 416 Sella Reconstruction and Closure  . . . . . . . . . . . . . 418 Postoperative Care  . . . . . . . . . . . . . . . . . . . . . . . . . . 419

22  Transorbital Surgery of the Skull Base Important Incisions and Approaches  . . . . . . . . . Medial Orbit: Precaruncular  . . . . . . . . . . . . . . . . . . Inferior Orbit: Lower Lid Preseptal Transconjunctival  . . . . . . . . . . . . . . . . . . . . . . . . . . . . Lateral Orbit: Lateral Retrocanthal  . . . . . . . . . . . . Superior Orbit: Superior Lid Crease/ Blepharoplasty  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

390 391 394

Rhino-/Neurosurgical Instrumentation  . . . . . . . 403 Surgical Technique—General Hints  . . . . . . . . . . . 404 Postoperative Care  . . . . . . . . . . . . . . . . . . . . . . . . . . 408

21  Transnasal Endoscopic Surgery of Pituitary Tumors  Planning for Pituitary Surgery  . . . . . . . . . . . . . . . Transnasal Approaches to the Pituitary Gland  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Uni-nostril Approaches  . . . . . . . . . . . . . . . . . . . . . . . Bi-nostril Approaches  . . . . . . . . . . . . . . . . . . . . . . . .

388

Associated Techniques  . . . . . . . . . . . . . . . . . . . . . . . Repair of Cerebrospinal Fluid Leak  . . . . . . . . . . . . Access to the Frontal Sinus  . . . . . . . . . . . . . . . . . . . . Orbital and Optic Nerve Decompression  . . . . . . . Useful Equipment and Setup  . . . . . . . . . . . . . . . . .

424 428 428 429 431 431

427

23  Evidence Base in Rhinosinusitis and Endoscopic Sinus Surgery Diagnosis  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 432 Medical Treatment  . . . . . . . . . . . . . . . . . . . . . . . . . . 432

432

Acute Sinusitis  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 432 Chronic Bacterial Rhinosinusitis  . . . . . . . . . . . . . . 433

XIII

Table of Contents Fungal Rhinosinusitis  . . . . . . . . . . . . . . . . . . . . . . . . Chronic Rhinosinusitis Without Nasal Polyposis  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Chronic Rhinosinusitis with Nasal Polyposis  . . . Surgical Treatment  . . . . . . . . . . . . . . . . . . . . . . . . . . The Extent of Surgery  . . . . . . . . . . . . . . . . . . . . . . . .

434 434 434 435 436

The Effect of Type I Hypersensitivity or IgEmediated Disease  . . . . . . . . . . . . . . . . . . . . . . . . . . . . Cystic Fibrosis  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Ciliary Dyskinesia and Immunodeficiencies  . . . . Recalcitrant Chronic Rhinosinusitis  . . . . . . . . . . . Allergic and Nonallergic Rhinitis  . . . . . . . . . . . . .

436 436 437 437 437

Appendix:  Information for Patients Undergoing Endoscopic Sinus Surgery 438 Endoscopic Sinus Surgery  . . . . . . . . . . . . . . . . . . . . What is Endoscopic Sinus Surgery?  . . . . . . . . . . . What Can I Expect When I Have This Operation?  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . What Complications Can Occur?  . . . . . . . . . . . . . . Douching  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Pharyngeal/Laryngeal Hypersensitivity  . . . . . . . What is This?  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Regimen to Break the Cycle  . . . . . . . . . . . . . . . . . . . Nasal Allergy  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . What is an Allergen?  . . . . . . . . . . . . . . . . . . . . . . . . . Intermittent Allergy  . . . . . . . . . . . . . . . . . . . . . . . . . Persistent Allergy  . . . . . . . . . . . . . . . . . . . . . . . . . . . . Diagnosis  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Treatment  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Sinus Infection  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

438 438 438 438 440 440 440 440 441 441 441 441 441 441 443

Associated Causes  . . . . . . . . . . . . . . . . . . . . . . . . . . . Symptoms  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Management  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Complications  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Nasal Polyps  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Conditions Associated with Nasal Polyps  . . . . . . Symptoms and Signs  . . . . . . . . . . . . . . . . . . . . . . . . . Unilateral (One-sided) Polyps  . . . . . . . . . . . . . . . . . Investigations  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Treatment  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Advice for Patients after Endoscopic Surgery for Nasal Polyps  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . The Complications of Endoscopic Surgery for Nasal Polyps  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . “Telephone Consultations”  . . . . . . . . . . . . . . . . . . .

443 443 443 443 444 444 444 444 444 444 444 445 445

Bibliography446

Index455

XIV

List of Videos

1 Mucociliary transport 2 Nasal airflow 3 Patient consultations 4 Middle turbinate lateralisation 5 Functional endoscopic sinus surgery and olfaction 6 Cadaver posterior ethmoidectomy 7 Posterior ethmoidectomy, sphenoidotomy 8 Posterior ethmoidectomy 9 Transethmoidal approach to the sphenoid 10 Spenopalatine artery bleed 11 Sphenopalatine artery ligation 12 Removal of meningioma at orbital apex 13 Intrathecal fluorescein and encephalocele 14 Meningocele 15 Uni-nostril approach to the pituitary 16 Cadaver uncinectomy and maxillary sinusotomy 17 (a) Uncinectomy; (b) Reduction of concha bullosa and retrograde uncinectomy 18 Anterior ethmoidectomy and piriform-turbinoplasty

19 Partial anterior ethmoidectomy and piriform-turbinoplasty 20 Further partial anterior ethmoidectomy 21 Sphenoid sinus 22 Optic nerve in sphenoid sinus 23 The frontal recess 24 Cavernous sinus 25 Resection and reconstruction of skull base for olfactory neuroblastoma 26 Cadaver skull base anatomy 27 Anterior approach to the maxillary sinus 28 Anterior approach to the maxillary sinus 29 Median drainage procedure 30 Piriform-turbinoplasty 31 Piriform-turbinoplasty 32 Preparation of the mucosa 33 Medial maxillectomy 34 Clival chordoma: transnasal endoscopic and transcranial retrosigmoidal approach

XV

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1  Principles of Practice Accurate Diagnosis Is the Key to Success A good surgeon should also be a good physician. The best results are often obtained by optimizing medical treatment both preoperatively and postoperatively (Fig. 1.1a,b). Optimizing medical treatment before surgery makes it less traumatic, reduces the chances of complications, and helps to preserve olfactory mucosa. To optimize medical treatment, the surgeon needs to have an understanding of the pathology of the mucosal disease. Postoperative medical treatment is frequently required to maintain the improvement that surgery has produced. A good surgeon may avoid or delay the need for surgery and obtain good symptomatic relief by medical means. The surgeon may

decide, after discussion with the patient, that surgery will not help the particular symptoms that they have and advise against surgical intervention. It is often more difficult to convince a patient that surgery is not in his or her interest, rather than proceeding, but in the long run it is to everyone’s benefit. History and examination should allow basic categorization of the disease, but these are often insufficient to make an accurate diagnosis. It is often necessary to undertake other investigations or to have a trial of medical treatment to clarify the underlying pathology. Each of the clinical appearances shown in Table 1.1 can be associated with different pathological processes (Figs. 1.2a–f, 1.3a–d, 1.4a–d, 1.5a–d). Try to arrive at a diagnosis that fits into one of the broad groups that are used for the classification of rhinosinusitis. These groups are shown in Table 1.2. In the light of history and examination, along with the relevant investigations, the physician can obtain an idea of the underlying pathology. Based on this, medical and surgical treatment can be maximized.

Focus on the Patient’s Main Complaint The patient may mention any of a large array of symptoms in nasal disease. There are four primary symptoms that are always worth asking about: 1. Nasal obstruction 2. Sense of smell 3. Secretions 4. Pain or pressure.

a

It is important to rank these symptoms in their order of priority to the patient. This not only helps to make a diagnosis, but it focuses the surgeon’s mind on how best to meet the patient’s needs. In the notes underline the patient’s main complaint.

Dealing with the Patient’s Expectations

b Fig. 1.1a,b  Nasal polyps. a Before medical treatment. b After medical treatment.

The patient’s priorities may differ from what the surgeon can achieve. For example, the patient’s main concern might be their postnasal discharge, but the surgeon may only be able to improve the symptoms of obstruction with little alteration to the postnasal drip (Fig. 1.6a–d). It is therefore vital that the surgeon is forthcoming and makes it as clear as possible to the patient which symptoms can and cannot be improved or resolved. When the

1

1  Principles of Practice Table 1.1  Simplified table of macroscopic clinical appearance in rhinosinusitis and criteria to classify length of history along with possible diagnoses based on clinical appearance

Length of history

Observation

Possible diagnosis—NOT diagnostic on its own

Acute

Subacute

Chronic

 3 weeks,  3 months

Erythema

Infective, allergic, nonallergic, chronic rhinosinusitis

Edema

Active or postinfective, allergic, nonallergic, chronic rhinosinusitis

Hyperplastic mucosa

Chronic rhinosinusitis

Polyposis

Idiopathic polyposis, allergic fungal polyposis

Granular mucosa

Wegener granulomatosis, sarcoidosis

Purulent secretion

Infective rhinosinusitis

Dry mucosa

Postsurgical, environmental, rhinitis medicamentosa

a

b

c

d Fig. 1.2a–f  Endoscopic appearance of a range of pathological conditions. a Idiopathic rhinitis with erythema. b Hyperplastic mucosa due to allergic rhinitis.

2

c Severe hypertrophy with edema. d Polyposis in a nonatopic patient.

Dealing with the Patient’s Expectations Table 1.2  Classification of rhinosinusitis

Type of rhinosinusitis

Comments

Infectious Viral Bacterial (including tuberculosis, leprosy, syphilis) Fungal Noninfectious Allergy

Seasonal (intermittent); perennial (persistent)

Chronic rhinosinusitis Chronic rhinosinusitis with polyposis Nonallergic rhinitis with eosinophilia (NARES) Hormonal

High-estrogen contraceptive pill; pregnancy

Autonomic/neurogenic

Primary symptom is rhinorrhea often reduced by ipratropium bromide; few other nasal symptoms; patients often elderly. Important not to include in idiopathic group

Sarcoidosis Vasculitis

Wegener granulomatosis

Drug induced

b-blockers

Rhinitis medicamentosa

Excessive use of local sympathomimetic agents

Occupational Atrophic Entopy

No systemic markers of atopy (skin prick test negative, no raised specific immunoglobulin E) but challenge/washings/biopsy show local immunoglobulin E in mucosa

Idiopathic

Some overlap in nomenclature as the cause of NARES is unknown

f

e

◁ continued e Granular mucosa.

f Dry mucosa.

3

1  Principles of Practice

a

b

c

d Fig. 1.3a–d  Endoscopic appearance of a range of pathological conditions. a Normal middle meatus. b Serous secretions in marked allergic rhinitis.

c Purulent bacterial secretions. d Purulent fungal secretions.

physician overlooks these reservations, the patient is likely to be disappointed with the outcome. Be aware that some patients may believe that even symptoms that they have not mentioned will be cured by any surgery. Some patients will have well-formed ideas before they attend, whereas others will come with an open mind. It is worth finding out what the main motives for the visit are before examining the patient and particularly before embarking on any treatment. Many patients are seeking reassurance that they do not have cancer or a life-threatening illness and that is all they want. Patients might reasonably be expected to want a diagnosis, a prognosis, an explanation of their symptoms in the light of the disease process, and a treatment plan. However, they may have a preconception about the cause of their symptoms that differs from the medical diagnosis. This is often the case in patients with “sinus headache,” facial pain, or catarrh. It is worth taking time to discover what the patients’ understanding of their disease process is so that their ideas about their symptoms and disease

can be taken into consideration when explaining the cause of these processes. Reassurance may be readily received after a clear explanation that recognizes the symptoms that the patient is experiencing, outlines their cause, and addresses the patient’s concerns. However, in a small proportion of anxious individuals, the effect of firm reassurance after a thorough examination and explanation may fade with time. It is often counterproductive to ask these individuals to return because this may reinforce their concerns that the doctor may have some ongoing doubt. Some patients come hoping, if not expecting, a cure for their symptoms. Many find it difficult to accept that there is no cure. Many patients have tried alternative therapy before seeking specialist advice. Many have browsed the Internet looking for advice, but it is not easy for anyone without knowledge in the area in question to decipher what is good information. If a patient attends with printed extracts it is worth studying these in front of the patient,

4

Dealing with the Patient’s Expectations

a

b

c

d Fig. 1.4a–d  Endoscopic appearance of a range of pathological conditions. a Endoscopic appearance of granulations. b Crusts in Wegener granulomatosis. c Coronal computed tomography scan showing the mucosal changes consistent with Wegener granulomatosis; there is often bony erosion as well.

d Collapse of the nasal dorsum often seen in nasal Wegener granulomatosis.

time allowing, so that he or she can see that your advice is given having considered this information. Anyone offering medical advice should not overplay the benefit of any treatment they propose. To be overenthusiastic or excessively optimistic runs the risk of the patient being disappointed. That does not mean that all sense of hope for an improvement should be dashed but

it is wise to qualify what the patient might realistically expect. This situation is not helped by claims that a treatment “works” or has been shown to produce a “statistically significant improvement,” when in reality the studies on which these are based only show that the mean patient symptom score has reduced from say 8 to 5 out of 10 in severity; in other words the patient still has a mean

5

1  Principles of Practice

b

a

d

c Fig. 1.5a–d  Endoscopic appearance of a range of pathological conditions. a Pale cobblestones in sarcoidosis. b Hyperemic mucosa on the middle turbinate—a variation of normal.

c Purulent secretions in cystic fibrosis. d Dry mucosa with stagnant mucus in the right nasal airway.

symptom score of 5 out of 10. Many rhinological studies show that, after treatment, high residual symptom scores remain. The patient’s expectations should ideally coincide with the surgeon’s prognosis. Hence, it is worth communicating to him or her which specific symptoms will not be helped. It is often worthwhile making this clear in any correspondence to the referring doctor and sending the patient a copy.

these patients are somatizing or have medically unexplained symptoms. Somatizing patients attribute their distressing symptoms to a physical illness that cannot be fully accounted for by organic disease. Often the distress caused by the symptoms is out of proportion when compared with that of someone with organic disease and there may be symptoms of depression and anxiety. Approximately 25% of patients attending an ear, nose, and throat surgeon are somatizing. Typical symptoms include fullness in the head or ears, dizziness without vertigo, catarrh or a dry sore throat. There are often many symptoms that change in nature over time. It is common for these patients to have seen many doctors. It is important to exclude any organic pathology that can present with these symptoms by performing a thorough examination and any relevant investigation.

Some Psychological Aspects of Nasal Symptoms In rhinology many patients have symptoms that do not appear to be due to organic disease and a proportion of

6

Tailor the Surgery to Fit the Extent of the Problem

a

b

c

d Fig. 1.6a–d  Endoscopic appearance of a range of pathological conditions. a The amount of secretions produced per day from the upper and lower respiratory tract. b Thick postnasal mucus in the pharynx.

c Thin tenacious mucus in the pharynx. d Purulent secretions from the middle meatus tracking over clear secretions.

If the patient is thought be somatizing then it is important to minimize the number of investigations, avoid unnecessary treatment, and address any psychological problems, while fully acknowledging the patient’s symptoms. Explanations that recognize the symptoms and offer a tangible and involving explanation are more likely to satisfy patients and empower them (Dowrick et al 2004). By legitimizing the patient’s symptoms, yet not colluding with the patient by acquiescing with their explanation, and offering a tangible mechanism that the patient ‘owns’ and gives him or her an opportunity for self management, the patient is less likely to make further demands on health care. The presentation of normal test results accompanied by reassurance has little effect on patients’ doubts and anxieties. Central to making a difference to the patient is finding out what his or her fears are (Balint 2000). Cognitive behavior therapy, the treatment of comorbid depression and anxiety, and, in patients with moderate psychological problems, psychiatric help are the mainstays of treatment (van der Feltz-Cornelis et al 2012). If the patient’s ability to function is impaired by the condition it may be necessary to seek psychiatric help.

Optimize Medical Treatment While it is accepted that medical treatment will complement surgery in making the mucosa as healthy as possible, it is less well recognized that it can be a useful predictor of what can be achieved by surgery. For example, in a patient with anosmia and nasal polyposis, the use of oral and topical steroids can indicate the patient’s remaining olfactory potential. If the patient has no sense of smell after a course of oral steroids (Fig. 1.7a–d), not even temporarily, then the surgeon must be very guarded in promising the patient that his or her sense of smell will be improved by surgery.

Tailor the Surgery to Fit the Extent of the Problem There is a price to be paid for extensive tissue removal. That price may include the loss of olfactory mucosa, frontonasal stenosis, altered sensation, dryness, and an

7

1  Principles of Practice

a

b

c

d Fig. 1.7a–d  Endoscopic and computed tomographic appearance before and after medical treatment. a,b Endoscopic views before and after oral steroids.

c,d Computed tomographic images before and after oral steroids.

increased risk of violating the boundaries of the paranasal sinuses (Fig. 1.8a,b). If a full thickness mucosal defect is created there will be persistent crusting until the mucosa has regenerated and it may take up to 1 year for cilia to return to normal so mucus can stagnate and dry causing debris that can collect for many months. Surgery is primarily aimed at improving ventilation of the sinuses and restoring mucociliary clearance. Removal of tissue alone does not cure mucosal disease. After a trial of medical treatment, it is possible to estimate the extent of surgery that will be of most benefit. This means that it is often possible to preserve valuable tissue, such

as mucosa in the olfactory cleft, that might otherwise be removed (Fig. 1.9a–d). Far less surgery is needed if medical treatment has been given preoperatively.

8

Minimize Surgical Morbidity Morbidity can be caused by poor surgical technique, and in particular may arise from excessive tissue removal. Good surgical technique is based on setting explicit goals and achieving these with the minimum amount of tissue trauma.

Minimize Surgical Morbidity

a

b Fig. 1.8a,b  Endoscopic appearance after extensive surgery. a Endoscopic views after overzealous removal of olfactory mucosa.

b Computed tomographic images after overzealous removal of olfactory mucosa.

b

a

c Fig. 1.9a–d  Endoscopic appearance of a range of pathological conditions. a Right nasal airway showing severe nasal polyposis after oral steroids just before surgery. b Perioperative view after ethmoidectomy. c Perioperative gentle lateralization of the middle turbinate (note preservation of olfactory mucosa). d Postoperative computed tomographic view to show open olfactory cleft.

d

9

1  Principles of Practice

How Can This Be Achieved? Work out what surgical steps are needed and then address them systematically. This strategy will not only avoid unnecessary tissue removal but is also very time efficient. Progress is made step by step rather than by exploring the sinuses in a haphazard way. It is clear to the experienced surgeon when observing surgeons who are unfamiliar with operating because the purpose in their movements is limited and they often spend a lot of time aimlessly sucking and prodding. You must decide what needs to be done, and in particular which step needs to be done next, and then do this as atraumatically as possible. This means: —— Punching tissue rather than tearing it —— Preserving mucosal integrity in the frontonasal recess —— Respecting olfactory mucosa —— Avoiding mucosal damage to adjacent surfaces (Fig. 1.10a,b). The surgeon must be aware of the variations that can occur in anatomy and the potential to cause damage to the surrounding structures.

Sense of Smell Should Be Preserved at All Costs Surgeons unfortunately often underestimate the importance of sense of smell to the patient. It is a sense that is all too often forgotten and may escape the notice of both surgeon and patient. The reason may be that the loss of this sense often creeps up on the patient slowly or that

the patient does not recognize that this loss is responsible for the reduced enjoyment of food. In any case, the rewards for preserving or restoring their sense of smell are enormous. The surgical strategy to achieve this goal centers on maximum preoperative medical treatment to minimize trauma to the olfactory mucosa, and to respect all olfactory mucosa whenever possible by leaving it alone, even if it is polypoid.

The Importance of Postoperative Treatment Unfortunately, surgery on its own cannot achieve or maintain healthy nasal mucosa in most patients with chronic rhinosinusitis. Accompanying medical treatment takes on a central role. During the operation, diseased mucosa is removed that has not recovered during preoperative medical treatment, thereby optimizing the drainage zones from the sinuses. Surgery may be able to overcome mucosa–mucosa contact and restore mucociliary clearance, remove diseased tissue, and allow access to topical nasal treatment, but surgery in and of itself cannot cure intrinsic nasal disease (Fig. 1.11a,b). Patients need to be made aware of the need for continuing treatment to achieve the best possible result and an improved quality of life. One way of getting this message across to your patients with intrinsic mucosal disease is to tell them that it is like “asthma of the nose,” and they will need to keep the lining under control by regular medical treatment. This will help to prevent disappointment.

a

b Fig. 1.10a,b  Punches and through-cutting instruments minimise mucosal trauma. a Use of Hajek forceps to neatly remove the mucosa and bone of a right uncinate process.

10

b Through-cutting forceps joining natural and accessory ostia.

Minimize Surgical Morbidity

a

b Fig. 1.11a,b  Preserve olfactory mucosa where possible. a Nasal polyps in the olfactory area medial to the middle turbinate, deliberately not removed at surgery.

b The superior turbinate can now be seen after lateralization of the middle turbinate along with 2 months of topical nasal steroids.

11

2  Pathophysiology of Rhinosinusitis A key aim for both surgeons and physicians is to arrive at a diagnosis. This is not always straightforward given the poor specificity and sensitivity of nasal symptoms and signs in making many rhinologic diagnoses. However, making a diagnosis helps to determine which treatment strategy is most likely to be effective. Implicit in this is the belief that the treatment will provide symptomatic help for the attributed diagnosis. Treatment works well for many specific diagnoses as is described later in this book, e.g., allergic aspergillosis,

a frontoethmoidal mucocele or inverted papilloma. However, there are many rhinologic conditions that pose both a diagnostic and a treatment challenge because we have a limited understanding of their pathophysiology, e.g., chronic rhinosinusitis and idiopathic rhinitis. This chapter tries to face up to what we do not know about these conditions and put this problem into a clinical context. Fortunately, although we may not fully understand the pathogenesis of some of these conditions, classifying these patients using clinical characteristics has enabled

Table 2.1  Classification of rhinosinusitis

Type of rhinosinusitis

Comments

Allergic rhinosinusitis Seasonal

Intermittent (IgE-mediated)

Perennial

Persistent (IgE-mediated)

Allergic fungal rhinosinusitis (IgE-mediated)

Diagnostic criteria: Antigen-specific IgE/IgG raised, eosinophil count raised, total serum IgE raised. Mucin—eosinophils, Charcot–Leyden crystals, scanty fungal hyphae (Gomeri methenamine silver stain, periodic acid Schiff, Fontana–Masson stain, calcofluor white method)

Supported by a positive nasal challenge with a negative reaction to a control chalEntopy or local allergic rhinitis (local allergy in the absence of atopy-negative lenge, IgE in washings, or immunocytochemical evidence of local IgE production skin prick tests and normal specific IgE) Nonallergic rhinosinusitis Rhinitis medicamentosa

Drug induced (history, and stopping medication with resolution support diagnosis)

Infections Viral Acute bacterial Chronic bacterial Fungal Cystic fibrosis Vasculitus

Wegener granulomatosis, Churg–Strauss syndrome

Sarcoid Atrophic Hormonal

Estrogen related: stopping the contraceptive pill or hormone replacement therapy improves symptoms, or the end of pregnancy resolves symptoms

Occupational

Usually irritant, care should be taken as it perhaps provokes allergic hyper-reactivity, occasionally allergic. Removal from environment improves symptoms. Challenge helps confirm allergy if there is an allergic basis

Ozena Empty nose syndrome Autonomic rhinitis

Rhinorrhea as a primary symptom responsive to ipratropium bromide spray four times daily

Structural

Adenoidal hypertrophy, post laryngectomy

Chronic rhinosinusitis Chronic rhinosinusitis with polyposis

12

Chronic Rhinosinusitis

Definition of CRS

Fig 2.1  Where there is controversy about classification

Inflammation of the nose/paranasal sinuses with two or more of the following symptoms (Fokkens et al 2012): —— Blockage/congestion —— Anterior or postnasal discharge —— Facial pain/pressure (on its own rarely due to rhinosinusitis) —— Reduction in or loss of smell and either —— Endoscopic signs of polyps/mucopurulent discharge/ edema or —— Mucosal obstruction of the middle meatus and/or —— Computed tomographic mucosal changes within the ostiomeatal complex and/or sinuses.

Nonallergic noninfective perennial rhinitis (NANIPER) Nonallergic rhinitis with eosinophilia (NARES)

O V E R L A P

Noneosinophilic nonallergic rhinitis (NENAR) Blood eosinophilic NAR syndrome (BENARS) Idiopathic rhinitis Chronic rhinosinusitis without polyps Chronic rhinosinusitis with polyps Neurogenic

some progress to be made in treating these groups (Table 2.1 and Fig. 2.1). It is useful to try to address what we know about the etiology of mucosal disease to place what we are doing in context. The term rhinosinusitis is better than rhinitis because almost all nasal conditions are not solely limited to the mucosa of the sinuses or the nasal airway.

Chronic Rhinosinusitis It is thought that chronic rhinosinusitis (CRS) is not one uniform disease but the result of many different pathogens, allergens, or foreign proteins on hosts with different gene expression at the mucosal level. This results in different immune responses, inflammatory mechanisms, and regulation of these responses. At present the clinical definition of CRS is very broad and is based on clinical symptoms, computed tomography, and endoscopy but not on pathology.

There are many theories and studies of CRS in different population groups and as a result there is little consensus. One of the problems is that, understandably, most studies center on one area of investigation. A holistic picture that analyzes clinical groups along with pathologic groups has been difficult to achieve. Whatever the mechanism that causes mucosal thickening, there appears to be a balance between the upregulators of inflammation and/or reduced apoptosis, and the downregulators of these processes (Fig. 2.2). This is akin to the dynamics that are found in the fibrinolytic and thrombogenic system that exists in blood. Each individual has a different ability to express certain cytokines or have a mechanism to downregulate inflammatory or neurogenic mediators that will influence whether any insult to the nasal lining has a limited or persistent effect. To illustrate the dynamic and complex nature of this balance, ~ 15% of an asymptomatic population have positive skin prick tests and 5% have raised specific immunoglobulin E (IgE) but have no symptoms or signs of allergic rhinitis.

Mucosal homeostasis: a dynamic system

Downregulators s

Fig. 2.2  Mucosal homeostasis: a dynamic system.

Allergens Infectious agents Viral Bacterial Fungal

Mucosal barrier Immunity

Mucosal disease

Mechanical irritants

Upregulators

13

2  Pathophysiology of Rhinosinusitis The analogy to the blood’s fibrinolytic and thrombo- —— Osteitis (it is uncertain whether this is a reaction to genic system is pertinent but it is important to appreciate inflammation or a cause of persistent disease) (Lee et that in CRS it is not a simple summative system. For examal 2006). ple all the upregulators listed below do not simply add up together to be balanced against the downregulators. The Fungal interaction of different cytokines and chemokines, and —— A non-IgE-mediated, mixed T helper type 1/type 2 the influence of mast cells and lymphocytes, are more cytokine response to fungi. A 60-kDa component complex. This is illustrated by the lack of direct evidence of Alternaria degranulates eosinophils. Eosinophils that allergy is a major source of sinonasal inflammation release major basic protein. Alternaria proteins are in CRS (Pant et al 2009). recognized by antigen-presenting cells and present It is important to appreciate that most individuals them to T cells whose response attracts and activates with CRS do not have an infective basis for their disease. eosinophils. Cytokines with a nonspecific protease However, in those who do have persistent or recurrent response are released. It is not clear whether this is a infection as the initiator of their disease, it is vital to condisease-specific response. sider their immunity.

Upregulators (Many Influenced by Genetic Factors) Cellular Basis of IgE-mediated Inflammation —— Mast cells and basophils express interleukin-4 (IL-4), IL-13, and CD40 ligand and therefore have the potential to augment/amplify IgE synthesis in a nonspecific manner.

Cytokines Involved in Mast Cell Maturation and Survival Include IL-4, IL-5, IL-6, IL-8, IL-9, IL-13, and Interferon-γ —— Basophils are detectable in the bronchial mucosa in atopic asthma, and they increase in numbers and express IL-4 during allergen-induced late responses. —— Eosinophils produce lipid mediators, including leukotriene C4 and platelet-activating factor. They also produce a range of cytokines, including IL-4, IL-5, and granulocyte–macrophage colony-stimulating factor (GM-CSF). Chemokine receptor 3 and very late antigen 4 (VLA-4) occur in response to chemokines, particularly eotaxin and RANTES (regulated upon activation, normal T-cell expressed and secreted). —— Adhesion of eosinophils to the vascular endothelium is dependent on binding of vascular cellular adhesion molecule-1 (VCAM-1) produced from the vascular endothelium to its ligand VLA-4 on the eosinophil surface. —— Tumor necrosis factor-α. —— GM-CSF. —— Reduced apoptosis (Powe et al 2009).

Bacterial —— Biofilms that harbor bacteria which produce toxins. Those with Pseudomonas spp. are associated with more severe disease (Foreman et al 2011) —— Bacterial toxins

14

Superantigen Hypothesis —— Staphylococci secrete superantigen toxins, which stimulate T cells. T cells produce cytokines and local polyclonal IgE and eosinophils are recruited. Specific IgE directed against toxins in polyp tissue is found in 50% of patients with idiopathic polyposis (not found in CRS without polyposis). A staphylococcal protein A has been found to cause mast cell degranulation. Staphylococci are present in many patients with nasal polyposis and it is not clear whether they are causative or the result of colonization of the mucus that tends to stagnate because of the dysfunctional ciliary clearance that occurs with nasal polyps (Bachert et al 2001).

Protease Activity —— House dust mite allergen, Der  p  1 (Kauffman et al 2006; Furmonaviciene et al 2007) —— Alternaria —— Staphylococcus aureus.

Neuronal —— Sensory nerves themselves may produce inflammation by an antidromic axon reflex, which causes sensory nerves to release neuropeptides such as substance P and neurokinin A. —— Nerve growth factor, responsible for maturation and development of sensory nerves, is present in nasal fluids of patients with chronic allergic rhinitis and is increased after allergen challenge.

Other Factors —— —— —— ——

Damaged epithelium may amplify any response Mechanical irritation Chemical exposure Free light chains are raised in both allergic and nonatopic rhinitis mucosa suggesting a role in nasal hypersensitivity (Powe et al 2010a).

Comments on Specific Conditions

Rare Conditions —— Primary ciliary dyskinesia —— Immunodeficiency —— Cystic fibrosis.

Limited Evidence Associated with Anatomical Factors Downregulators (Many Influenced by Genetic Factors) Cellular Mechanisms —— —— —— ——

IL-10 can suppress inflammation Transcription factor Fox P3 IL-6 role in inhibitory local innate immune responses Transforming growth factor-b (TGF-b) (also has some proinflammatory effects) —— Sialic acid-binding, immunoglobulin-like lectin-8 (siglec-8) receptor —— “Functional” IgG antibodies may downregulate antigen-specific T-cell responses —— Regulatory T cells might also downregulate T-cell responses through cell–cell contact, as well as through the direct effect of these cytokines

Innate Immunity —— Nitric oxide —— Defensins —— Pattern recognition of damage associated with foreign proteins that induce a reaction to help maintain the barrier (Tan et al 2010) —— SPINKS5, a polyvalent antiprotease that encodes LEKT1, which is a protease inhibitor and helps to protect gap junctions —— S100 proteins with direct antimicrobial and antifungal properties —— IL-22 activates epithelial cells in the innate response —— Mucociliary clearance —— Toll-like receptors (Vanhinsbergh et al 2007; Tan et al 2010)

Mast Cells —— Mast cells can cleave IgE with a protease and may play a role in limiting the late phase reaction (Rauter et al 2008; Hakim-Rad et al 2009).

Mucosal Barrier —— Pseudostratified columnar epithelium —— Pattern recognition receptors recognize damage and initiate a response, e.g., Toll-like receptors —— Tight junctions —— Mucociliary clearance

—— Defensins —— Lysosymes —— Mucus

Comments on Specific Conditions Allergic Rhinosinusitis Allergic rhinitis and seasonal or childhood asthma appear to share a unified disease pathway attributed to an inflammatory cell cascade involving T helper type 2 cells with the production of allergen-specific IgE antibodies from activated B cells (plasma cells). CD4+ T cells, also called T helper cells, IL-4, IL-5, and IL-13 are all involved in the allergic response. IgE is taken up by receptors on mast cells and when cross-linked by allergen, degranulation occurs with the release of inflammatory mediators. Mast cells are abundant in the nasal mucosa of allergic rhinitis mucosa and submucosal lung tissue, consistent with their role in maintaining inflammation in allergic airway disease. Much is made of the balance or dynamics of the predisposition toward either a T helper type 1 (defense against pathogens) or a T helper type 2 (important in parasitic immunity and allergy) pattern of cytokine production, although, as our understanding progresses, this view appears to be simplistic. However, degranulation can be caused by IgG and immunoglobulin-dependent pathways that include Toll-like receptors, complement proteins, calcium-binding proteins, and some cytokines.

Entopy or Local Allergy Approximately 20% of symptomatic people who are skin prick test negative and have normal IgE levels have a positive nasal challenge to house dust mite but not to saline. They also have local IgE in their secretions. There is compelling evidence that has shown that IgE is produced locally within the nasal mucosa in atopic subjects (Huggins and Brostoff 1975; Durham et al 1997; Kleinjan et al 1997; Cameron et al 1998; Kleinjanajk et al 2000; Smurthwaite et al 2001; Takhar et al 2005; Roden et al 2010). Interestingly, some patients with apparently nonallergic rhinitis share similar histologic mucosal features characterized with increased numbers of mast cells and eosinophils and produce local IgE (Powe et al 2001, 2003, 2004, 2006, 2010b). The diagnostic measures proposed in this group include the detection of specific IgE in the nasal secretions after exposure to the aeroallergen along with the local production of tryptase and eosinophil cationic protein (Rondón et al 2010).

15

2  Pathophysiology of Rhinosinusitis

Nonallergic Rhinitis Listed above are the recognized causes of nonallergic rhinitis. However, this leaves a group whose etiology is unclear. The terms nonallergic noninfective perennial rhinitis (NANIPER), nonallergic rhinitis with eosinophilia (NARES), noneosinophilic nonallergic rhinitis (NENAR), blood eosinophilic NAR syndrome (BENARS) and idiopathic rhinitis have all been used (see Table 2.1). There are no specific diagnostic tests for this group because they are largely a diagnosis of exclusion (e.g., no vasculitis, hormonal, or environmental causes, rhinitis medicamentosa). The cause of idiopathic rhinitis, or those with nonallergic rhinitis where no cause in the list above is present, has evaded medical science (Carney and Jones 1996). This is in part because most studies focus on one area of investigation and an analysis that examines this clinical group along with the pathology has yet to be done. “It is likely that neuronal mechanisms, T cells, innate immunity and possibly auto-immune responses all play a role in nonallergic rhinitis and may also contribute to the symptoms of allergic rhinitis” (Bousquet et al 2008).

A Note on the Term “Nasal Polyposis” The term nasal polyp is very nonspecific as it is not a diagnosis but a sign. A minority can result from a bacterial infection or allergic fungal sinusitis and, if they are unilateral, neoplasia needs to be excluded. The most common type of nasal polyposis is associated with late-onset asthma and this patient group is 10 times more likely to have nasal polyposis than the rest of the population. The prevalence of idiopathic nasal polyps is ~ 4% in the population. The

a

term idiopathic nasal polyposis is best used to describe these individuals where the cause is uncertain although both staphylococcal superantigens and an immunologic response to fungal spores have been implicated. The term idiopathic nasal polyposis is preferable at present because it helps to remind us to exclude other recognized causes such as allergic fungal sinusitis or polyposis secondary to bacterial infection. In idiopathic nasal polyposis high levels of IL-5, IL-13, eosinophil cationic protein, TGF-b, eotaxin, RANTES, matrix metalloproteinases 7 and 9, and eosinophils are characteristic in most western populations. Raised levels of B-cell attracting chemokine-1 and stromal cell-derived factor-1a and their receptors may be partially responsible for the increase in B cells and the eosinophilic inflammation seen in CRS with nasal polyps. The complexity of the dynamics at the subcellular level is shown by the finding that 192 genes were upregulated at least twofold, and 156 genes were downregulated by at least 50% in nasal polyp tissue (Liu et al 2004). Mucociliary clearance is dysfunctional in CRS with nasal polyposis but this is probably a secondary phenomenon (Mason et al 1996).

Chronic Rhinosinusitis Without Nasal Polyps These patients have a tendency to a T helper type 1 cell cytokine expression (Daines and Orlandi 2010). Various cells and cytokines have been found to be raised in CRS without nasal polyps including macrophages, mast cells, eosinophils (although fewer than in CRS with nasal polyposis), IL-1, IL-6, IL-8, tumor necrosis factor-a, TGFb1, IL-3, GM-CSF, intracellular adhesion molecule-1, myeloperoxidase, and eosinophil cationic protein. Neither IL-5 nor VCAM-1 was raised and the levels of IL-22 were reduced.

b Fig. 2.3a,b  Idiopathic nasal polyps and computed tomography scan.

16

Practical Comments

a

b Fig. 2.4a,b  Nasal polyps associated with aspirin sensitivity and computed tomography scan.

a

b Fig. 2.5a,b  Chronic rhinosinusitis with osteitis and computed tomography scan.

Practical Comments Patients with CRS and polyps tend to do better than those without polyps after endoscopic sinus surgery. Aspirin-sensitive patients with nasal polyposis often have worse disease as well as a poor response to steroids and all too frequently surgery provides only short-term benefit (Figs. 2.3a,b and 2.4a,b). Patients with CRS and osteitis are a very difficult subgroup. In spite of medical and surgical treatment these patients tend to have a more resistant disease process (Fig. 2.5a,b). Most patients with CRS have no evidence of atopy but those who do are very difficult to manage surgically. Thankfully most of these patients respond well to steroids (Fig. 2.6).

Fig. 2.6  Chronic rhinosinusitis with no evidence of atopy.

17

3  Who? Optimizing Diagnosis and Selection of Patients for Surgery Symptom-oriented Patient Selection

History—Interpreting Nasal Symptoms

The initial goal is to make a correct diagnosis. Many patients with rhinologic symptoms do not need surgery. The art of a good rhinologist is to select “who” will benefit from surgery. While surgery can provide an invaluable benefit in restoring patients’ health and well-being, advocating surgery is not an appropriate response to all symptoms that our patients may report.

Nasal Obstruction

Which are the Cardinal Symptoms? What Criteria in the History are Best to Focus on?

This is the main reason for operating, as it is one symptom that surgery can almost be guaranteed to help in chronic rhinosinusitis with nasal polyposis (Fig. 3.1). However, results are disappointing in allergic rhinitis and chronic rhinosinusitis without nasal polyposis. However, be careful about operating on anyone whose primary symptom is not nasal obstruction—think twice!

A Summary of the Diagnostic Approach History—Interpreting Nasal Symptoms —— —— —— —— —— ——

Nasal obstruction Disorders of smell Rhinorrhea Crusting Facial pain and pressure Relevant medical history –– Aspirin or nonsteroidal anti-inflammatory sensitive –– Late-onset asthma –– Response to medical treatment –– Medication

Clinical Examination —— —— —— —— ——

Examination of the nose Nasal endoscopy Posterior oropharynx Neck Eyes and cranial nerves

Investigations —— —— —— —— —— —— —— —— —— ——

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Skin prick tests Total and specific immunoglobulin E Immunity testing Other hematologic test Ciliary dysmotility/structural studies Sweat test Serum biochemistry Culture Radiology Histopathology

Fig. 3.1  Gross polyposis where the patient will appreciate the improvement in their airway after removal of the polyps.

Also be careful about operating on someone who complains about nasal congestion but in whom there is no objective sign of poor airflow. These patients may have a form of altered sensation due to a neurologic condition called midfacial segment pain. Another cause is a dry lining when the subjective sensation of airflow is reduced as the receptors lining the nasal mucosa do not work well under these conditions (Fig. 3.2). If you are operating to help someone whose primary symptom is an obstructed airflow and they have idiopathic nasal polyps, it is imperative that you explain to them before surgery that they will not be cured and that they will need to comply with continuing postoperative medical treatment. Even then it is likely that they will need further surgery for recurrent polyposis in future. Otherwise you will have a disappointed and disaffected patient after surgery! The wise words of Ian Mackay are worth reflecting on. “You want to be the last surgeon to operate on someone with idiopathic nasal polyps.” This implies that

History—Interpreting Nasal Symptoms

a Fig. 3.2  Dry lining with mucous stagnation. The patient lacked a sensation of airflow.

they usually recur, but often at some point in time that is impossible to discern, the patient’s immunity changes and their polyps no longer return. The patient then thinks that it is the last surgeon that did a “proper” job, when it is their immunity that has corrected the situation! Ask the patient whether they have unilateral obstruction or bilateral obstruction, or whether it alternates from side to side. Bilateral nasal obstruction is often associated with generalized rhinosinusitis, as is obstruction that alternates from side to side. If this is the case, it is likely that the patient has generalized swelling of the nasal mucosa from any cause that can produce bilateral rhinosinusitis. The nasal cycle happens in ~ 80% of patients every 3 to 8 hours, with one side being congested while the other is clear (Fig. 3.3a–c). Any disease that causes a generalized swelling of the intranasal lining may lead to the nasal cycle being “disclosed” so that the patient notices that one side is partially blocked. In the disease-free individual, the amount of swelling of the nasal lining that occurs in the nasal cycle is usually insufficient to cause any symptoms. If the patient has persistent unilateral nasal obstruction, the most common cause is septal deviation (Fig. 3.4). If there is any other pathology, such as a malignancy, there are often other associated symptoms in the history, such as a bloody mucous discharge, loose teeth, diplopia, or distortion of the cheek (Fig. 3.5). Bilateral marked nasal obstruction associated with a reduction in taste and smell is often due to idiopathic polyposis. These patients often respond well to maximum medical treatment but when this has failed they are good candidates for surgery because their nasal obstruction can be helped. Nevertheless, the patient needs to be told that surgery is not a cure and they will need long-term medical treatment to maintain any improvement.

b

c Fig. 3.3a–c  Nasal cycle. a,b The inferior turbinates. c Axial magnetic resonance image showing one side congested at one point in the nasal cycle.

19

3  Who? Optimizing Diagnosis and Selection of Patients for Surgery

Fig. 3.4  A septal deviation in the right nasal airway.

Fig. 3.5  A unilateral mass producing nosebleeds—an angiofibroma.

“Blockage” without Airway Obstruction Be specific in asking the patient whether the sensation is of “blockage” or if there is a feeling that their nasal airflow is impaired. There is a subtle but important distinction between these two symptoms. Someone with an impairment in their airflow normally has a mechanical obstruction, whereas a patient who complains of “blockage” without any airflow obstruction is less likely to have intranasal pathology that will benefit from surgery. Be careful about operating on someone who has a sensation of “blockage” but whose airflow is normal, because these patients may have a feeling of pressure under the bridge of the nose, on either side of the bridge of the nose, or behind the eyes or supraorbital and infraorbital margins. This sensation of pressure is often not related to the obstruction of the ostiomeatal complex, as is implied in most orthodox texts. These patients often have a variation of a tension-type headache called midfacial segment

20

pain that affects the midface. It gives them a feeling of blockage in this area (Jones 2001a) and can produce a sensation of pressure or congestion rather than pain. These symptoms usually respond to low-dose amitriptyline ( Video 3). There are several other different conditions that can cause a sensation of blockage when the airway is good and it is important to make sure that you diagnose the right one as the treatment for them varies a great deal. For the receptors within the nose to feel airflow they need to register a change in humidity and temperature. If the lining is dry then the sensation of airflow is reduced. These patients often sniff to enhance the sensation of airflow and this in turn may exacerbate the problem by causing secondary nasal valve collapse. Sniffing menthol helps temporarily because it stimulates the receptors and relieves the lack of sensation. A lack of sensation with a dry lining is not uncommon in patients who have had a lot of nasal surgery and in particular turbinate surgery of any kind. At a glance, little may appear to be abnormal but on closer examination the septal mucosa does not have any moisture on it. Sometimes there will be obvious crusting but the patient may have cleared any debris before attending. An explanation that this is the problem along with advice on regular douching is required, but, more importantly, instruction is necessary that the prolonged application of petroleum jelly over several months is often needed to allow the mucosa to recover. Petroleum jelly is placed on the little finger inside the nostril margin and then sniffed up and “milked” up by squeezing the nostrils. Collapse of the nasal valve area can cause nasal obstruction but it is often blamed as the cause when it is secondary to other factors. The external valve is made of the ala, the skin of the vestibule, the nasal sill and the contour of the medial crus of the lower lateral cartilages. The nasal valve area and internal nasal valve are two entities that should not be confused. The nasal valve area is the narrowest portion of the nasal passage. It is bounded medially by the septum and the tuberculum of Zuckerkandl; superiorly and laterally by the caudal margin of the upper lateral cartilages, its fibroadipose attachment to the pyriform aperture, and the anterior end of the inferior turbinate; and inferiorly it is made of the floor of the pyriform aperture (Fig. 3.6). The nasal valve, on the other hand, is the specific slitlike segment between the caudal margin of the upper lateral cartilage and the septum and it is measured in degrees at ~ 15°. The mucosal soft tissue changes that affect the inferior turbinate and septum are the commonest causes that narrow the nasal valve area and in turn this can cause secondary collapse of the nasal valve. Nasal valve problems can follow excessive resection of the lower lateral cartilages, or be the result of a long returning of upper lateral cartilages, the inherent concave shape of the lower

History—Interpreting Nasal Symptoms

Fig. 3.6  A diagram of the nasal valve area. Yellow is the inferior turbinate, blue is the septum, green is the nasal floor, and red is the lateral nasal vestibule and upper lateral cartilages.

lateral cartilages, no overlap between the upper and lower lateral cartilages, inherently weak upper and lower lateral cartilages, soft tissue stenosis, a narrow pyriform aperture, or facial nerve palsy affecting the dilator muscles. A diagnosis of nasal valve dysfunction can be made by simple inspection and watching the patient breathe at rest (Fig. 3.7a,b). Inspection during increasing rates of inspiration can reveal various degrees of collapse of the nasal valve. There are no reliable objective measurements. Using a Jobson–Horne probe it is possible to gently support the upper lateral cartilage and ask the patient if it provides symptomatic benefit (Fig. 3.8). If artificially supporting the nasal valve, or opening the soft tissues of the alar region along with the nasal valve with a Jobson– Horne probe, does not provide good subjective improvement in airflow, then valve surgery is unlikely to be of any benefit. The Cottle sign, distracting the nasal valve by pulling on the soft tissues of the cheek (Fig. 3.9), is a nonspecific sign and often provides symptomatic improvement in most primary and secondary causes affecting the nasal valve, and it is of little diagnostic use. It is important not to overlook these problems because surgery to the paranasal sinuses will be unhelpful.

a

Disorders of Smell The patient whose sense of smell returns after oral steroids, only to deteriorate thereafter, is the patient whose sense of smell may benefit from surgery. A patient with anosmia who has had previous surgery is unlikely to regain any sense of smell if systemic steroids have not helped. However, a patient with anosmia who has not

b Fig. 3.7a,b  Primary valve collapse occurs when a patient breathes gently (a) compared with at rest (b).

21

3  Who? Optimizing Diagnosis and Selection of Patients for Surgery

Fig. 3.8  A fine instrument gently supports the lateral aspect of the nasal valve area—if this provides good symptomatic benefit then this may be a factor in the symptom of nasal obstruction.

Fig. 3.9  Cottle sign is poor at defining the site of the cause of any nasal obstruction.

had previous surgery and did not respond to oral steroids still has a small chance of regaining his or her sense of smell through an ethmoidectomy and gentle lateralization of the middle turbinate. It is vital that the middle and superior turbinate are treated with absolute care in these patients when surgery is performed to open the olfactory cleft. Hyposmia is the commonest disorder of smell and is normally caused by any inflammation of the nasal lining of any cause ranging from a cold, severe allergic rhinitis, and chronic rhinosinusitis, to sarcoid or a vasculitis (Jones and Rog 1998). Partial anosmia (an ability to detect some, but not all, qualitative olfactory sensations) usually follows when there has been some damage to the olfactory mucosa or bulb. This may follow an influenza-like illness where the virus is neuropathic to the olfactory apparatus or following trauma with either a head injury or nasal surgery. The extreme end of this spectrum is anosmia. What we do not know is, from a cohort of people who have had a neuropathic virus or head injury causing severe damage

to their olfactory mucosa, how many recover and after what length of time. In secondary care we see individuals whose sense of smell has only partially returned or failed to return and these may represent a minority who have not recovered as many may have done so in the first few weeks. It is difficult to predict the outcome in any individual and there are reports of an individual’s sense of smell returning up to 7 years after these events, even though the basal cells that replace the neuroepithelium do so approximately every 40 days. Frontal blows are a common site of trauma that results in olfactory loss but occipital blows, in themselves much less common, are more likely to result in total anosmia. Amnesia for longer than 24 hours is an indicator of a poorer prognosis (Jones et al 1997b). However, although it is often premature to dismiss the possibility that some or all of their sense of smell may return, it is unwise to predict that it will improve because recovery occurs in fewer than 10%, most occurring within 6 months. Congenital anosmia is associated with some patients with Turner syndrome and with patients with premature

22

History—Interpreting Nasal Symptoms baldness, vascular headaches, and other abnormalities. This presents remarkably late as the individual knows nothing different. Patients with anosmia or severe hyposmia need to be advised about using smoke alarms. They may become fastidious about cleaning both themselves and their surroundings and overuse fragrances for fear of there being a bad smell that they cannot detect. Parosmia or cacosmia (the presence of an unpleasant odor when a normal odor is presented), from the Greek kakos “bad” and osme “smell,” can be even more disturbing than anosmia. These patients may also have had an influenza-like illness or head trauma but the neuronal pathways to the glomeruli in the olfactory bulb have become disrupted. Typically a particular substance such as coffee, perfume, or smoke will initiate another sense of smell such as a chemical-like sensation, or, even more distressing, a smell of feces. In some individuals all olfactory substances induce the same sensation. It is important to exclude other causes such as anaerobic organisms in the paranasal sinuses, diseased teeth, and occasionally organisms within the vestibular hairs. The risk of mild hyposmia and anosmia following nasal surgery is ~ 30% and 1%, respectively (Kimmelman et al 1994; Briner et al 2003). Nasal and paranasal surgery can affect the olfactory pathway by direct trauma to the olfactory epithelium on the middle or superior turbinate, septum or cribriform plate, or by obstructing the olfactory cleft with adhesions. The olfactory mucosa should be preserved if at all possible because to remove it will significantly affect an individual’s quality of life.

Olfactory Hallucinations or Phantosmia These terms apply to the perception of an odor in the absence of an olfactory stimulus. Olfactory hallucination can be a symptom of various non-nasal conditions associated with a head injury, epilepsy, migraine, cluster headache, schizophrenia, depression, bipolar mood disorders, eating disorders, substance abuse, iatrogenic causes, cerebral aneurysm, or tumors (Fig. 3.10). Migrainous olfactory hallucinations are rare and there is usually a clear temporal relationship between episodes of headache and olfactory hallucination. Epileptic olfactory auras are rare. Electroencephalogram changes during the olfactory hallucination indicate an epileptic origin of the aura. Phantosmia following head injury is uncommon. Iatrogenic olfactory hallucination is sometimes seen in epileptic patients on dopaminergic therapy in the early stage and these patients frequently also have a synchronous visual hallucination. Olfactory hallucination is relatively rare in psychotic patients. The presence of olfactory hallucination along with psychosis indicates serious psychopathology with a poor prognosis. Various modalities of treatments for idiopathic

Fig. 3.10  Anterior skull base meningioma that caused a gradual deterioration of the patient’s sense of smell.

olfactory hallucinations have been reported in the literature and include surgical extirpation of the olfactory neuroepithelium and ablation of the olfactory bulb. Rhinosinusitis, viral infection of the upper respiratory tract, and head injury with cribriform plate fracture have been reported to be associated with phantosmia and sometimes with simultaneous parosmia.

Rhinorrhea Anterior Rhinorrhea Anterior rhinorrhea is usually secondary to viral or allergic rhinitis. The reason for anterior rhinorrhea in a viral rhinitis is not only an increase in mucus production but also paralysis of the cilia. The degree of cilial stasis that is needed to produce anterior purulent bacterial rhinorrhea is very marked in bacterial infections and normally occurs only in cystic fibrosis and ciliary dyskinesia. Unilateral clear rhinorrhea should be investigated to exclude a cerebrospinal fluid leak. A specimen of the discharge must be sent for analysis of b2-transferrin by immunofixation (Fig. 3.11); this test has a high specificity and has superseded all other diagnostic techniques. Unilateral autonomic rhinitis can look very much like cerebrospinal fluid rhinorrhea, and it is essential that fluid be sent for b2-transferrin analysis before surgery is contemplated. Other causes that can feign a cerebrospinal fluid leak are mucous retention cysts bursting or nasal secretions pooling in the maxillary or other sinus and draining when leaning forward or when the head is placed in a certain position.

23

3  Who? Optimizing Diagnosis and Selection of Patients for Surgery

a Fig. 3.11  Immunofixation of b2-transferrin is specific and sensitive for diagnosing a cerebrospinal fluid leak.

Clear rhinorrhea caused by allergic rhinitis normally responds well to antihistamines. Topical nasal steroids can also help. When these measures are not enough then an ipratropium nasal spray taken four times a day along with an antihistamine and steroid spray will often suffice. Vidian neurectomy has been advocated but its effect lasts only 6 to 9 months even if fragments of bone are placed in the canal.

Posterior Rhinorrhea As with facial pain, be very cautious about recommending surgery if posterior rhinorrhea is the patient’s primary symptom (Fig. 3.12a,b). Surgery can help reduce the discoloration of the postnasal mucus by helping drainage, but it is important not to promise the patient a “cure” because the mucus secretion may be due to systemic mucosal disease. Because of this, ongoing medical treatment is often important. Patients with asthma can expect an improvement in their lower respiratory symptoms. It is also important to take time to explain to the patient the connection between the upper and lower respiratory tract. Ask the patient about the color of the mucus. Is it clear, yellow, or green, or does it vary in color? Many who mouth breathe or snore when they sleep wake up with some discolored mucus which has collected in their nasopharynx or oropharynx and has dried in this area and become discolored with oropharyngeal commensals or smoke particles. It is therefore important to ask patients who complain of discolored mucus if it is just in the morning or whether it becomes clearer throughout the day. If they say it is always discolored it is useful to ask them to blow into a handkerchief and have a look! If they do blow out green mucus into their handkerchief, it is likely that they have a chronic infective rhinosinusitis. This is relatively unusual, but when it does occur a 2-week course of a broad-spectrum antibiotic that also

24

b Fig. 3.12a,b  Visible signs of mucus are uncommon and make it more likely that there is sinus pathology. a Clear mucus from the accessory ostia. b Mucus tracking back from the sphenoethmoidal recess from the middle meatus.

covers anaerobes usually clears the infection (Clifton and Jones 2007). Patients with nasal polyposis often produce a lot of yellow-stained mucus, which is due to the presence of eosinophils; this discoloration does not necessarily mean that it is infected. The mainstay of treatment for this condition is oral steroids followed by topical nasal steroids, and compliance is important. A separate group of patients with primary ciliary dyskinesia, cystic fibrosis, or immunodeficiency will present with discolored secretions (Fig. 3.13) that they can blow out into a tissue, or that can be seen with an endoscope in the middle meatus or tracking down from the sphenoethmoidal recess. Surgery is disappointing in these groups because it does not address their underlying pathology. Surgery can help to reduce the discoloration of the postnasal mucus in patients with genuine chronically infected rhinosinusitis when medical treatment has failed by aiding drainage. They may need to douche regularly if the cilia are not functioning or in abnormal mucus

History—Interpreting Nasal Symptoms

Fig. 3.13  Stagnant mucus in primary ciliary dyskinesia.

production such as in cystic fibrosis. In those with idiopathic nasal polyposis who often have associated lateonset asthma, it is important not to promise the patient a “cure” because mucus secretion is part of their systemic mucosal disease. Because of this, ongoing medical treatment is often important. Patients with asthma can expect a temporary improvement in their lower respiratory symptoms after sinus surgery but it is important to take time to explain to the patient the connection between inflammation of the upper and lower respiratory tract, and that surgery cannot cure the cause of the inflammation of their whole upper and lower respiratory tract.

Catarrh and Postnasal Drip “Catarrh” means different things to different patients. You need to be quite specific in your history-taking to find out what they mean by it. Ask whether it is a sensation of mucus coming down the back of the throat, at the level of the soft palate, or if there “something” lower down around the level of the cricoid cartilage. Ask the patient to point with one finger to the area or level where they feel the sensation. Ask whether it is clear or mucky, and if it is mucky is that mainly in the morning, and clearer during the day? How much do they produce? Does it make them sniff, snort, clear their throat repeatedly, or hawk? Normally, the paranasal sinuses produce a half a cupful of mucus a day, and this is swallowed along with 1.5 L of saliva. The sensation of an increase in mucus production felt in the back of the throat is sometimes called “postnasal drip.” Patients often complain of a sensation of “something” in the back of the throat that they cannot clear and persistently attempt to clear their throat. Frequently, these symptoms are a result of a hyperawareness of normal mucus. It is particularly important to warn

these patients that this symptom cannot be helped by surgery. Other strategies, however, may help these patients; for example, breaking a cycle of repeated throat clearing, snorting, or hawking by swallowing ice-cold sparkling water instead without doing any of the aforementioned for a week (see p. 440, “Regimen to Break the Cycle”). However, paranasal sinus disease can lead to more mucus being produced. This includes all the causes of chronic rhinosinusitis and in particular the subgroup with nasal polyposis. The presence of nasal obstruction and hyposmia complemented by endoscopic signs will differentiate these patients from those who have a hyperawareness of mucus. It is important that these problems are distinguished from habitual snorting, dry swallowing (swallowing without drinking or eating), or clearing of the throat: this is often part of a habitual cycle which accompanies a hyperawareness of normal mucus. The snorting and throat clearing appear to maintain, if not exacerbate, the sensation that mucus is present. Often the snorer whose uvula is edematous complains of a sensation of “something” around the soft palate, and they may use the term “catarrh” to describe this (Fig. 3.14). To further complicate matters, some patients with globus pharyngeus may complain of catarrh because they have a sensation of something (or mucus) at the level of the cricoid cartilage. It is far more common for patients to have a hyperawareness of normal postnasal mucus, and through repeated clearing of their throat or snorting to have “sensitized” these areas to the half a cup of mucus that is normally produced from the paranasal sinuses each day, as well as the liter of saliva that is swallowed. In this context it is worth considering that, of the large number of people with allergic rhinitis who have a definite increase in their mucus production, few complain of catarrh (Fig. 3.15). A strategy to break the cycle of repetitive throat clearing, dry swallowing, and hawking is to advise the patient to strictly avoid all of these for 1 week and instead swallow ice-cold water that will stimulate the back of the throat and take away the desire to clear the throat. They must be disciplined about doing this and rotate bottles of ice-cold water from the fridge regularly and have some by their bedside. An explanation that the secretions that they have become aware of are healthy and can be swallowed without causing any problems also helps. An audit of this strategy has shown that it works well in a large proportion of patients with these symptoms (Acharya et al 2007).

Postnasal Drip Syndrome Some patients complain of “something” dripping down from the nasopharynx, a need to clear the throat, a tickle in the throat, and posterior nasal discharge, therefore overlapping the symptoms with catarrh. Postnasal drip syndrome has been described as one of the “pathogenic

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3  Who? Optimizing Diagnosis and Selection of Patients for Surgery esophagobronchial reflex via the vagus nerve. This condition is also worth considering in patients who throat clear. A trial of a proton pump inhibitor may be worth considering.

Chronic Cough

Fig. 3.14  Edematous uvula in a snorer.

Fig. 3.15  A snorer who mouth breathes and has dried, discolored mucus in the morning and pharyngitis. During the day the mucus was clear, as were the sinuses.

triad of the causes of chronic cough” together with asthma and gastroesophageal reflux. It has been suggested that the symptoms are the result of mechanical stimulation in the upper airway and specifically due to secretions dripping into the hypopharynx. However, it has no clear definition and there is no physiologic reason why secretions should “drip” in this way—nasal mucus is normally tenacious and cannot drip like water from a tap. Most authorities in this field believe that nasal disease has a role in the production of chronic cough through a continuum or “global” airway inflammation affecting the upper and lower airway and not through any “drip.” Symptoms of heartburn, dysphagia, dysphonia, globus, acid regurgitation, and a bitter taste in the mouth suggest a diagnosis of gastroesophageal reflux disease but this condition has been shown to be asymptomatic or “silent” in many patients. It has also been implicated in chronic cough, dysphonia, globus, throat clearing, dysphagia, and excessive throat mucus. The two potential pathophysiologic mechanisms are aspiration of gastric contents irritating the larynx or tracheobronchial tree, and an

26

Respiratory tract infections are the commonest cause of an acute cough that, by definition, should have resolved within 2 months. Patients with a cough lasting longer than this period are defined as having a chronic cough. Studies of the etiology of chronic cough suggest that ~ 95% of symptoms in immunocompetent, nonsmoking patients with a normal or near-normal chest radiograph are caused by asthma, gastroesophageal reflux disease, chronic bronchitis, bronchiectasis, eosinophilic bronchitis, or the use of an angiotensin-converting enzyme inhibitor. Less common causes such as bronchogenic carcinoma, left ventricular failure, sarcoidosis, and tuberculosis may explain the remaining 5%. Physiologically, cough is a defense mechanism protecting the tracheobronchial tree. Afferent receptors are believed to be innervated through the vagus nerve via the pharyngeal, superior laryngeal, and pulmonary branches. Innovation of the tracheobronchial region has a great role in the generation of cough as in the larynx, as evidenced by the poor or absent cough of lung–heart transplant recipients with absent pulmonary vagal innervation. Stimulation of the vagus can also initiate cough whether it is by stimulating the external auditory canal or by instilling acid into the lower third of the esophagus. As mentioned in the last section, there is no good evidence to support postnasal drip as a cause of chronic cough. In the literature there is no diagnostic test to define those who are labeled as having postnasal drip syndrome other than a response to a first-generation antihistamine. Nasal disease is more likely to result in cough through the co-existing involvement of the lower airways through an as yet undefined pathway, and eosinophil and mast cell mediation appear a likely mechanism (Fig. 3.16). Studies have shown that 60 to 78% of people with asthma also suffer with rhinosinusitis. How gastroesophageal reflux disease may trigger cough is not entirely clear. The two potential pathophysiologic mechanisms are aspiration of gastric contents irritating the larynx or tracheobronchial tree, and an esophagobronchial reflex via the vagus nerve. A trial of a proton pump inhibitor for 2 months can be both diagnostic and therapeutic.

Sneezing Most people sneeze, but more than four sneezes a day are almost pathognomonic of allergic rhinitis. If a patient sneezes a great deal in the morning, then you should be suspicious that they have an allergy to house dust mite, having been exposed to it over the previous few hours

History—Interpreting Nasal Symptoms many, although a minority find that a nasal spray can initiate a sneezing bout. Sprays that contain benzalkonium chloride as a preservative tend to initiate sneezing bouts more than those that do not. A small proportion of patients have incapacitating sneezing bouts that can last for hours. Most of these patients are young adolescents or children and psychogenic factors play a major role. Cognitive behavior therapy, treating anxiety, or suggestion therapy can help. Surgery has no role in the management of sneezing.

Crusting Fig. 3.16  Diagrammatic representation of the concept of the whole respiratory tract being a single airway.

in their bedding (Fig. 3.17a,b). Itchy and watery eyes are in keeping with an allergic rhinitis, whether this is persistent or intermittent. The best treatment for this is nonsedative antihistamines that normally work well and a topical nasal steroid provides supplementary help in

This symptom should alert you to the possibiility of the patient having a systemic disease such as Wegener granulomatosis or sarcoidosis (Fergie et al 1999), and the relevant investigations should be undertaken to exclude these (Jennings et al 1998).

Facial Pain and Pressure Facial pain and pressure are often wrongly attributed by patients and their primary care physicians as being due to rhinosinusitis (West and Jones 2001).

a

b Fig. 3.17a,b  An external clinical sign in allergic rhinitis. a A nasal salute in allergic rhinitis.

b The crease over the bridge of the nose created by repeated rubbing.

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3  Who? Optimizing Diagnosis and Selection of Patients for Surgery In patients with chronic pain involving the face and/or head, it is important to see whether their symptoms are associated with, or exacerbated by, an upper respiratory tract infection and, furthermore, to see whether there is a temporal relationship with any purulent discharge. If they have no significant nasal symptoms and if their nasal endoscopy is normal, it is unlikely that their facial pain is due to rhinosinusitis. However, patients who have facial pain and purulent secretions at endoscopy do well with surgical or medical treatment—over 80% will be helped. Beware if pain and pressure are the patient’s main symptoms. The majority of patients with nasal polyposis have no facial pain or pressure from rhinosinusitis unless there are purulent secretions present and their is an acute episode with obstruction of the sinus ostia (Fahy and Jones 2001). However, if patients have symptoms of pain or pressure in addition to nasal obstruction and a loss of sense of smell, especially if the pain and pressure get worse with a cold or when flying or skiing, then you can advise the patient that these symptoms may be helped by surgery. It is important to be aware of other causes of facial pain that are much more common. Even in an ENT clinic only ~ 16% of those who have been referred with a provisional diagnosis of facial pain due to rhinosinusitis turn out to have pain that is related to paranasal sinus disease (West and Jones 2001).

are isolated reports of sphenoidal sinusitis that can cause headaches but these are extremely rare, there are usually systemic signs such as pyrexia, endoscopic signs, or there is a raised C-reactive protein, and most of these patients respond to antibiotics. Patients with a headache often make a self-diagnosis of “sinusitis” because they know that some sinuses lie within the head. With the advent of nasal endoscopy and computed tomography (CT), along with the finding that many patients’ symptoms of headache or facial pain persist after sinus surgery, it has become apparent that this is not the case. Also of note is that over 80% of patients with purulent secretions visible at nasal endoscopy have no headache or facial pain (Clifton and Jones 2007) (Fig. 3.18). Even if patients with intermittent symptoms of headache or facial pain, and who believe that it is due to infection, are asked to attend the clinic when they are symptomatic, the majority are found not to have any evidence of infection and another neurologic cause for their pain is often responsible (Stewart and Michael 2002; Tepper 2004).

Useful Generalizations —— The vast majority of patients who present with a symmetrical frontal or temporal headache, sometimes with an occipital component, have tension-type headache. —— Unilateral, episodic headaches are often vascular in origin. —— Symmetrical symptoms of facial pressure, particularly if it is long standing, is usually due to midfacial segment pain, a version of tension-type headache that affects the midface.

Sinogenic Pain Sinusitis rarely causes headache, let alone facial pain, except when there is an acute bacterial infection when the sinus in question cannot drain. These patients usually have a history of a viral upper respiratory infection immediately before this, and they have pyrexia with unilateral nasal obstruction. The vast majority of patients with acute sinusitis respond to antibiotics. Patients with more than two episodes of genuine bacterial sinusitis in 1 year should be investigated for evidence of poor immunity. Patients with chronic bacterial sinusitis rarely have any pain unless the sinus ostia become blocked in an acute exacerbation and then their symptoms are the same as acute sinusitis (Clifton and Jones 2007). There

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Fig. 3.18  Purulent secretions in the right middle meatus—the patient had no pain as is often the case.

Over 90% of self- and doctor-diagnosed sinus headaches meet the International Headache Society criteria for migraines. Many migraine sufferers had at least one unilateral nasal symptom of congestion, rhinorrhea, or ocular lacrimation, and redness or swelling during an attack that caused confusion and led them to think their sinuses must be the cause (Fig. 3.19). One series showed that nearly 90% of participants with self- or physician-diagnosed sinus headache met the International Headache Society criteria for migraine-type headache and responded to triptans (Cady and Schreiber 2004). They note that during a migrainous episode there is engorgement and erythema of the nasal mucosa along with rhinorrhea, and after subcutaneous sumatriptan both the symptoms and endoscopic signs resolve. An

History—Interpreting Nasal Symptoms Migraine Stabbing

Throbbing

Piercing Supra-orbital Facial Frontal Parietal Occipital Temporal

Photophobia Pallor or Flushing Nausea

Fig. 3.19  Symptoms that can occur in migraine.

interdisciplinary consensus group recently agreed that “the majority of sinus headaches can actually be classified as migraines” and that “unnecessary diagnostic studies, surgical interventions, and medical treatments are often the result of the inappropriate diagnosis of sinus headache” (Levine et al 2006). Chronic sinusitis is usually painless, with episodes of pain occurring during acute exacerbations which are often precipitated by an upper respiratory tract infection or when there is obstruction of the sinus ostia. An increase in the severity of pain on bending forward is traditionally thought to be diagnostic of sinusitis, but this is nonspecific as many types of facial pain and headache are made worse by this. The key points in the history of sinogenic pain are an exacerbation of pain during an upper respiratory tract infection, an association with rhinologic symptoms, and a response to medical treatment.

Midfacial Segment Pain A relatively recently described condition, which affects about a third of patients with facial pain seen in ENT clinics, is midfacial segment pain. This is a version of tensiontype headache that affects the midface, although 60% have a coexisting headache, and has been shown not to be related to sinusitis (Jones 2007). The definition of midfacial segment pain is: —— A symmetrical sensation of pressure, tightness, or “blockage” (but without airway obstruction). —— Can affect the nasion, under the bridge of the nose, either side of the nose, the periorbital or retro-orbital regions, or across the cheeks (Fig. 3.20a–f). Approximately 60% also have the symptoms of tension-type headache. —— There may be hyperesthesia of the skin and soft tissues over the affected area. Lightly touching the skin can cause discomfort. —— Nasal endoscopy is normal. —— CT of the paranasal sinuses is normal (note: a third

of asymptomatic patients have incidental mucosal changes on CT). —— The symptoms may be intermittent ( 15 days/month). —— There are no consistent exacerbating or relieving factors, although a short placebo effect may be reported after some medication. This is not consistent and quickly wears off. —— There are no nasal symptoms (but note that ~ 20% of most populations have intermittent or persistent allergic rhinitis, which may occur incidentally in this condition) ( Video 3). Patients with midfacial segment pain describe a symmetrical feeling of pressure, heaviness, or tightness and they may say that their nose feels blocked when they have no airway obstruction. There are no consistent exacerbating or relieving factors and patients often take a range of analgesics but they have no, or minimal, effect. Patients may be convinced that their symptoms are due to sinusitis as they know that their sinuses lie under this area with the exception of the bridge of the nose; indeed, their primary care physician may have treated them as having sinusitis for many years. Patients often describe tenderness on touching the tissue of the forehead or cheeks, leading them to think there is underlying inflammation of the bone. However, on examination there is hyperesthesia of the skin and soft tissues in these areas; gently touching these is enough to cause discomfort and there is no evidence of underlying bony disease. This is similar to the tender areas over the forehead and scalp seen with tension-type headache. They may say that the skin of the infraorbital margin region or cheeks swells up, but there are no objective signs—this symptom appears to be due to an alteration in sensation in this area. Nasal endoscopy is normal. As around one in three asymptomatic people have incidental changes on their CT images, this may confuse the picture. The majority of patients with this condition respond to low-dose amitriptyline, but usually require up to 6 weeks of 10 mg (occasionally 20 mg) at night before it works (Agius et al 2013). Amitriptyline should then be continued for 6 months before being stopped, and the 20% of patients whose symptoms return when amitriptyline is stopped need to restart it if the pain returns. It is our practice to inform patients that amitriptyline is also used in higher doses for other conditions such as depression, but its effectiveness in midfacial segment pain is unrelated to its analgesic properties, which would take effect much more quickly and normally require 75 mg. It is often reassuring for patients to know the dose used for depression is some seven or more times the dose used in tension-type headache or midfacial segment pain and that no other antidepressant works for this condition. If amitriptyline fails, then relief may be obtained from gabapentin or pregabalin.

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3  Who? Optimizing Diagnosis and Selection of Patients for Surgery

a

b

c

d

e

f Fig. 3.20a–f  The different patterns of pain distribution in midfacial segment pain.

If patients with midfacial segment pain undergo septal or sinus surgery it makes no difference in approximately a third, in a third it makes their symptoms worse, and in the remaining third it helps their pain but only for a few weeks and rarely more than a few months. It is as though the surgical stimulus alters the “balance” of neuronal activity in the trigeminal caudal nucleus for a short time. It is possible that the placebo effect or cognitive dissonance may also be responsible for a temporary symptomatic improvement (Homer et al 2000). The term midfacial segment pain avoids the use of the term “tension,” which often results in a long and relatively unproductive

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discussion with the patient about the role of stress in their condition.

Facial Pain Due to Vascular Causes Unilateral, Episodic Headaches, or Facial Pain These are often vascular in origin. Vascular pain of various types can be associated with autonomic rhinologic symptoms such as nasal congestion and rhinorrhea and this has led to confusion in arriving at a correct diagnosis (Erros et al 2007). Vascular causes of facial pain include

History—Interpreting Nasal Symptoms atypical forms of migraine cluster headache, paroxysmal hemicrania, chronic paroxysmal hemicrania, hemicrania continua, and short-lasting neuralgiform pain with conjunctival injection and tearing.

Migraine Migraine is typically episodic, lasting 4 to 72 hours and throbbing in nature. Although classical migraine often has a prodromal state and is usually preceded by an aura that frequently contains visual phenomena, facial migraine often has none of this. The pain is typically unilateral but may be bilateral. Nausea, vomiting, and photophobia often accompany the pain. The pain can affect the face as well as the head and a minority can have pain confined to the periorbital area, rarely affecting the cheek and nose alone (Fig. 3.19). The treatment options for acute migraine attacks include the triptans (e.g., sumatriptan, naratriptan, rizatriptan, zolmatriptan), ergotamine or dihydroergotamine, aspirin, paracetamol, codeine phosphate, ibuprofen, or naproxen, with or without metoclopramide. Preventive therapy includes pizotifen (weight gain is a common side effect and reduces its acceptability), propranolol, and amitriptyline. Acute antimigraine therapy is most likely to be beneficial if it is started early in an attack ( Video 3).

Cluster Headache Cluster headache is both severe and uncommon. It is characterized by recurrent, strictly unilateral attacks of headache that typically wake the patient and are retroorbital or centered at the medial aspect of the orbit, of great intensity, and last up to 1 hour. There is often ipsilateral rhinorrhea, nasal obstruction, and lacrimation (Fig. 3.21). It is called cluster headache because there are active or inactive bouts separated by clinical remission when the patient is completely pain free. Treatment includes sumatriptan and oxygen ( Video 3).

Burning Piercing

Red eye Watery eye Dry/runny nose Ptosis

Unilateral Fig. 3.21  Symptoms of cluster headache.

Paroxysmal Hemicrania This has been described as an excruciating unilateral pain that is usually ocular and frontotemporal, with shortlasting (2–45 minutes), frequent attacks (usually more than five a day). At least one of the following autonomic symptoms should be present: nasal congestion, rhinorrhea, lacrimation, conjuctival injection, or, rarely, ptosis, eyelid edema, increased local sweating, and facial flushing. Approximately one in four patients develop a chronic form. The average age at onset is usually 30 to 40 years, but the age spectrum is wide. The condition’s complete or rapid response to indometacin is said to differentiate paroxysmal hemicrania from cluster headache.

Hemicrania Continua Hemicrania continua is a unilateral headache that is moderately severe without side shift, continuous but with fluctuations, with complete resolution of pain with indomethacin, and exacerbations that may be associated with autonomic features such as conjunctival injection, lacrimation, and photophobia to the affected side.

SUNCT Short-lasting neuralgiform pain with conjunctival injection and tearing (SUNCT) is one of the rarest idiopathic headache syndromes. There is trigeminal pain, particularly in the orbital or periorbital areas, associated with autonomic symptoms in which conjunctival injection and tearing are the most prominent features. Attacks last between 15 and 60 seconds and recur between 5 and 30 times an hour. These attacks may be precipitated by chewing movements and ingesting of certain foods such as citrus fruits. Treatment is not always straightforward and a trial of lamotrigine, carbamazepine, or topiramate may help.

Other Symptoms That Are Difficult to Interpret Facial Swelling without Any Objective Signs, or Tenderness of the Soft Tissues of the Face It is not uncommon for patients to say that their cheeks swell when they have facial discomfort when there are no objective signs, even when they are symptomatic. They often turn to their partner to confirm this, yet they have no objective signs. Some patients with facial pain of vascular origin release neuropeptides in the distribution of their pain. This may be responsible for some sensation of facial swelling, and they may even have a facial flush. Another reason some patients complain of facial swelling without any signs, particularly when it is bilateral, is that they have an altered sensation in the affected area akin to the feeling of facial swelling that occurs after a dental

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3  Who? Optimizing Diagnosis and Selection of Patients for Surgery local anesthetic. This can occur in conjunction with the hyperesthesia that many of these patients feel in midfacial segment pain. Facial swelling, and in particular swelling of the cheek, is unusual with infective rhinosinusitis except where accompanied by periorbital cellulitis (Fig. 3.22). The most common causes of swelling of the cheek are of dental origin. The rare sinus causes include maxillary mucoceles, tumors, or where there is a dehiscence in the wall of the maxillary sinus, but these are unusual. It is very rare for infective rhinosinusitis to cause swelling of the cheek.

strategy is to explain that it is not diseased mucus and not going to cause any harm. Measures that may help include douching regularly, hydration, and humidification of the environment. If not being able to “blow my nose” is associated with crusting, then an atrophic lining may be responsible, or occasionally sarcoid or vasculitis, and then these need to be excluded.

Lethargy and Dark Rings Under the Eyes These are nonspecific symptoms that are not associated with sinusitis. They are symptoms that are more frequently associated with midfacial segment pain.

Halitosis Pseudo-halitosis or Halitophobia

Fig. 3.22  Periorbital cellulitis.

“Clicking” Sinuses This is not a common symptom but it has a similar significance to the sensation of the ears popping. The fact that that the sinuses do click may indicate that the pressure is equalizing as the sinus ostia open. This may indicate some minor mucosal hypertrophy or some increase in secretions but it is rarely associated with significant sinus disease. As an isolated symptom it does not warrant intervention and as part of a collection of symptoms it should be ignored other than to explain to the patient that it is not a cause for concern.

“Nothing Comes Out When I Blow my Nose” As a solitary symptom this is not one that is associated with any pathology. Often patients who complain of this have a coexisting awareness of “something” at the back of the soft palate and they may snort or dry swallow. This is akin to the hyperawareness of mucus that is described above. Occasionally thick mucus can be seen at endoscopy or in the nasopharynx and the increased viscosity of the mucus makes it difficult to dislodge. This can occur secondary to turbinate surgery or a dry environment, dehydration can contribute, the aging process sometimes affects the mucus–secreting glands, post radiotherapy, and as a result of any cause of cilial dysfunction. The main

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This is common and approximately half of patients who complain of halitosis have no odor. It may not be something that you are familiar with doing but it helps to ask the patient to breathe out through their mouth while you smell their breath while leaning over them from the side. This lets the patient know that you have taken their complaint seriously. It is remarkable how frequently you will find patients have no halitosis whatsoever. When a patient is told there is no smell they often say that it was good that day. They can be offered the opportunity to return when they are symptomatic and when they do so there is rarely any change.

Oral Halitosis Oral halitosis is by far the most common cause as it is responsible for more than 90% of cases and poor oral hygiene and periodontal disease are the primary culprits. Debris in tonsil pits can collect anaerobes in the extruded dead white cells and this has an offensive smell. The debris is best not removed mechanically but dealt with by hydrogen peroxide gargles and in time the pits usually shrink. Patients often seek tonsillectomy for this problem but regular hydrogen peroxide gargles and convincing patients not to instrument their tonsillar pits with fingernails, hairgrips, or anything else works after a few months. A coated tongue is often implicated by patients but is often not the cause. When a coated tongue is the cause, no particular bacterial genus has been found to be responsible, and it appears that halitosis may be the result of interactions between various species. Regular mouthwashes with cetylpyridinium chloride plus chlorhexidine and zinc lactate or cetylpyridinium reduce breath odour in 2 to 4 weeks. Tongue brushing is another alternative. Oral malignancy can produce a particularly foul anaerobic smell and the whole oral cavity including the posterior third of the tongue, the retromolar trigone, and sublingual area should be inspected.

Clinical Examination Extra-oral Halitosis Extra-oral halitosis can come from the nose, the lower respiratory tract, exhalation of blood-borne compounds, systemic diseases, metabolic disorders, medication, and some foods. The paranasal sinuses are rarely a cause and when they are it is usually due to anaerobic organisms collecting around a foreign body, rhinolith, or from a dental infection that has involved the maxillary sinus.

Relevant Medical History The main relevant points are whether there is a history of late-onset asthma or bronchiectasis that would indicate involvement of the lower respiratory tract. Aspirin sensitivity is associated with severe polyposis. Infections elsewhere in the body raise the possibility of an immunodeficiency. If the patient with purulent rhinosinusitis is not responding to the appropriate antibiotics, then the possibility of an immunodeficiency, ciliary dysmotility, or an atypical infection, e.g., aspergillosis, should be considered. If the patient has had previous sinus surgery that did not help, think twice before operating again. If surgery failed the first time, why should it work the second time? Thickened mucosa on CT is very common after sinus surgery, particularly of the maxillary sinus, and it does not mean that this is the cause of any residual symptoms (Fig. 3.23a,b). If the patient has ongoing symptoms it is important to go over the history, examination, and response to

medical treatment in detail before embarking on surgery again. Is the patient systemically well or unwell—if the patient is systemically unwell and looks and feels ill, then consider connective-tissue disease and in particular vasculitis. Symptoms suggestive of a bleeding disorder and the use of anticoagulants should be sought.

Clinical Examination —— —— —— —— ——

Examination of the nose Nasal endoscopy posterior oropharynx Neck Eyes and cranial nerves.

Examination will provide objective information to support or cast doubt on the provisional diagnosis that may be made based on the history. Rigid nasal endoscopy is invaluable in assessing the lining of the nose and middle meatus, as well as that in the sphenoethmoidal recess (Fig. 3.24a,b). If nasal endoscopy is normal, the surgeon should be very wary about attributing any symptoms to rhinosinusitis. If the patient says that they are going through a good period and that this is not a representative time, then it is advisable to see them when they are symptomatic to confirm that rhinosinusitis is the cause of their problem.

b

a Fig. 3.23a,b  Typical computed tomography images in two different patients showing changes after surgery. These mucosal changes in themselves do not mean that further surgery is warranted.

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3  Who? Optimizing Diagnosis and Selection of Patients for Surgery

a

b Fig. 3.24a,b  Subtle changes of ethmoiditis visible only on close-up endoscopic examination.

The majority of patients with allergic rhinitis have mucosal changes confined to the inferior turbinate, but some will have more generalized edema and this endoscopic appearance should be interpreted in light of their symptoms. Patients with late-onset asthma and rhinitis have more generalized mucosal disease affecting the lining of their nasal airway. It is important to look for the granulations associated with Wegener granulomatosis or sarcoidosis, as surgery will not help patients with these conditions (Fig. 3.25). Check that there is no displacement of the orbit, which can occur with a mucocele (Beasley and Jones 1995b; Muneer et al 1998).

Investigations

Fig. 3.25  A nonspecific but abnormal mucosa that warrants further investigation, in this case Wegener granulomatosis.

Fig. 3.26  Skin prick test that is positive to a range of inhaled allergens.

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Investigations are tailored to the history.

Skin Prick Tests Skin prick tests are helpful in determining whether someone has an allergic rhinitis and in demonstrating to them that it is their response to allergens that is partially or totally responsible for their symptoms (Fig. 3.26). This can help motivate a patient to comply with treatment and consider allergen avoidance.

Investigations

Total or Specific Immunoglobulin E Tests Total or specific immunoglobulin E (IgE) tests are less specific and sensitive than skin prick tests but can help support a diagnosis in patients who are on antihistamines or steroids or in whom a skin prick test is not helpful, e.g., in dermatographism. In patients who have lower respiratory tract symptoms in whom a diagnosis of asthma has not been made, it is helpful to do a peak flow reading as 20% of patients with idiopathic nasal polyps have coexisting asthma (Fig. 3.27).

Fig. 3.27  A peak flow meter is useful in a rhinology clinic.

Immunity Testing Watch out for immune dysfunction in recurrent or chronic purulent sinusitis. Adults should not suffer from more than two episodes of genuine acute bacterial sinusitis a year. If they do, then their immunity should be checked. The Jeffrey Modell Foundation (www.info4pi.org) lists 10 warning signs of primary immunodeficiency.

It is important to remember that primary immunodeficiencies, especially antibody deficiencies, can present at any age. The incidence of common variable immunodeficiency has two peaks, one in the first 5  years of life and again in the second decade, but it should still be considered in the elderly. Antibody deficiencies are the commonest primary immunodeficiency, and are also the most likely to present with recurrent ENT infections. Primary defects of cell-mediated immunity, neutrophil function, or complement activity are relatively rare, and while ENT infections may occur in these diseases, they are more likely to present with features outside the upper respiratory tract. The initial investigations should include a full blood count and differential white cell count and total immunoglobulin levels for IgG, IgA, and IgM. The collection of any organisms found in the nasal airway is best done by passing a culture swab through a sterile protective sheath of a large intravenous cannula to avoid picking up the commensals from the nasal vestibule. Titers of specific IgGs for tetanus, Haemophilus influenzae, and pneumococcus, and investigation of the patient’s humoral response are indicated; if their IgG titers are low, patients should be vaccinated against these diseases, and the titers should then be repeated after 1 month to check that they have improved (Cooney et al 2001). An abnormal response needs to be discussed with an immunologist. The fasting glucose should be measured and you should consider whether an human immunodeficiency virus (HIV) test might be appropriate (Fig. 3.28). If these tests are normal, but in the light of the patient’s progress or response to treatment there is concern about their immune function, then further investigations should be performed in consultation with an immunologist. The decision to test for HIV in a patient with recurrent otorhinologic infections should be precipitated by a history of risk factors for HIV or infections with fungi such as Candida or Aspergillus or herpes viruses. If such

Ten Warning Signs of Primary Immunodeficiency (Jeffrey Modell Foundation) 1. Eight or more new ear infections within 1 year 2. Two or more serious sinus infections within 1 year 3. Two or more months on antibiotics with little effect 4. Two or more pneumonias within 1 year 5. Failure of an infant to gain weight or grow normally 6. Recurrent deep skin or organ abscesses 7. Persistent thrush in mouth or elsewhere on skin, after age 1 8. Need for intravenous antibiotics to clear infections 9. Two or more deep-seated infections 10. A family history of primary immunodeficiency

Fig. 3.28  Middle meatal mucopus in a patient with acquired immune deficiency syndrome.

35

3  Who? Optimizing Diagnosis and Selection of Patients for Surgery factors are present then all blood samples and biologic materials should be labeled as high risk to avoid potential hazards to those handling these samples. Remember that counseling and informed consent are required before taking blood for HIV testing.

Other Hematologic Tests Titers of c-antineutrophil cytoplasmic antibody are both specific and sensitive in diagnosing Wegener granulomatosis. The angiotensin-converting enzyme level is a screening test for sarcoidosis but has poor specificity. C-reactive protein is a broad screening test as a marker for systemic inflammation.

Ciliary Motility/Structural Studies Primary ciliary dysmotility syndromes commonly have otorhinolaryngologic infection as a prominent part of their history at diagnosis. Co-existent bronchiectasis, infertility in men and situs inversus are suggestive. The simple saccharin test is a useful screening test, but falsepositive results may occur in the presence of infection. Phase-contrast microscopy of a nasal brushing or electron microscopic examination of a nasal biopsy are more accurate ( Video 1).

Sweat Sodium Concentration Cystic fibrosis is a possible but unlikely cause of isolated recurrent upper respiratory tract infections. A child with chronic sinusitis associated with intranasal polyposis should have cystic fibrosis excluded, as mild forms of the disease can occur. Sweat sodium concentration remains the standard investigation, but genetic testing for some alleles of cystic fibrosis is now available.

Radiology Computed tomography should be interpreted in the light of history and endoscopic findings (Fig. 3.29) but this should be interpreted in the context of the history and examination (Scadding et al 2008a,b) as the prevalence of incidental mucosal changes in an asymptomatic population is ~ 30% (Marshall and Jones 2003). In the diagnosis of rhinosinusitis, the use of CT alone can be misleading (Jiannetto and Pratt 1995; Bhattacharyya et al 2010). A review of the presence of the various anatomical variations does not differ between a symptomatic and an asymptomatic population, making it unlikely that these are very important in either initiating or sustaining paranasal sinus disease (Willner et al 1997; Jones 2002). CT provides an excellent map to help the sinus surgeon operate (Mason et al 1998b). CT provides information about the extent of mucosal disease but this correlates poorly with symptoms, surgical findings, and histopathology. CT does provide invaluable information to help in the diagnosis of atypical sinus infections, malignancy, and in the management of the complications of rhinosinusitis. A normal CT in a patient with facial pain should make the doctor consider another diagnosis. In essence, CT helps to support a clinical diagnosis but it should not be interpreted out of context and it is therefore vital that doctors communicate the clinical picture to their radiologic colleagues or that they learn to interpret the images. The prevalence of incidental changes on magnetic resonance images is considerable and therefore this imaging technique is of limited use in the diagnosis of rhinosinusitis (Cooke and Hadley 1991).

Serum Biochemistry Diabetes, malnutrition, hepatic and renal failure, lymphoproliferative disorders, and therapy with certain drugs (e.g., steroids) or radiotherapy are relatively common causes of impaired immune function. Most of these will be evident from the history, but the addition of a basic biochemical profile is appropriate. Urea and electrolytes (U&Es), liver function tests (LFTs), and fasting blood sugar level are sufficient.

Culture The problem of culturing secretions in the nasal airway is that they are often contaminated by organisms from the nasal vestibule. In unresponsive patients it can help to obtain samples for bacterial and fungal culture, both to identify unusual organisms and to guide treatment according to sensitivities.

36

Fig. 3.29  Incidental mucosal changes are found in one in three asymptomatic people.

Disease-oriented Patient Selection

Histology In patients with a granular mucosa where a vasculitis or sarcoid are suspected a biopsy is advisable.

Who Will Most Likely Benefit from Surgery? In determining which patients to select for surgery, the decision must be founded on the likelihood that surgical treatment is capable of offering the desired improvement. Patients with a diagnosis of rhinosinusitis and nasal polyposis who do not have an adequate improvement in their symptoms after maximum medical treatment are most likely to profit to some extent from surgery. These patients may have had a very good initial response to oral steroids, but their symptoms of hyposmia and congestion may return within a few weeks, even with continued topical treatment. The key questions are: What symptoms do the patients have, and how pronounced are they? It helps to ask the patient what is their most troublesome symptom and then write down their symptoms in order of severity in the notes. As a generalization, patients who complain of marked nasal obstruction and hyposmia can often be helped whereas patients with symptoms of catarrh and facial pain cannot. Another key point in making your selection about whether or not to operate is whether the patient has had previous sinus surgery that did not help. If so, think twice before operating again. If surgery failed the first time, why should it work the second time? It is important to be sure that the surgery was performed well the first time, that the sinus ostia are open, and that there is no significant residual disease. Postsurgical mucosal thickening on CT, particularly of the maxillary sinus, is very common and it does not mean that this is the cause of any residual

symptoms. In this situation, it is important to go over the history, examination, and response to treatment in detail before embarking on surgery again.

Disease-oriented Patient Selection Which pathologic processes benefit from surgery? The symptom-oriented approach applies to the majority of patients with rhinosinusitis, whether they have polyps or not. However, there are specific diseases that deserve special mention.

Chronic Infective Rhinosinusitis Patients with chronic infective rhinosinusitis who have not responded to medical treatment usually benefit from surgery unless they have an immunodeficiency or a disorder of ciliary motility (Fig. 3.30a,b).

Aspergillosis/Fungal Disease In purulent rhinosinusitis that does not respond to two or more courses of antibiotics, the possibility of a fungal infection, and an Aspergillus infection in particular, should be considered. An accurate diagnosis of fungal disease centers on culture, skin prick tests, CT scans, and in allergic aspergillosis titers of Aspergillus precipitins.

Mycetoma/Saprophytic Fungal Disease Adults who have a unilateral nasal discharge visible at nasal endoscopy that fails to respond to a broad-spectrum antibiotic with an anaerobic cover should be suspected of

a

b Fig. 3.30a,b  A patient with purulent secretions that partially responded to prolonged medical treatment but remained symptomatic.

37

3  Who? Optimizing Diagnosis and Selection of Patients for Surgery having a fungal sinusitis. A paranasal sinus fungus ball or sinus mycetoma is a noninvasive fungal infection that is seen in immunocompetent persons. CT is useful as it can help to make a diagnosis because of the relatively specific findings (Fig. 3.31a,b). The maxillary sinus is most commonly involved, with partial or complete opacification, bone thickening, and sclerosis or bone destruction. CT often shows some calcification within the involved sinus. Histopathologic investigation should reveal that this material is composed of a dense matted conglomeration of fungal hyphae, separate from the mucosa of the sinus. Aspergillus fumigatus is the most frequently isolated organism. Surgical removal of the fungus ball is the treatment of choice.

Allergic Aspergillosis Among all the patients who present with nasal polyposis are a group with allergic fungal sinusitis. These patients can have unilateral or bilateral polyps and they often

respond to some extent to both topical and systemic steroids (Simmen et al 1998). Although there are no unique pathognomonic symptoms, patients often have thick yellow–green nasal or sinus mucus. This condition occurs in young immunocompetent adults with chronic relapsing rhinosinusitis unresponsive to antibiotics, anthistamines, or corticosteroids. Although patients do not have underlying immunodeficiencies, 50 to 70% are atopic. There is no male or female predominance. Cases of allergic fungal sinusitis have been described from different parts of the world, but the condition appears to be most prevalent in the warm humid areas of the southern United States where it accounts for ~ 7% of all sinus surgery. The nasal polyposis may form an expansive mass that causes bone necrosis of the thin walls of the sinuses and produces some proptosis, or quite an alarming picture on CT as the erosion of bone can look as though there is a malignant process (Fig. 3.32). CT scans often reveal a characteristic serpiginous sinus opacification of more than one sinus, mucosal thickening, and erosion of bone, but this does not represent tissue invasion. The diagnosis of allergic fungal sinusitis requires the presence of chronic rhinosinusitis in an otherwise immunocompetent individual; the microscopic examination of the characteristic allergic mucin to determine the presence of eosinophils and fungal elements; histologic examination of sinus tissue to rule out invasion; radiographic studies to assess the extent of disease; and laboratory testing for eosinophilia, total serum IgE, specific IgE against fungal antigens, and a positive skin prick test to fungal antigens. Fungal cultures are required to identify the responsible fungus. The criteria for diagnosis have undergone numerous revisions; however, most authors agree on the following: the presence in patients with chronic rhinosinusitis, confirmed by CT scan, of characteristic allergic mucin

a

b Fig. 3.31a,b  Clinical and computed tomography (CT) appearances of fungal mycetoma. a Fungal debris in the middle meatus. b Coronal CT scan with mycetoma.

38

Fig. 3.32  Typical appearance in allergic fungal sinusitis with altered density and some erosion.

Disease-oriented Patient Selection containing clusters of eosinophils and their by-products; and the presence of fungal organisms within that mucin detectable on staining or culture. In addition there is evidence of type 1 (IgE-mediated) hypersensitivity to fungi. Various dematiaceous (brown-pigmented) environmental molds, including Alternaria, Bipolaris, Cladosporium, Curvularia, and Drechslera species, can also be responsible. The treatment of allergic fungal sinusitis includes surgical debridement to remove polyps and the allergic mucin containing fungal debris, which is thought to cause the immune reaction. Medical treatment is also required because it is unlikely that all fungal elements can be removed and postoperative systemic corticosteroids reduce recurrence of disease. In many studies there is a high recurrence rate (Kupferberg et al 1997; Kuhn and Javer 2000). Allergic aspergillosis has been likened to allergic bronchopulmonary aspergillosis; in other words it is a systemic reaction to an allergen in the respiratory tract (Schubert 2004). The authors have found that using preoperative itraconazole for 4 weeks markedly reduces the extent of surgery that is required, and given along with a 6-week course of postoperative itraconazole reduces recurrence rates (Andes et al 2000; Daudia and Jones 2008). In addition oral corticosteroids reduce symptomatic recurrence but should be avoided in patients with diabetes, blood dyscrasias, and immunodeficiencies because they can convert the fungus into the invasive form. Other conditions where oral steroids should be used with caution include glaucoma, osteoporosis and hepatitis, among a range of contraindications. Topical steroids also help in reducing symptomatic recurrence.

Chronic Invasive Fungal Sinusitis Chronic (invasive) fungal sinusitis is a slowly progressive disease that is seen in both immunocompromised and immunocompetent individuals. Granulomatous invasive fungal sinusitis often presents with long-standing symptoms of nasal obstruction, unilateral facial discomfort or enlarging mass, or with a silent proptosis. This condition may begin as a paranasal sinus fungus ball and then become invasive, perhaps as a result of the immunosuppression associated with diabetes mellitus or corticosteroid treatment. If left untreated, the infection can spread to invade adjacent structures, including the orbit and brain. In patients with chronic invasive sinusitis, noncontrast CT scans will reveal a hyperdense mass within the involved sinus with associated erosion of the sinus walls. There is profuse fungal growth with localized tissue invasion, and noncaseating granulomas with giant cells. The granulomatous response is often intense enough to cause pressure necrosis of bone and can cause proptosis. Unless removed, the fungal mass can spread into the orbit and brain.

Chronic (invasive) fungal sinusitis requires long courses of itraconazole, unless the disease is of the acute fulminant type with blood vessel invasion when intravenous antifungals are needed. Chronic invasive sinusitis is often advanced by the time of diagnosis, with erosion out of the ethmoidal sinuses, or into the cranial cavity or orbit. It is important to distinguish a chronic expanding fungal disease that comprises a mycetoma that can erode bone and expand into neighboring areas, from chronic invasive aspergillosis that not only leads to bone loss on CT but, most importantly, penetration of soft tissues (Fig. 3.33a–c). Itraconazole has revolutionized the treatment of this condition and a 12-month course will often make surgery unnecessary and cure the patient (Browning et al 2006). It is important to monitor liver function and morning cortisol before and after 1 month of treatment with itraconazole, and liver functions monthly thereafter.

Fulminant Aspergillosis Acute fulminant (invasive) fungal sinusitis is a rapidly progressive disease that is most commonly seen in immunocompromised individuals or patients with diabetes with uncontrolled ketoacidosis. Immunocompetent individuals are seldom affected. The infection can spread from the nasal mucosa and sinus into the orbit and brain. Prolonged neutropenia and metabolic acidosis are well recognized as important risk factors for rhinocerebral mucormycosis and fulminant aspergillus sinusitis among patients with hematologic malignancies, hematopoietic stem cell transplant recipients, and individuals with diabetes mellitus. Other contributing factors include the use of corticosteroids, deferoxamine, and HIV infection. In immunocompromised persons, acute invasive fungal sinusitis presents with fever, unilateral facial swelling, unilateral headache, nasal obstruction or pain, and a serosanguinous nasal discharge. Necrotic black lesions on the hard palate or nasal turbinate are a characteristic diagnostic sign. As the infection spreads into the orbit, periorbital or perinasal swelling occurs and progresses to disfiguring destruction of facial tissue. Ptosis, proptosis, ophthalmoplegia, and loss of vision can occur. The commonest causes of acute fulminant sinusitis are molds of the order Mucorales, including the species Rhizopus and Rhizomucor. Other less frequent causes of fulminant sinusitis include Aspergillus species, particularly A. flavus and A. fumigatus. In the immunocompromised or diabetic patient with acute invasive sinusitis, lipid-based amphotericin B at dosages of 3 to 5 mg/kg or higher or voriconazole are best. The administration of lipid-based amphotericin B is preferable for patients in whom the conventional formulation is contraindicated because of renal impairment, or who develop side effects that would otherwise necessitate discontinuation of the drug. New antifungal drugs are being developed, and it is worth consulting a microbiologist.

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3  Who? Optimizing Diagnosis and Selection of Patients for Surgery

b

a Fig. 3.33a–c  Features of fulminant invasive aspergillosis. a Preoperative coronal computed tomography scan in invasive fungal sinusitis. b Postoperative coronal computed tomography scan in invasive fungal sinusitis. c Histology showing Aspergillus invading a blood vessel (arrow).

Maxillary Sinusitis Secondary to Dental Disease In anyone with unilateral maxillary sinusitis the teeth should be examined as a possible cause (Hoskison et al 2012). If maxillary sinusitis persists in spite of good root canal or apicectomy treatment, then sinus surgery can help to eradicate residual sinus disease. If there is any history of a periapical abscess, a discharging sinus in the buccal sulcus, a complex root canal filling or a difficult extraction (particularly the upper second premolar and first molar) where a root may have been retained or an oroantral fistula created, then a primary dental cause should be sought before doing any sinus surgery. Sinus surgery done when there is residual dental disease will not work. When a maxillary sinusotomy is performed and the contents of the sinus consist of foul-smelling pus then an underlying dental cause should be excluded, and if present, dealt with (Fig. 3.34).

Antrochoanal Polyp Surgery is always indicated for this type of polyp because it does not respond to medical treatment. If the whole base of the polyp in the maxillary sinus is removed, the prognosis is good; otherwise, the polyp recurs (Fig. 3.35a–d).

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c

Inverted Papilloma These patients have a unilateral nasal polypoidal mass and their CT scan shows flecks of calcification, osteitis,

Disease-oriented Patient Selection Fig. 3.34  Unilateral maxillary sinusitis secondary to dental disease. Note the periapical rarefaction.

b

a

d Fig. 3.35a–d  Features of an antrochoanal polyp. a b c d

An antrochoanal polyp in the nasopharynx. An antrochoanal polyp in the nasal airway. Coronal computed tomography scan of an antrochoanal polyp. Surgical specimen of an antrochoanal polyp with its pedicle.

c

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3  Who? Optimizing Diagnosis and Selection of Patients for Surgery and erosion. Surgery is indicated not only to confirm the diagnosis but to try and eradicate the disease. It is vital to send the whole specimen for histologic examination, as 8 to 15% of inverted papillomas are associated with malignancy or atypia (Mirza et al 2007).

Unilateral Nasal Polyps Associated with Neoplasia Surgery is necessary for biopsy and/or excision (Fig. 3.36a,b). Any unilateral nasal polyp should be treated with suspicion, even if it looks harmless (Fig. 3.37). It may disguise an underlying tumor or atypical infection (Fig. 3.38). A biopsy should be taken to ensure that no infection or tumor has been overlooked.

Benign and Malignant Tumors Today, many tumors can be removed endonasally. Here, the complete removal of the tumor base is critical. Knowledge of the tumor’s pathology is critical in formulating a treatment plan. For example, while an endoscopic medial maxillectomy will suffice for inverted papilloma without malignancy, it would not suffice for a poorly differentiated squamous cell carcinoma where a maxillectomy and radiotherapy would give a better prognosis.

Pediatric Rhinosinusitis The main treatment strategy should be conservative and not surgical.

b

a Fig. 3.36a,b  Clinical signs of malignancy in the paranasal sinuses. a A unilateral nasal lesion due to adenocarcinoma.

b Endoscopic appearance of an adenocarcinoma of the ethmoidal sinuses.

Fig. 3.37  A unilateral polyp may disguise an underlying tumor or atypical infection. A neurofibroma originating from the right sphenopalatine area.

Fig. 3.38  A harmless-looking polyp medial to the middle turbinate and an infective-looking polyp at the origin of the turbinate—at histology an adenocarcinoma.

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Disease-oriented Patient Selection It is well recognized that adenoidal hypertrophy and allergic rhinitis are common in children, as are recurrent upper respiratory tract infections (Fig. 3.39). The main causes of symptoms associated with rhinosinusitis in children are rhinorrhea, nasal obstruction, mouth breathing, hyponasal speech, and snoring. In children, adenoidal hypertrophy reduces in size and the number of colds decreases in frequency by the age of 8 to 10 years (Fig. 3.40a–c). Parents may exert a great deal of pressure in the pursuit of their child having no symptoms, but this strategy is flawed. Explain to anxious parents that simple, noninvasive measures such as teaching nose-blowing, the use of saline sprays, or a trial of allergen avoidance, and age-appropriate topical nasal anti-inflammatory sprays should be tried before surgery is contemplated. Because such infections are so common, antibiotics given for chronic nasal discharge often have short-lived effects. Rhinorrhea, snoring, mouth breathing, nasal obstruction, and hyponasal speech are very common symptoms in childhood. Mucosal hypertrophy is very common and this is illustrated by Gwaltney’s findings that 95% of subjects with a history of a recent viral upper respiratory tract infection, with no preceding problems, had changes

in their sinuses on CT scans (Fig. 3.41) (Gwaltney et al 1994). The main factors that influence pediatric symptoms are the frequency of upper respiratory tract infections, the relatively immature immune system present in children, the prevalence of allergic rhinitis, and adenoidal hypertrophy. Infection on its own is not an adequate explanation for the protracted inflammation which some children have in their paranasal sinuses. Wald in 1995 said “The primacy of infection as the pathophysiologic explanation for continued inflammation of the paranasal sinuses is quite unlikely” and that remains the case today. It is worth explaining to parents that children aged 2 to 5 years average eight upper respiratory tract infections a year (Wald 1992). In a Dutch study, parents of 228 out of 1000 children reported that their child had had a cold or flu during the single 3-week study period. Awareness of these figures alone will often do much to reassure parents (Bruijnzeels et al 1998). In an acute viral rhinitis there is often fever, malaise, and possibly a cough with a serous nasal discharge at first, which then becomes mucopurulent before settling spontaneously in ~ 10 days. However, up to 13% of children aged 1 to 3 years will have symptoms for more than 15 days (Wald et al 1991).

Fig. 3.39  Children below the age of 6 years average eight upper respiratory tract infections a year. Clear periods between infections will help to distinguish upper respiratory tract infections from other causes of rhinosinusitis.

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3  Who? Optimizing Diagnosis and Selection of Patients for Surgery

a

c Fig. 3.40a–c  The adenoid usually involutes before 7 years of age. a

Adenoidal hypertrophy: this usually involutes without intervention by the age of 8 years. b,c Lateral soft tissue plain radiographs, found by chance, of the same child over several years showing natural involution of the adenoid (we no longer perform plain lateral soft tissue radiography).

b

Children under the age of 3½ years rarely blow their nose and stagnant secretions collect in the nasal airway only for those in the nasal vestibule to become colonized with nasal commensals that discolor them. If swabs are taken from the middle meatus in these children and the secretions cultured, the majority do not culture anything. Culturing purulent secretions rarely contributes to management. A study of the bacteriology of purulent secretions obtained under endoscopic control from the sinus ostia or cavity in 394 patients with chronic rhinosinusitis and 139 controls showed no difference in the positive culture rate between these two groups (Klossek et al 1998). The prevalence of allergic rhinitis in children is ~ 20%. While most parents recognize hay fever or seasonal allergic rhinitis, few are aware that many children who have allergic rhinitis have symptoms all year round because

44

Fig. 3.41  A computed tomography scan of an asymptomatic child having the investigation for an unrelated reason, showing coincidental mucosal changes—a common finding.

they are allergic to perennial allergens such as house dust mites or pet allergens.

Disease-oriented Patient Selection Adenoidal hypertrophy is common with a tendency to spontaneous involution by the age of 8 to 10 years. The symptoms and signs that parents mention include snuffles in a baby, snoring, mouth breathing, feeding problems, bad breath, cough, and hyponasal speech. The parents are often very concerned while the child often appears unperturbed about their symptoms. Facial pain and headache are very rare symptoms in children with rhinosinusitis. One useful question is “Does the child have any periods when their nose is clear, or do they have persistent symptoms week after week?”. If they have periods when they are clear it is more likely that they fit into the category of having multiple upper respiratory tract infections (see Fig. 3.39). If they are never clear then it is worth asking about symptoms that indicate that perennial allergic rhinitis may be part of the problem. Do they have asthma, sneeze a lot, have itchy eyes, or is there a family history of seasonal asthma or rhinitis, as these features are associated with allergic rhinitis? Another common factor contributing to persisting symptoms is adenoidal hypertrophy but it is difficult to differentiate this from perennial allergic rhinitis on the basis of symptoms alone. A child who mouth breathes is often labeled as having adenoidal hypertrophy but a child with turbinate hypertrophy due to an allergic rhinitis can look the same. A history of more than four sneezing bouts a day, particularly in the morning, and a family history of seasonal rhinitis or asthma make a diagnosis of allergic rhinitis more likely and a trial of topical nasal steroids worthwhile, although compliance under the age of 6 is poor. If snoring is a major problem it is worth asking if the child regularly stops breathing for more than 10 seconds, even when they do not have an active respiratory tract infection, as this raises the possibility that they may have sleep apnea and this needs further investigation. A unilateral smelly nasal discharge means that a foreign body should be excluded. Gastroesophageal reflux has been implicated as a possible contributing factor in rhinosinusitis, but this has yet to be proven as both conditions are common and their coexistence may be coincidental. Nasal symptoms do not cause eating problems that would directly reduce a child’s intake, although a loss of sense of smell reduces their ability to taste.

have a unilateral antrochoanal polyp, another third have polyps secondary to an infective process that is associated with the mucus retention that occurs in cystic fibrosis, and the remainder are associated with a range of inflammatory conditions, although many remain idiopathic. In one series the etiology of pediatric polyposis was idiopathic in 55% (Triglia et al 1992). Unilateral polyps are most commonly due to an antrochoanal polyp but other pathology such as an encephalocele, inverted papilloma, hemangioma, angiofibroma, nasal glioma, or malignancy must be excluded (Fig. 3.42).

Clinical Signs

If allergy is suspected, skin tests can be performed in children after about the age of 5 years in those who are unperturbed by the test. This test has very good specificity and moderately good sensitivity. It not only helps the clinician but illustrates to the parents and older child the allergens that are responsible. It illustrates that surgery will not cure this aspect of the problem. The main perennial allergens are house dust mite and pet proteins. An alternative is to test for specific IgE, especially in children who are taking antihistamines or who have eczema or dermatographism.

It is said that very pale or boggy bluish turbinate mucosa is indicative of an allergic rhinitis but this is an unreliable sign and does not allow differentiation between the allergic, infective, or postinfective states. Nasal polyps in children are uncommon. The term “a nasal polyp” is not a diagnosis but a sign of inflammation of the lining of the nose that can be the result of a range of significant diseases. Most pediatric nasal polyps appear to be the result of inflammation. Approximately a third

Fig. 3.42  Sagittal magnetic resonance image showing an encephalocele in an infant with a unilateral polyp.

Antrochoanal polyps result from mucosal retention cysts in the maxillary sinus that have prolapsed through either the infundibulum or accessory ostia. The best way of reducing the chances of them recurring is to remove the mucosa around their base so that scar tissue forms. A strategy to manage nasal polyps is outlined in Fig. 3.43.

Investigations

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3  Who? Optimizing Diagnosis and Selection of Patients for Surgery

Unilateral

Pediatric nasal polyps

CT

Antrochoanal polyp Remove, including base of polyp Encephalocele MRI Resect and repair defect Biopsy Further management based on histology and staging Tumor

History of cystic fibrosis

Macrolide antibiotic + topical nasal steroids (often poor response)

Surgery + douching (high rate of recurrence)

No cause found Bilateral

No history of cystic fibrosis

Investigate for primary ciliary dyskinesia, immunodeficiency, allergic aspergillosis and treat appropriately

Fig. 3.43  Algorithm for the management of pediatric nasal polyps.

Nasal endoscopy has little to offer in a child under ~ 8 years as visibility is often restricted and it can upset the child. CT is not indicated in most patients given the prevalence of incidental findings (~  50%). Its use is restricted to the complications of sinusitis or when an atypical infection or tumor is suspected. Anatomical variations appear to play little if any role in the prevalence of pediatric sinusitis and this is shown in a study by Willner et al 1997, who found that anatomical “abnormalities” appear to be a range of normal variations that did not correlate with disease.

Treatment In children who do not respond to conservative management or who repeatedly fail to improve, even temporarily with medical management, it is worth considering whether there is an immunologic defect or an abnormality in mucociliary clearance. Reduced levels of immunoglobulins to pneumococcal, Haemophilus or tetanus antigen are a marker of reduced immunity. Vaccination can be given and then the antibody titers are retested after 1 month to see that they are in the normal range. If not, a referral to an immunologist is indicated. If a child has persistent lower as well as upper respiratory tract problems it is worth testing their peak flow in case they have asthma. If they develop bronchiectasis, persistent purulent sinusitis and middle ear effusions, or persistent discharge through a grommet, primary ciliary dyskinesia should be considered.

46

Studies of the natural history of persistent purulent rhinorrhea unresponsive to treatment have produced the useful information that by the age of 7 over 95% had resolved without any further action (Otten et al 1991). Antibiotics make very little difference other than in the short term.

Endoscopic Sinus Surgery in Children Endoscopic techniques can reduce the surgical morbidity and achieve better symptomatic control than conventional surgery in cystic fibrosis, allergic fungal sinusitis, antrochoanal polyp, mucoceles, repair of cerebrospinal fluid leaks, intracranial complications, mucopyoceles, a periorbital orbital abscess, traumatic injury to the optic canal, fibrous dysplasia causing optic nerve decompression, dacryocystitis, choanal atresia, unilateral fungal sinusitis, some meningoencephaloceles, and some neoplasms. Few studies of endoscopic sinus surgery in children treated for rhinosinusitis report more than an 80% improvement in symptoms and when these results are compared with the reported improvement that occurs without any treatment (Otten et al 1992), surgery does not compare favorably. The adage of primum non nocere or “first, do no harm” should underlie the management of pediatric sinusitis. Rhinosinusitis in children is not a surgical disease; “watchful waiting” is advised. Any treatment should have

Summary

a

b Fig. 3.44a,b  Surgery is not always indicated. a A patient with bilateral nasal polyps visible at endoscopy, but who is asymptomatic.

b A patient with allergic rhinitis whose symptoms are unlikely to be helped by surgery.

safety as its first priority, as the problem usually resolves over time without intervention. It is likely that growth and maturation of the immunologic response to pathogens play a major role in resolution of the disease (Jones 1999a; Howe and Jones 2004). There is no evidence that the majority of children who have persistent symptoms attributed to rhinosinusitis develop into adults with chronic sinus disease (the exceptions are those with cystic fibrosis, ciliary dyskinesia, and immunodeficiencies). The first-line treatment should involve harmless measures such as teaching nose blowing, saline sprays, short courses of topical decongestants, and, probably most of all, an explanation to the parents. Allergen avoidance in children with coexisting allergic mucosal disease may help, as will regular topical nasal steroids for symptoms of obstruction and nonsedative antihistamines for itchy eyes, sneezing, and rhinorrhea. In the rare situation when antibiotics are given for purulent nasal secretions they should be given with the expectation that reinfection is likely to occur within the next few weeks. The place of radiology in the management of children with rhinosinusitis is very limited and is confined to the few who develop the complications of sinusitis or in whom a tumor or atypical infection are suspected.

findings. Beware that patients often expect that all their symptoms will be cured by surgery, even those symptoms that they have not mentioned. Be sure to clarify those

Summary Who Not to Select for Surgery Never coerce any patient into having surgery for rhinosinusitis (Fig. 3.44a,b). The patient has to want to proceed, knowing what can realistically be achieved and what risks are involved. At the same time, do not be forced into operating by a patient who has unrealistic expectations and whose symptoms do not correlate with clinical

Fig. 3.45  The skyscraper analogy helps to explain the “ups” and “downs” of controlling nasal symptoms through the medical and surgical treatment of rhinosinusitis. The surgeon can use this illustration to explain symptom goals to patients.

47

3  Who? Optimizing Diagnosis and Selection of Patients for Surgery symptoms that may be helped and those that are unlikely to improve. Patients occasionally have sizable nasal polyps without any symptoms. Before operating, you would be well advised to manage these patients medically, delaying surgery until they develop symptoms.

Patient Expectations Finally, we need to make sure that patients understand that it is usually not possible to cure them of their polyps forever or to eradicate all their symptoms. We explain to our patients that their symptoms are like a person trying to get from the ground floor of a skyscraper to the top floor in order get a good view. On the ground floor, they feel blocked, with a poor sense of smell and postnasal mucus. Medical treatment can get them up a few flights of stairs, and oral steroids may get them near the

48

top in a lift, but the lift often comes down again. Surgery together with medical treatment will help them to get a better view for a longer period, but it will not necessarily get them to the top floor (Fig. 3.45). While symptoms of obstruction are often greatly improved, those of a sensation of postnasal discharge may well not be altered. Hyposmia is often improved if the mucosa in the olfactory cleft is preserved and medical treatment is continued. Only a minority of patients with nasal polyps have symptoms of pain or pressure. If their symptoms are exacerbated by a respiratory tract infection or a change in barometric pressure, they are more likely to benefit from surgery. Be cautious if their pain or pressure does not have these features, as it may be incidental and not helped by surgery.

4  When? Medical Treatment and Timing of Surgery Having made the diagnosis and tried medical treatment, and, importantly, excluded patients who are not suitable for surgery, the goal is to prepare the patient for surgery. For the timing of surgery, it is important to maximize medical treatment just before operating so that the patient’s mucosa is as healthy as possible. This will not only help the patient’s symptoms but also minimize inflammation if surgery is required, and help access and reduce intraoperative bleeding. For example, in polyposis a course of oral steroids in the 5 days before surgery will considerably reduce the amount of bleeding as well as increase access and visibility. In patients with an untreated bacterial infection, surgery will result in a more bloody and difficult operation. Even if antibiotics have been unable to eradicate all infection it is best to reduce the bacterial load as much as possible, and hence inflammation and propensity to bleed preoperatively. Steroids and macrolide antibiotics can also reduce the amount of inflammation and perioperative bleeding. Treating any allergic component will minimize the amount of “hyperreactivity” of the mucosa. This will reduce the amount of exudate that forms after surgery, lessen the formation of adhesions, and help the preservation of olfactory mucosa.

a

Optimizing Medical Treatment Before Surgery The Management of Chronic Rhinosinusitis with Polyposis The majority of patients with nasal polyposis respond to medical treatment. The main treatment of idiopathic nasal polyposis comprises topical nasal steroids, douching and the treatment of any bacterial infection if there are any purulent secretions (Fig. 4.1a,b). If topical nasal steroids fail, oral steroids should be tried unless there are contraindications. In patients with gross polyposis, we often give oral steroids initially, not only to help the patient immediately but also to see “how far up the skyscraper they can go” (Fig. 4.2). The use of macrolide antibiotics for 3 months has been shown to be of benefit in many patients (Lund 2005; Aouad and Chiu 2011; Fokkens et al 2012) (Table 4.1). Patients who have failed medical treatment and are to have surgery still require maximum medical treatment just before their surgery. This comprises douching, antibiotics if there is any infective component, and, most importantly, systemic steroids. It is important that

b Fig. 4.1a,b  A patient with recurrent polyposis after previous surgery who had a coexisting infection and responded to antibacterial treatment and topical nasal steroids.

patients know how to douche, not only to prepare the nose preoperatively, but also to get them into the habit of doing it as they will need to do it postoperatively. Douching is very important to help clear altered blood and mucus from the mucosa until the cilia recover.

The Use of Systemic Steroids Systemic steroids are normally reserved for patients with rhinosinusitis and polyposis, although they can help those patients with allergic rhinitis who are resistant to other forms of treatment. We give only short courses of oral steroids so as to minimize side effects. Normally, topical nasal steroids, along with allergen avoidance and antihistamines, will control symptoms

49

4  When? Medical Treatment and Timing of Surgery circumstances, oral steroids may reverse the mucosal edema, but the degree of success varies, as does the duration of the improvement. The reasons for using oral steroids in rhinosinusitis with nasal polyposis are: —— To reduce polyp bulk, allowing access for topical steroids —— To determine the extent of the “olfactory reserve” —— To preoperatively help reduce mucosal inflammation.

Fig 4.2  Skyscraper illustrating levels of treatment success. We use this illustration when discussing treatment options with patients.

(Fig. 4.3a,b). However, a small group of patients do have symptoms such as mucosal edema that persist even when they have complied with treatment for over 8 weeks. This is more common in nonallergic patients, particularly those with late-onset asthma. Under these

In the majority of patients, the effect of a trial of oral steroids is variable, in spite of maintenance treatment with topical steroids. Some patients respond very well and for a long time, whereas others may be helped for only a short period. In these patients, surgery may help if obstruction or hyposmia are their main symptoms, although it is vital that the patient is aware that surgery is not a “cure” for their mucosal disease. If surgery is planned, a further course of preoperative steroids will reduce bleeding and the level of surgery required. By allowing more mucosa to be preserved, particularly in the olfactory cleft, adhesions will be minimized and postoperative recovery will be improved as ciliary recovery will be better. In patients with marked allergic or nonallergic rhinitis, in whom other treatments have failed or in the immediate preoperative period, a dose of 30 to 70 mg (depending on body mass) of prednisolone with breakfast (for 4 to 7 days) is recommended as a means of maximizing the anti-inflammatory component of medical treatment of nasal polyposis (Figs. 4.4a,b, 4.5a,b, 4.6). It is important to check that there are no contra­ indications (diabetes, cardiac disease, gastric or duodenal ulcers, osteoporosis, etc.). Patients should be warned of the potential side effects: patients sometimes become

Table 4.1  Treatment evidence and recommendations for adults with chronic rhinosinusitis with and without nasal polyposis (adapted from Fokkens et al 2012)

Chronic rhinosinusitis with polyposis

Chronic rhinosinusitis without polyposis

Therapy

Level of evidence

Grade of recommendation

Relevance

Level of evidence

Grade of recommendation

Relevance

Oral antibiotic  6 months in spite of topical treatment. With opening of the olfactory cleft (see text), the results are better Mucus:  Disappointing Pressure or pain:  Rarely a symptom except in cases of acute infection; this is helped

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6  Why? The Goals of Surgery

a

b Fig. 6.1a,b  Endoscopic views showing mucosal response to treatment. a Preoperative views before sphenoethmoidectomy.

b Postoperative views after sphenoethmoidectomy—this illustrates many of the goals listed.

Rationale and Goals of Surgery in Specific Conditions The reasons for surgery in specific conditions other than rhinosinusitis are more straightforward and are listed below.

Periorbital Abscess —— Drainage of pus defined on computed tomography (Fig. 6.3a,b).

Barotrauma —— Ventilate the sinus and preserve mucosa at all cost.

Choanal Atresia

Fig. 6.2  Root canal filling material within the maxillary sinus associated with a persistent fetid purulent discharge.

of inflammatory mediators or reduced immunity. There may be a genetic predisposition, e.g., atopy and allergic rhinitis, or in a few cases an inherited immunodeficiency; but in many there are inflammatory changes that are poorly understood, e.g., late-onset asthma and polyposis. Clearly surgery cannot stop these inherent inflammatory disease processes.

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—— Endoscopes aid access and visibility to allow an adequate airway and create space. —— Cause as little trauma as possible to the mucosa (Fig. 6.4a,b).

Epistaxis —— Localizing the site of bleeding is of the utmost importance. —— Avoid packing as this causes trauma to the nasal mucosa, making it difficult to find the site (Fig. 6.5a,b). —— A primary aim is to occlude the vessel near its distal site ( Videos 10, 11).

Rationale and Goals of Surgery in Specific Conditions

a Fig. 6.3a,b  A left periorbital abscess (a), also shown on axial computed tomography (b). b

a

b Fig. 6.4a,b  Surgical view of left choanal atresia in a newborn child with bilateral atresia.

Distal Nasolacrimal Duct Obstruction —— A dacryocystorhinostomy creates a nasal fistula or rhinostomy in distal nasolacrimal duct obstruction (Fig. 6.6a–c). —— A dacryocystorhinostomy is not effective in the presence of coexisting proximal obstruction. —— A dacryocystorhinostomy may help functional outflow obstruction to a moderate extent.

Unknown Pathology/Biopsy —— Histology is vital to make the right treatment plan (Diamantopolous et al 2000) (Fig. 6.7a–g).

—— Endoscopic access and visibility are often best at visualizing and removing diseased tissue (Howard and Lund 1993). —— Studying the computed tomography image helps to define the site for biopsy while magnetic resonance imaging (MRI) helps to differentiate secretions from soft tissue (Fig. 6.8a,b). —— Inflammatory polyps occur around a malignancy so it is important to avoid sampling only these. —— Endoscopic biopsy is associated with less morbidity than an external approach in many circumstances, e.g., the pterygopalatine fossa or orbit. —— An exception is an angiofibroma, where preoperative histology is not required because its MRI features are diagnostic (Fig. 6.9a,b).

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6  Why? The Goals of Surgery

a

b Fig. 6.5a,b  Torrential epistaxis (arrow) from one branch of the sphenopalatine artery stopped by endoscopic cautery.

b

a Fig. 6.6a–c  Epiphora due to a dacryolith in the nasolacrimal sac.

c

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Rationale and Goals of Surgery in Specific Conditions

a

b

c

d Fig. 6.7a–g  Biopsy is key in establishing a diagnosis. e

a Patient 1. A harmless-looking polyp in the right middle meatus. b A computed tomography image of the harmless-looking polyp in (a), which proved to be an adenocarcinoma. c Patient 2. Lymphoma of the left orbit that also produced a nasal polyp. A biopsy of this helped make the diagnosis. d Coronal computed tomography scan of this patient. e Patient 3. Facial appearance showing displacement of right eye. Fig. 6.7f–g  ▷

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6  Why? The Goals of Surgery ◁ continued

f f Endoscopic appearance. g Magnetic resonance image of a melanoma in the right paranasal sinuses that presented with epiphora and epistaxis.

g

a

b Fig. 6.8a,b  MRI helps to define where the tumor is as opposed to secretions. a Coronal computed tomography scan of left-sided inverted papilloma showing uniform opacification of the paranasal sinuses.

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b Magnetic resonance imaging in the same patient, clearly defining where the inverted papilloma are based.

Rationale and Goals of Surgery in Specific Conditions

a

b Fig. 6.9a,b  Angiofibroma. a Sagittal magnetic resonance imaging of an angiofibroma showing voids where there are vessels.

b Axial magnetic resonance imaging showing the tumor coming from the sphenopalatine area.

Benign Tumors

the lesion and the risk of complications needs to be weighed up very carefully. This is particularly important in a tumor that is close to the carotid artery, cavernous sinus, optic nerve or orbital apex, e.g., fibrous dysplasia, chordoma, osteoma at the orbital apex or adjacent to the carotid artery. —— An endoscopic approach often reduces the morbidity of surgery, and access and visibility can be helped with magnification and angled lenses.

—— Ensure total resection is achievable endoscopically, or warn the patient if an external approach may be needed (Fig. 6.10a,b). —— Endoscopic postoperative monitoring helps to detect any recurrence. —— Although in benign disease complete removal is the goal, this may not be achievable in some instances. The balance between the completeness of removal of

a

b Fig. 6.10a,b  Adenoameloblastoma. a Adenoameloblastoma that originated from the right maxilla, for which a lateral rhinotomy or midfacial degloving may be needed to complete the resection.

b A biopsy can be obtained endoscopically with less morbidity, but external approaches are occasionally needed for resection.

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6  Why? The Goals of Surgery —— There are circumstances when an external approach is warranted or should remain an option for the surgeon to convert to (large angiofibroma, skull base tumors where the extent of intracranial extension/dural invasion is uncertain) (Fig. 6.11a,b).

Mucoceles —— The primary goal is marsupialization and not enucleation. —— Wide drainage with preservation of mucosa around the lumen to reduce the incidence of stenosis and reformation (Fig. 6.12a,b). —— If accessible, endoscopic drainage provides less morbidity.

b Fig. 6.11a,b  An external approach is sometimes warranted. a Axial magnetic resonance imaging of a clival chordoma. Note its proximity to the basilar artery. b Endoscopic operative view of the basilar artery; the chordoma was removed using a lateral suboccipital endoscopic approach in conjunction with a transnasal endoscopic approach.

a

a Fig. 6.12a,b  Characteristic appearance of a left frontal mucocele. a Clinical view. b Computed tomography views showing a left frontal mucocele. b

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Rationale and Goals of Surgery in Specific Conditions

Antrochoanal Polyp —— Remove the entire polyp along with its stalk and, importantly, its base to stop recurrence (Fig. 6.13a,b).

a

a

b

b Fig. 6.13a,b  Features of an antrochoanal polyp. a Axial computed tomography scan. b Endoscopic view of an antrochoanal polyp that has extended into the nasopharynx and oropharynx.

Inverted Papilloma —— The key goal is to remove all macroscopic disease. —— This tissue must be examined for atypia or malignancy. Malignant transformation is rare if there is no evidence of atypia or malignancy in the resected tissue (Mirza et al 2007) (Fig. 6.14a–c). —— You need to inform the patient if external access may be needed, e.g., disease within the lateral aspect of the frontal sinus (MRI preoperatively helps to differentiate inverted papilloma from retained secretions; Video 12).

c Fig. 6.14a–c  Inverted papilloma. a Endoscopic view of right inverted papilloma. b Coronal magnetic resonance imaging in the same patient. c The specimen should be checked for any evidence of atypia or malignancy.

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6  Why? The Goals of Surgery

Malignant Tumors —— The old idea that an “en bloc” resection is mandatory has been discredited. It is now appreciated that even with the widest craniofacial approach this rarely happened and that skull base tumors were picked off the periorbita, dura, or bony remains of the skull base. It is now accepted that in most circumstances it is possible to obtain as much, if not better, surgical clearance with the benefit of magnification using endoscopes (Fig. 6.15a–c). —— The ability to resect and repair large areas of the skull base and periorbita endoscopically allows many skull base tumors to be removed endoscopically (Fig. 6.16a–d). —— There are circumstances when an external approach may be needed and the surgeon should be able to convert to this approach (large angiofibroma, skull base tumors where the extent of dural invasion is uncertain because MRI can overstage the extent of disease but not always).

a

Repair of Dural and Skull Base Defects —— Confirm that it is a true cerebrospinal fluid leak (b2-transferrin) (Fig. 6.17a–c). —— The etiology of the CSF leak needs to be considered, especially in spontaneous leaks because there may be a high-pressure system that needs treating. —— Precisely localize the defect. —— Endoscopic multilayered occlusion gives the best results. —— Tell patients with defects in the lateral part of the frontal sinus that they may need an external approach. —— May not be suitable if there is an associated malignancy. —— High-pressure leaks (normally in the group of patients with a spontaneous leak) may also need a shunt ( Videos 13, 14).

b

Pituitary Surgery —— To provide access and visibility for tumor removal ( Video 15).

Decompression of the Orbit —— The orbit may require decompression for cosmetic reasons. —— Decompress the orbital contents to stop damage from corneal exposure, reduce pain, or if optic nerve function is compromised (Fig. 6.18a,b). —— Helps in dysthyroid eye disease with reducing vision when steroids and radiotherapy fail.

c Fig. 6.15a–c  a Endoscopic view of right paranasal sinus adenocarcinoma. b Coronal magnetic resonance imaging of the same patient. c Postoperative view 4 years after surgery.

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Rationale and Goals of Surgery in Specific Conditions

a

b

c Fig. 6.16a–d  a The whole of the anterior skull base has been removed along with an aesthesioneuroblastoma. b Fascia lata placed over the defect. c Postoperative view 2 years later.

Decompression of the Optic Nerve —— Carry out early in the presence of reduced vision after trauma to the optic nerve when there is disruption of its bony surround. —— Visual evoked potentials are important as a useful objective test in lightly anesthetized or unconscious patients (Jones 1997) (Fig. 6.19a–c). —— If there is no significant bony disruption then surgery has as yet to be shown to have any benefit over systemic steroids.

d d Sagittal computed tomography scan—note the pedicle of the posteriorly based vascular flap.

Penetrating Injuries of the Skull Base —— Having ensured that any penetrating objects are not abutting into intracranial vessels, they can be removed if there is ready access to neurosurgical and interventional neuroradiologic assistance. —— Repair the defect.

77

6  Why? The Goals of Surgery

«

+

b

a Fig. 6.17a–c  Cerebrospinal fluid leak. a Clear unilateral rhinorrhea due to a cerebrospinal fluid leak. b Endoscopic view of the left sphenoidal sinus showing a cerebrospinal fluid leak from the sphenoidal sinus between the optic nerve («) and carotid artery (+). c Axial computed tomography scan showing the same defect (arrow) as in (b) but with a fluid level of cerebrospinal fluid.

c

a

b Fig. 6.18a,b  Decompression of the orbit. a Bilateral proptosis in dysthyroid eye disease at danger from corneal ulceration.

78

b Coronal magnetic resonance image showing muscle hypertrophy due to dysthyroid eye disease.

Quality of Life

Quality of Life Chronic rhinosinusitis has a significant adverse effect on patients’ perception of quality of life (Gliklich and Metson 1995). Over the last few years, there has been an increasing realization that improving nasal symptoms has a dramatic effect on patients’ enjoyment of life that goes far beyond the nose (Fig. 6.20). Discussion of this issue is also important in convincing healthcare providers that sinus surgery is of great value. Endoscopic sinus surgery for chronic sinusitis results in an improvement in a general indicator of health, namely the SF-36 “Health Survey Questionnaire,” as well as in disease-related symptoms (Winstead and Barnett 1998). The greatest negative general health impact of chronic rhinosinusitis in the study by Winstead and Barnett was on bodily pain, social functioning, and vitality when compared with a control group. These criteria were improved 12 months after surgery, along with physical functioning, mental health, and emotional status. Endoscopic sinus surgery has also been shown to improve pulmonary function in patients with asthma and chronic rhinosinusitis (Ikeda et al 1999), with an improvement in their average peak expiratory flow and a reduction in their need for corticosteroids. In spite of these positive studies, we need to improve our understanding of the pathophysiology of rhinologic conditions, their definition, and the staging procedures, and to validate all of these in order for us to improve the way we compare treatment strategies.

a

b

c Fig. 6.19a–c  Decompression of the optic nerve. a Left enophthalmos, periorbital ecchymosis, and subconjunctival hemorrhage secondary to a fracture of the medial wall of the orbit. b An axial computed tomography scan showing disruption of the medial wall of the orbit toward its apex (arrow). c Perioperative endoscopic view showing the bony spicule that was pressing on the optic nerve.

Fig. 6.20  A smell scientist testing new odors.

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7  Applied Anatomy for Endoscopic Sinus and Skull Base Surgery In collaboration with Hans Rudolf Briner Surgery of the paranasal sinuses and the adjacent orbit and skull base requires a thorough knowledge of anatomy. Anatomical landmarks allow a surgical procedure to be performed in a step-by-step manner, which means that the dissection and the resection of tissue should only be continued after identifying the anatomical landmarks in the area that is approached. This anatomical landmarkorientated step-by-step principle helps the surgeon to navigate in the surgical field and reduces the risk of causing complications by preventing a loss of orientation. This chapter focuses on the anatomical landmarks and the anatomical areas at risk that are important for the surgeon for the following anatomical regions: —— Ethmoidal infundibulum —— Maxillary sinus —— Anterior ethmoid —— Posterior ethmoid —— Sphenoidal sinus —— Frontal sinus —— Pterygopalatine fossa —— Cavernous sinus —— Pituitary gland —— Cribriform plate.

Ethmoidal Infundibulum —— Landmarks: –– Anterior superior insertion of the middle turbinate (axilla of the middle turbinate) –– Nasolacrimal duct –– Posterior edge of uncinate process –– Natural ostium of the maxillary sinus. —— Areas at risk: –– Lamina papyracea and orbit lateral to the uncinate process –– Lacrimal sac and duct. The first step in sinus surgery is usually to open the ethmoidal infundibulum (infundibulotomy). To perform an infundibulotomy, the inferior and middle part of the uncinate process has to be identified and resected. The anatomical landmarks defining the superior and anterior borders of the approach to this area are the anterior superior origin (axilla) of the middle turbinate and the nasolacrimal duct, the latter being covered by part of the frontal process of the maxillary bone and the lacrimal bone (Fig. 7.1). The next landmark is the posterior border of the uncinate process, which sometimes becomes visible only after gentle medialization of the middle turbinate (Fig.

80

Fig. 7.1  Anterior superior origin or axilla of the right middle turbinate (ball probe) and position of the nasolacrimal duct (arrow). Right nasal airway.

7.2). The posterior edge of the uncinate process is often readily visible but sometimes it “fades away” because its edge turns laterally out of view. When this is the case it is best to check its position by palpating it with the end of a ball probe to locate it. After resection of the uncinate process, the natural ostium of the maxillary sinus becomes visible. It is located just lateral to the sagittal plane where the uncinate process inserts into the lacrimal bone (Fig. 7.3). Structures at risk are the lamina papyracea and the adjacent orbit as well as the lacrimal sac and duct (especially if backbiting forceps are used to remove more than Videos 16, 17). the uncinate process) (Fig. 7.4;

Maxillary Sinus —— Landmarks: –– Insertion of the uncinate process –– Anterior lacrimal crest –– Natural ostium of the maxillary sinus –– Accessory ostium of the maxillary sinus (if present) –– Ethmoidal bulla –– Lamina papyracea –– Floor of the orbit –– Insertion of the inferior turbinate at the medial wall of the maxillary sinus.

Maxillary Sinus

Fig. 7.2  Posterior border of uncinate process at the end of the ball probe. The middle turbinate is gently medialized by the shaft of the ball probe. Right nasal airway.

Fig. 7.3  Natural ostium of the maxillary sinus, which becomes visible after resection of the uncinate process. Right nasal airway.

Fig. 7.4  Position of the lamina papyracea and orbit (ball probe), and the area of lacrimal sac and duct (arrow). Right nasal airway.

Fig. 7.5  The ethmoidal bulla. Right nasal airway.

—— Areas at risk: –– Lamina papyracea and adjacent orbit –– Nasolacrimal duct –– Maxillary branch of sphenopalatine artery.

ostium of the maxillary sinus, which is found posterior to the natural ostium; however, it is not always present. There is a risk of misinterpreting the accessory ostium as the natural ostium. If an ostium is seen when there has not been any previous surgery it is likely to be an accessory ostium. An opening is rarely seen in the uncinate process, just anterior and medial to the natural ostium of the maxillary sinus. A constant landmark is the ethmoidal bulla, which is the first cell posterior to the uncinate

The main landmark to approach the maxillary sinus is its natural ostium, which lies just lateral and posterior to the insertion of the uncinate process at the anterior lacrimal crest (Fig. 7.3). Another landmark can be an accessory

81

7  Applied Anatomy for Endoscopic Sinus and Skull Base Surgery process and it is inserted into the lamina papyracea at the medial part of the orbit (Figs. 7.5 and 7.6). Following the lamina papyracea inferiorly, it turns into the floor of the orbit, which is the roof of the maxillary sinus (Fig. 7.7). The insertion of the inferior turbinate usually determines the level of the inferior border of the maxillary

sinus opening at the medial wall of the maxillary sinus (Fig. 7.8). Structures at risk are the lamina papyracea with the adjacent orbit, the nasolacrimal duct, and, lying in the medial wall of the maxillary sinus, the maxillary branch of the sphenopalatine artery (Fig. 7.9).

Fig. 7.6  Lamina papyracea (after resection of the ethmoidal bulla). Right nasal airway.

Fig. 7.7  Floor of the orbit. Right nasal airway.

Fig. 7.8  Area of the insertion of inferior turbinate at the medial wall of the maxillary sinus. Right nasal airway.

Fig. 7.9  The site of the maxillary branch of sphenopalatine artery. Right nasal airway.

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Posterior Ethmoid

Anterior Ethmoid —— Landmarks: –– Natural ostium of the maxillary sinus –– Floor of the orbit –– Ethmoidal bulla –– Basal lamella –– Anterior ethmoidal artery –– Roof of the ethmoid. —— Areas at risk: –– Lamina papyracea and adjacent orbit –– Anterior ethmoidal artery –– Roof of the ethmoid –– Lamella lateralis of the ethmoid and cribriform plate –– Maxillary branch of the sphenopalatine artery.

is made of frontal bone). The lamella lateralis is located between the roof of the ethmoid and the superior origin of the middle turbinate (Fig. 7.12) and an injury here may induce a cerebrospinal fluid leak ( Videos 18, 19, 20).

Posterior Ethmoid —— Landmarks: –– Basal lamella –– Lamina papyracea –– Dorsal wall of maxillary sinus –– Ethmoidal crest

Proceeding on from the anatomical landmarks of the maxillary sinus, additional landmarks are the ground lamella, which is formed where the middle turbinate inserts into the lateral nasal wall and forms the division between the ethmoid into anterior and posterior ethmoidal cells (Fig. 7.10). The anterior ethmoidal artery is often located in the ethmoidal roof and occasionally is running “free” through the anterior ethmoidal sinuses, especially when the supraorbital ethmoidal cells are well pneumatized (Fig. 7.11). Other structures at risk include the maxillary branch of the sphenopalatine artery that runs forward from the base of the insertion of the middle turbinate into the lateral nasal wall and forward to supply the inferior and middle turbinate, the lamina papyracea with the adjacent orbit, the ethmoidal roof and anterior ethmoidal artery, and the lamella lateralis, which is the very thin bone that joins the cribriform plate to the fovea ethmoidalis (the roof of the ethmoidal sinuses but

Fig. 7.11  Roof of the ethmoid containing the anterior ethmoidal artery travelling medially as it comes anteriorly. Right nasal airway.

Fig. 7.10  Ground lamella. Right nasal airway.

Fig. 7.12  Lamella lateralis of the ethmoid. Right nasal airway.

83

7  Applied Anatomy for Endoscopic Sinus and Skull Base Surgery –– Sphenopalatine foramen –– Anterior wall of the sphenoid –– Natural ostium of the sphenoid –– Roof of the ethmoid. —— Areas at risk: –– Roof of the ethmoid –– Lamina papyracea and orbit –– Optic nerve –– Sphenopalatine artery and its branches –– Carotid artery. The ground lamella and the lamina papyracea define the anterior and posterolateral borders of the posterior ethmoid. The posterior wall of the maxillary sinus (Fig. 7.13) helps to define the coronal plane of the sphenopalatine foramen, which will be just posterior to this. Another useful landmark is the ethmoidal crest, which is positioned where the bone of the middle turbinate joins the palatine bone anterior to the sphenopalatine foramen (Fig. 7.14). Its triangular shape helps to find the sphenopalatine foramen, which is located immediately posterior to the ethmoidal crest. The anterior wall of the sphenoid, with its natural ostium, and the roof of the ethmoid define the posterior and superior borders of the sinuses (Fig. 7.15). Structures at risk in this area are the lamina papyracea with the orbit, the optic nerve, and the roof of the ethmoid (Fig. 7.16). Other risk areas are the branches of the sphenopalatine artery in the sphenopalatine foramen just posterior to the crista ethmoidalis (Fig. 7.14), and the carotid artery in the lateral wall of the sphenoid Videos 7, 8). (Fig. 7.16;

Sphenoidal Sinus —— Landmarks: –– Choana –– Posterior inferior insertion of the superior turbinate –– Anterior wall of the sphenoid –– Natural ostium of the sphenoid –– Sphenopalatine foramen. —— Areas at risk: –– Septal branch of the sphenopalatine artery –– Carotid artery

«

Fig. 7.14  Sphenopalatine vessels («) with the ethmoidal crest (ball probe). Right nasal airway.

Fig. 7.13  Posterior wall of the maxillary sinus (arrow) and position of the superior bony border of the sphenopalatine foramen (ball probe). Right nasal airway.

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Fig. 7.15  Natural sphenoidal ostium (ball probe) and anterior wall of the sphenoid (arrow). Right nasal airway.

Frontal Sinus

«

Fig 7.16  The roof of the ethmoid (ball probe), lamina papyracea (white arrow), optic nerve (black arrow), and carotid artery («). Right nasal airway.

Fig. 7.17  Posterior choana. Right nasal airway.

–– Cavernous sinus –– Optic nerve –– Pituitary gland. When the sphenoidal sinus is approached transnasally, the posterior choana is a basic landmark (Fig. 7.17). Superior to the posterior choana, the natural sphenoidal ostium is located at that level of the superior turbinate (Fig. 7.18). Approaching the sphenoid transethmoidally, the sphenopalatine foramen helps to identify the anterior wall of the sphenoid, which is located posterior and superior to the foramen (Figs. 7.14 and 7.15). Areas at risk are the septal branch of the sphenopalatine artery (Fig. 7.19) on the anterior wall of the sphenoidal sinus and the structures adjacent to the sphenoid, the cavernous sinus, Vidthe carotid artery, and the optic nerve (Fig. 7.20; eos 21, 22).

Frontal Sinus —— Landmarks: –– Anterior superior insertion of the middle turbinate (axilla of the middle turbinate) –– Lamina papyracea –– Ethmoidal bulla –– Anterior ethmoidal artery –– Roof of the ethmoid –– Lacrimal bone, lacrimal sac –– Frontal process of the maxillary bone— “frontal beak” –– Dorsal wall of the frontal sinus –– Anterior nasal artery.

Fig. 7.18  Posterior inferior insertion of the superior turbinate (arrow) and natural ostium of the sphenoid (ball probe). Right nasal airway.

—— Areas at risk: –– Lamina papyracea and adjacent orbit –– Anterior ethmoidal artery –– Roof of the ethmoid –– Lamella lateralis of the ethmoid –– Anterior nasal artery. When approaching the frontal sinus, the same landmarks are used as for the ethmoidal infundibulum and the anterior ethmoid, because most frequently it is approached through the anterior ethmoidal sinuses. The landmarks

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7  Applied Anatomy for Endoscopic Sinus and Skull Base Surgery

«

Fig. 7.19  The septal branch of the sphenopalatine artery has been injected with pink latex to help visualize it as it passes on the anterior wall of the sphenoid, just visible where a sphenoidotomy has been enlarged inferiorly. Right nasal airway.

Fig. 7.20  Position of the pituitary gland (ball probe), cavernous sinus («), carotid artery (black arrow), and optic nerve (white arrow). Right side.

Fig. 7.21  The lacrimal bone (mucosa excised) with the nasolacrimal duct (ball probe) and axilla of the middle turbinate (arrow). Right nasal airway.

Fig. 7.22  The position of the ethmoidal roof (ball probe), anterior ethmoidal artery (dark arrow), and way to the frontal sinus (white arrow). Right nasal airway.

are the anterior superior insertion of the middle turbinate (axilla), the lacrimal sac and duct with the covering lacrimal bone (Fig. 7.21), the lamina papyracea, the ethmoidal bulla, the anterior ethmoidal artery, and the roof of the ethmoid (Fig. 7.22). For more extensive approaches to the frontal sinus, such as a median drainage procedure, the nasal process of the frontal bone (“frontal beak”) is a key landmark (Fig. 7.23). It is located superior and medial to the lacrimal sac. After removing the frontal beak, the

dorsal wall of the frontal sinus becomes more visible. When resecting the floor of the frontal sinus toward the midline, another constant landmark is found, the anterior nasal artery. It is one of the final branches of the anterior ethmoidal artery and it enters the nose just anterior to the cribriform plate (Fig. 7.24). Structures at risk are the lamina papyracea with the orbit, the anterior ethmoidal artery, the roof of the ethmoid with the lamella lateralis, Video 23). and the anterior nasal artery (Fig. 7.25;

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Pterygopalatine Fossa

«

Fig. 7.23  Ball probe pointing at the frontal process of the maxillary bone (“frontal beak”) and the lacrimal sac (arrow). Right nasal airway.

Fig. 7.24  View into the frontal sinus after partial resection of the frontal beak («). Dorsal wall of the frontal sinus (black arrow), anterior nasal artery (white arrow).

—— Areas at risk: –– Maxillary artery –– Descending palatine artery –– Maxillary nerve (V2) –– Orbit –– Carotid artery.

«

Fig. 7.25  Lamina papyracea (white arrow), roof of the ethmoid («), and anterior nasal artery (black arrow).

Pterygopalatine Fossa —— Landmarks: –– Dorsal wall of the maxillary sinus –– Floor of the orbit –– Sphenopalatine foramen –– Maxillary artery –– Descending palatine artery –– Foramen rotundum with maxillary nerve (V2) –– Vidian (pterygoid) canal.

The first landmark when approaching the pterygopalatine fossa is the posterior wall of the maxillary sinus, which defines its anterior border. Its superior border is the floor of the orbit and the medial border is the sphenopalatine foramen (Fig. 7.26). After resection of the bony wall of the posterior maxillary sinus, the fat and neurovascular structures of the pterygopalatine fossa can be dissected. The maxillary artery and the descending palatine artery (Fig. 7.27) are located anterior and medial to the maxillary nerve (Fig. 7.28). At its posterior border toward the sphenoid, the foramen rotundum with the maxillary nerve, and the Vidian (pterygoid) canal with its nerve and artery are additional landmarks (Fig. 7.29). An additional anatomical structure is the palatovaginal canal (palatosphenoidal canal), which lies lateral to the Vidian canal and contains a branch of the maxillary artery that leads to the roof of the nasopharynx. Areas at risk are the neurovascular structures of the pterygopalatine fossa itself (maxillary artery, descending palatine artery), the orbit, and the carotid artery. Surprisingly, it is not always easy to differentiate the maxillary nerve from the artery within the fat of the pterygopalatine fossa.

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7  Applied Anatomy for Endoscopic Sinus and Skull Base Surgery

Fig. 7.26  View to the posterior wall of the right maxillary sinus (ball probe) after partial resection of the medial wall of the maxillary sinus. Position of the sphenopalatine foramen (black arrow), floor of the orbit (white arrow).

Fig. 7.27  View to the right pterygopalatine fossa after resection of the posterior wall of the maxillary sinus. Maxillary artery (above ball probe), descending palatine artery (arrow).

«

Fig. 7.28  Right foramen rotundum with the maxillary nerve (white arrow), orbit («), and carotid artery (black arrow).

Cavernous Sinus —— Landmarks: –– Lateral wall of the sphenoid –– Carotid artery –– Pituitary gland. —— Areas at risk: –– Carotid artery –– Optic nerve

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Fig. 7.29  Right vidian (pterygoid) canal with its nerve and artery (white arrow), foramen rotundum with maxillary nerve (black arrow).

–– Cranial nerves: oculomotor, trochlear, ophthalmic, maxillary, and abducens. The cavernous sinus is lateral to the lateral wall of the sphenoid and lateral to the pituitary gland (Fig. 7.30). It is a venous confluence of the anatomical region containing the carotid artery and the oculomotor, trochlear, ophthalmic, maxillary, and abducens cranial nerves. Therefore, the whole cavernous sinus can be regarded as an “area at risk” ( Video 24).

Pituitary Gland

«

«

Fig. 7.30  Lateral wall of the right sphenoid indicating the area of the adjacent cavernous sinus (ball probe). Carotid artery (white arrow), optic nerve (black arrow), and pituitary gland («).

Fig. 7.31  Intrasphenoidal landmarks are the dorsal wall of the sphenoid (black arrow), the intersphenoidal septum («), the convex shape of the sella (ball probe), and the planum sphenoidale (white arrow).

Pituitary Gland

pituitary gland, a constant landmark is the planum sphenoidale. An important landmark in the lateral sphenoidal sinus is the bulge of the carotid artery. The carotid artery, as well as the cavernous sinus and the optic nerve, is an Video 15). area at risk (Fig. 7.32;

—— Landmarks: –– Anterior wall of the sphenoid –– Natural ostium of sphenoidal sinus –– Dorsal wall of the sphenoid –– Intersphenoidal septum –– Sellar floor –– Planum sphenoidale –– Bulge of carotid artery in lateral wall of the sphenoid. —— Areas at risk: –– Carotid artery –– Cavernous sinus –– Optic nerve. To approach the pituitary gland, a wide sphenoidotomy is necessary. Therefore it is important to identify the anatomical landmarks for the sphenoidal sinus when approaching the pituitary gland—namely the anterior wall of the sphenoidal sinus and the natural sphenoidal ostium (see Fig. 7.18). For a wide approach, usually some of the posterior nasal septum (rostrum) has to be resected; furthermore, an anterior and posterior ethmoidectomy helps to obtain a wide access to the lateral parts of the sphenoid. Intrasphenoidal landmarks are the intersphenoidal septum (which is often asymmetric), the dorsal wall of the sphenoid, and the convex shape of the sellar floor (Fig. 7.31). Superior and anterior to the

Fig. 7.32  Structures at risk in the lateral sphenoid are the optic nerve (ball probe), the carotid artery, (black arrow), and the cavernous sinus (white arrow). Right side.

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7  Applied Anatomy for Endoscopic Sinus and Skull Base Surgery

«

«

Fig. 7.33  Anatomy of the right olfactory cleft: superior insertion of middle and superior turbinate (ball probe), cribriform plate (arrow), and nasal septum («).

Fig. 7.34  Anterior border of the cribriform plate: posterior wall of the frontal sinus («) and anterior nasal artery (branch of the anterior ethmoidal artery, arrow). Ball probe pointing at middle turbinate.

Cribriform Plate —— Landmarks: –– Nasal septum –– Superior insertion of middle and superior turbinate –– Anterior nasal artery –– Dorsal wall of frontal sinus –– Planum sphenoidale. —— Areas at risk: –– Anterior nasal artery –– Cribriform plate (cerebrospinal fluid leak). The cribriform plate forms the roof of the olfactory cleft and is located between the nasal septum and the superior insertion of the middle and superior turbinate (Fig. 7.33). The anterior border is the dorsal wall of the frontal sinus and a constant landmark is also the anterior nasal artery, which leaves the bone of the anterior skull base just anterior to the cribriform plate and therefore also anterior to the olfactory fibers (Fig. 7.34). Structures at risk in this area are the anterior nasal artery and the cribriform plate itself; because it is so thin, dissection in this area runs the risk of causing a cerebrospinal fluid leak (Fig. 7.35; Videos 25, 26).

Acknowledgments The anatomical specimen was provided by the Institute of Anatomy, University of Zurich (O. Ullrich, M. Vich, M. Manestar, and A. Lang). The anatomical dissection was assisted by K. Makic and M. Johnke, Klinik Hirslanden, Zurich.

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Fig. 7.35  View to cribriform plate (arrow) and ethmoidal roof (ball probe) after resection of the middle and superior turbinate. Right side.

8  How? Operative Procedures: A Step-by-Step Safe and Logical Approach This chapter focuses on technique. As the chapter progresses, so does the complexity of the procedures described, but throughout we emphasize the need to consider whether the surgeon really needs to do more or not. The anatomy of the paranasal sinuses is varied and fascinating, which makes surgery both interesting and a challenge, but it has the potential to entice the enquiring surgeon to go “exploring” to discern and dissect the anatomy when such an expedition may not be warranted and may be precarious! It is wise to have a plan of what is going to be done preoperatively on the basis of the clinical findings and computed tomography (CT) scans. This may need to be modified on the basis of peroperative findings but be careful not to do more than is indicated; to do so may lead to trouble. The format is deliberately didactic to make clear to the reader the exact extent of Video 8). each procedure (Fig. 8.1;

Fig. 8.1  Three-dimensional diagrammatic scheme to represent the anatomical compartments and the surgical steps possible in endoscopic sinus surgery.

Terminology of Procedures —— Infundibulotomy (uncinectomy) ± Maxillary sinusotomy (I, II, III) —— Partial anterior ethmoidectomy —— Frontoethmoidectomy ± Frontal sinusotomy (I, II, III) —— Sphenoethmoidectomy ± Sphenoidal sinusotomy (I, II, III) —— Frontosphenoethmoidectomy ± Maxillary sinusotomy (I, II, III) ± Frontal sinusotomy (I, II, III) ± Sphenoidal sinusotomy (I, II, III) —— Sphenoidal sinusotomy (I, II, III)

Infundibulotomy (Uncinectomy) ± Maxillary Sinusotomy (I, II, III) (

Videos 6, 7, 8)

Terminology and Classification Infundibulotomy This is the removal of the uncinate process with preservation of the mucosa around the natural maxillary ostium (Fig. 8.2). The upper part of the uncinate process is left intact if it is attached to the skull base or middle

Fig. 8.2  Line diagram showing the area removed in an infundibulotomy (uncinectomy).

turbinate, in order to avoid any instrumentation near the frontal recess. It often seems easier to continue rather than to stop, but ask yourself why you should do any more surgery. Doing unnecessary surgery increases not only bleeding but the risk of complications such as adhesion formation, causing a cerebrospinal fluid leak and, in particular, damaging the frontal recess. This is a good example of “less is more.”

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Maxillary Sinusotomy I The natural maxillary ostium is enlarged posteriorly to a limited extent, and no more than 1 cm. If there is an accessory ostium, this is joined to the natural ostium (Fig. 8.3).

lacrimal sac, and inferiorly to the base of the inferior turbinate (Fig. 8.5).

Indications for Infundibulotomy and Maxillary Sinusotomy

Maxillary Sinusotomy II

Infundibulotomy

Open the antrostomy to a diameter of approximately 2 cm, opening it posteriorly and inferiorly (Fig. 8.4).

—— An infundibulotomy as a sole procedure is performed for isolated purulent maxillary sinusitis that does not respond to medical treatment. —— An infundibulotomy is the key first step in most procedures for chronic rhinosinusitis.

Maxillary Sinusotomy III The antrostomy is extended close to the level of the posterior wall of the maxillary antrum, anterior to the

Fig. 8.3  Line diagram showing the area of bone and mucosa to be removed in a maxillary sinusotomy type I.

Fig. 8.4  Line diagram showing the area of bone and mucosa to be removed in a maxillary sinusotomy type II.

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Maxillary Sinusotomy Following an infundibulotomy the maxillary sinus ostia can be seen. At this stage you should consider whether anything else needs to be done to the ostia at all because to do so runs a small risk of causing scarring and stenosis. Before you enlarge the ostia, think “why does it need to be enlarged?” There are few indications for minimally opening the ostia (Type I). —— Type I maxillary sinusotomy. Join accessory anterior or posterior fontanelles as they are said to run the risk of producing a circular motion of mucus from one ostium to the other, so providing a never-ending cycle that is prone to infection (Fig. 8.6a–c). —— Type II maxillary sinusotomy. This is most frequently performed for patients with chronic rhinosinusitis. —— Type III maxillary sinusotomy. There is some evidence that a type III maxillary sinusotomy helps patients with late-onset asthma as a smaller ostia is prone to closing from mucosal hypertrophy (Davis et al 1991).

Fig. 8.5  Line diagram showing the area of bone and mucosa to be removed in a maxillary sinusotomy type III.

Infundibulotomy (Uncinectomy) ± Maxillary Sinusotomy (I, II, III) Fig. 8.6a–c a

a Endoscopic view of circulating mucus between an incomplete opening of the anterior natural ostium and a large posterior ostium. b Coronal computed tomography scan showing the obstructed natural anterior ostium. c Coronal computed tomography scan showing the wider posterior ostium, away from the natural ostium.

a

b

c

—— If there is maxillary sinus pathology that requires more access; e.g., an antrochoanal polyp, where it is important to remove the base of the retention cyst, otherwise it will reform. —— Type III maxillary sinusotomy is needed to treat a mycetoma in the maxillary sinus (Fig. 8.7a,b), foreign body, or persistent maxillary sinus problems secondary to dental problems that have received treatment, and also in polypoid maxillary disease. —— In cystic fibrosis and primary ciliary dyskinesia, a wide ostium may help local irrigation and the mechanical clearance of retained secretions. —— In patients who are to undergo extensive ethmoidal surgery or surgery geared to improving their sense of smell, it is necessary to open the maxillary ostium inferiorly so that when the middle turbinate is lateralized to open the olfactory cleft, it is still possible for the sinus to drain and for the surgeon to obtain access to be able to inspect it (Fig. 8.8a,b). Note that in patients who need to have their olfactory cleft opened,

the maxillary sinusotomy should extend below the inferior edge of the middle turbinate so that it remains patent. —— A small proportion of patients have very thick inspissated mucopus within the maxillary sinus that often contains staphylococci; in these patients the cilia are slow to recover. In this situation a sump of mucus will collect in the base of the sinus postoperatively and this can perpetuate the problem of the cilia not regenerating. In this group a type III sinusotomy helps irrigation and drainage (the patient should lean forwards after douching, turn his or her head so that the sinus is raised with the ostia pointing down, and blow out to empty the contents of the sinus). In an even smaller proportion of patients even these measures will not prevent a sump of debris repeatedly collecting in the floor of the sinus and if after months of rigorous douching this does not resolve, an endoscopic medial maxillectomy can be considered that prevents a sump from forming.

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8  How? Operative Procedures: A Step-by-Step Safe and Logical Approach

a

b Fig. 8.7a,b a Endoscopic view of a mycetoma in the right maxillary sinus.

b Coronal computed tomography scan of the patient showing radiodense material in the right maxillary sinus indicative of aspergillosis.

b

a Fig. 8.8a,b a The maxillary sinusotomy is extended below the margin of the middle turbinate to help ensure that mucociliary clearance can take place.

b A line diagram of (a).

Anatomy The uncinate process is shaped like a rudder (Fig. 8.9); its superior extension can do one of the following: —— Merge with an agger nasi air cell or the lateral nasal wall to form a blind-ended pocket called the sulcus terminalis —— Insert into the skull base, forming an overhang that can limit anterior access to the frontal recess —— Insert into the middle turbinate and form a web that guards the frontal recess.

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Fig. 8.9  A disarticulated right uncinate process.

Infundibulotomy (Uncinectomy) ± Maxillary Sinusotomy (I, II, III) The uncinate process “guards” the natural maxillary ostium to form a slitlike corridor to it, the infundibulum ethmoidale (Fig. 8.10). The entrance to this corridor is the hiatus semilunaris (anterior), a crescent-shaped space at the posterior edge of the uncinate process (Fig. 8.11). The uncinate process is made up of very thin bone that attaches anteriorly to the bone adjacent to the nasolacrimal duct, so it is important not to come too far forward when removing the uncinate process. It extends upward to insert into the lateral nasal wall in approximately 70% of patients and into the skull base or the middle turbinate in the remaining 30%. The insertion of the uncinate process determines whether the frontal sinus drains directly into the middle meatus (type A) or into the infundibulum

ethmoidale lateral to the uncinate process (type B) (Fig. 8.12). The uncinate process is normally in a sagittal plane, although polyps in the infundibulum can push its posterior edge medially and give it the appearance of a middle turbinate (it may look as though there is a bifid middle turbinate as the turned back edge of the uncinate and the middle turbinate will be visible). This can be determined by gently running an instrument along the lateral wall of the nose and seeing if it meets a dead end before coming forward to the edge of the structure, in which case it will be the uncinate process. In less than 1% of healthy individuals, it can be paradoxical, curving forward on itself. It rarely contains a pneumatized cell. The uncinate

«

Fig. 8.10  The uncinate process (arrow) has been lifted forward to reveal the natural ostium of the maxillary sinus. The green wire is in the position of the infundibulum of the anterior ethmoidal sinuses.

Fig. 8.11  A window has been made in the middle turbinate to reveal the edge of the uncinate process (arrow), the hiatus semilunaris, and the ethmoid bulla («).

Fig. 8.12  This shows a type A uncinate process (left), where the frontal sinus drains directly into the middle meatus, and types B1 (center), where the uncinate process attaches to the skull base, and B2 (right), where the uncinate process attaches to the middle turbinate. Both B1 and B2 have the frontal sinus draining into the infundibulum ethmoidale.

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8  How? Operative Procedures: A Step-by-Step Safe and Logical Approach process is very thin and any incision through it needs to be only about 1 mm; any more and it could go through other structures that are more lateral to it. It is important to be aware of this and check the position of the uncinate process in relation to the lamina papyracea on the CT scan before starting. The uncinate process may attach to anterior ethmoidal air cells, but in many patients there are no cells between it and the orbit. Inferiorly, it is attached to the base of the inferior turbinate, and together these fill most of the bony defect of the medial wall of the maxillary sinus. The remainder of the medial wall of the maxillary sinus has no bone and is made up of mucosa. It forms the anterior and posterior fontanelles. An anterior branch of the sphenopalatine artery runs in the medial wall of the maxillary sinus and is sufficiently large that opening the maxillary ostium posteriorly to within 0.5 cm of the posterior wall of the maxillary sinus will lead to bleeding.

a

Surgical Technique Infundibulotomy It is best to assess the endoscopic findings and coronal CT images together to work out the position and insertion of the uncinate process before starting surgery. We recommend using a 0° endoscope for almost every procedure outside the frontal sinus. The optics of the 0° endoscope give minimal distortion and this reduces the likelihood of surgeons losing their orientation. Check that the maxillary sinus is not hypoplastic and whether there is a large infraorbital cell (Haller cell) present, as this may alter your approach. An infraorbital cell is an inferiorly placed anterior ethmoidal air cell that is attached to the floor of the orbit in the roof of the maxillary sinus. It is possible to enter a large infraorbital cell and think that you have done a maxillary sinusotomy when this is not the case. With a hypoplastic maxillary sinus you must stay low toward the base of the inferior turbinate to avoid entering the orbit. With a hypoplastic maxillary sinus it is very easy to enter the orbit and extreme care is needed. With an infraorbital cell you need to particularly check, when undertaking a middle meatal antrostomy, that you have opened the maxillary ostium widely, and not simply entered the infraorbital cell. Occasionally the lateral wall is dehiscent and then the orbit is easily entered. Under these circumstances, it is particularly helpful to perform ballottement of the closed eye while endoscopically inspecting the area to see whether the orbital contents prolapse into the nasal airway. It is important to do this at the beginning of surgery if there has been previous surgery or if there is marked polyposis and the CT shows erosion of the lateral wall of the nose. The uncinate process is defined endoscopically by palpating it laterally with the side of a Freer’s elevator or a ball probe (Fig. 8.13a–c). It is mobile, unlike the rigid anterior lacrimal crest. A curved seeker can be used to

c

b Fig. 8.13a–c  Palpating around the edge of the uncinate process with a ball probe.

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Infundibulotomy (Uncinectomy) ± Maxillary Sinusotomy (I, II, III) gently palpate the posterior edge of the uncinate process and then be passed around its inferior edge anteriorly to feel the site of the natural ostium. There are several ways to perform an uncinectomy. For the inexperienced surgeon, a retrograde approach is safer and runs less risk of inadvertently entering the orbit. A closed Stammberger Rhinoforce antrum punch (backbiter) is advanced into the middle meatus behind the posterior edge of the uncinate process and then rotated so that the “finger” of the back-biter opens upward. This finger can then be fed into the infundibulum and the back-biter can be rotated so that it lies horizontally (Fig. 8.14a–d). It is best to take the first bite as low as possible near the base of the uncinate process. When the back-biters are closed they should not meet any significant bony resistance because the uncinate process is thin. If anything more than minimal resistance is met, then the back-biters should not be closed because the nasolacrimal duct may be damaged. Back-biters can take more

than one bite at a time without having to be cleaned. The back-biters can then be fed upward to take a bite higher up (Fig. 8.15a,b), so creating a “door” of the uncinate process that can be opened or folded forward on its anterior hinge. The door of the uncinate process can then be removed using through-cutters, a Hajek punch, or one of the microdebriders that can “digest” bone (Fig. 8.16a–c). An alternative is to remove just the inferior strip with the back-biters and then use the 45° through-cutters to nibble away upward at the uncinate process incrementally. If an infundibulotomy is all that is indicated, there is no need to follow it up to the middle turbinate or skull base if it is attached there. The more experienced surgeon may perform an uncinectomy by palpating the lateral wall to define the position of the anterior lacrimal crest, which is totally rigid, unlike the uncinate process, which gives way to some extent. A sickle knife or a Freer’s elevator is used to incise the uncinate process near its top edge and then to run it down in a sagittal plane, being careful not to go through it

a

b

c

d Fig. 8.14a–d  The back-biter is fed around the edge of the uncinate process and an inferior horizontal bite is taken.

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8  How? Operative Procedures: A Step-by-Step Safe and Logical Approach

a

b Fig. 8.15a,b  The back-biter can be used to reduce the uncinate process, with multiple segments being removed.

a

b

c Fig. 8.16a–c  A Hajek punch is used to remove the uncinate process.

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more than 1 mm, and then extend the incision inferiorly (Fig. 8.17a,b). On the patient’s right side a c-shape of mucosa and uncinate is incised, and on the other side the shape is reversed. While the incision is being made, the shoulder of the sickle knife can be used to mobilize the uncinate process medially. The initial incision can be started half way up and then extended in either direction (Fig. 8.18a– d). If the incision is started high up there is an increased risk of entering the orbit. The sickle knife is used to medialize the uncinate process to reveal the infundibulum; the natural ostium may also be seen. The line diagrams illustrate one way of making this incision. The remaining superior attachment can be cut with Zurich scissors or Rhinoforce Blakesley (through-cutting) forceps and the same is done at its inferior attachment (Fig. 8.19a–h). With this maneuver, this segment of the uncinate process can be removed without tearing any mucosa. Often there are tags of mucosa that need to be trimmed with through-cutting forceps or a microdebrider. If the sickle knife comes up against hard bone then this is likely

Infundibulotomy (Uncinectomy) ± Maxillary Sinusotomy (I, II, III)

a

b Fig. 8.17a,b  The sickle knife is used with caution, incising only 1 mm, which is all that is needed to go through the uncinate process, and is kept in the sagittal plane as much as possible.

a

b

c

d Fig. 8.18a–d a A right uncinectomy with the uncinate process medialized to reveal the natural maxillary ostium. b One method for performing an uncinectomy is to initially incise downward with a sickle knife.

c Next, turn the sickle knife around and incise in the opposite direction. d The uncinate process is then medialized to help define its remaining superior or inferior attachments.

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8  How? Operative Procedures: A Step-by-Step Safe and Logical Approach

a

b

c

d

e

f Fig. 8.19a–h a Zurich scissors or through-cutting forceps are used to divide any remaining superior attachment of the uncinate process. b A line diagram of (a). c Zurich scissors are used to divide any remaining inferior attachment of the uncinate process.

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d A line diagram of (c). Blakesley forceps can be used to grasp the uncinate and rotate it laterally to free any remaining attachment. f A line diagram of (e).

Infundibulotomy (Uncinectomy) ± Maxillary Sinusotomy (I, II, III) ◁ continued

g

h g The natural maxillary ostium is exposed and a small part of the uncinate process is left attached both superiorly and inferiorly.

h A line diagram of (g).

to be the anterior lacrimal crest, meaning that the incision has been started too far anteriorly. Whichever method is used, as soon as the sickle knife has gone through the uncinate process, it should be medialized so that the operator can check the position of the uncinate process and the depth of the incision. It is best to use throughcutting forceps or scissors to cut mucosal tags, as to grasp them with forceps and pull runs the risk of tearing the mucosa off the lateral wall. When this happens, it can come off the lateral wall like steamed wallpaper being pulled. This would run the risk of causing stenosis of the frontonasal recess. If forceps are the only instrument available, then they should be rotated laterally toward the lateral wall to minimize the chance of peeling the mucosa off the lateral nasal wall. Remember that while the uncinate process inserts into the lamina papyracea or lateral nasal wall in 70% of patients, in the other 30% of patients it is attached to the skull base or middle turbinate, and under these circumstances it will extend up to the “armpit’ where the middle turbinate attaches to the lateral nasal wall and guards the frontal recess. It is unnecessary to remove the uncinate process this high up in these circumstances, unless there is good reason for operating in the frontal recess area. Whichever method is used, there is usually a small “stub” of uncinate process remaining at its inferior attachment just medial to and below the natural maxillary ostia (Fig. 8.19g,h). This little piece of bone is best dissected out with the end of a fine ball probe and the mucosal remnants shaved off or trimmed with side-biting forceps. The natural ostium can usually be visualized, but if not it can be palpated gently with a ball probe, a curette, or an olive-ended right-angled sucker unattached to the suction tube (Fig. 8.20a–f). When this is done, minimal pressure should be required and it is important to direct the end of the seeker downward and laterally and to search

for it from the level of the attachment of the inferior turbinate so as to minimize the chance of inadvertently entering the orbit. If the maxillary ostium cannot be seen it is likely that an insufficient amount of uncinate process has been removed; this can be trimmed with either backbiting forceps or side-biting forceps until it is visible. Sometimes palpating the lateral nasal wall will produce a bubble out of the ostium that will locate its position. In an infundibulotomy, where there is no reason to enlarge the natural ostium, it is important not to scuff the mucosa on the posteroinferior aspect of the natural maxillary ostium, as mucociliary clearance passes around this aspect along the lateral wall of the nose under the ethmoidal bulla. Unless there are good reasons for opening the maxillary ostium it is best left alone as opening it runs the risk of causing scar tissue around its margin that may interfere with mucociliary clearance ( Videos 16, 17, 18).

Alternative Surgical Techniques Occasionally, in a very narrow nose, where access is restricted by a narrow pyriform aperture, finding the maxillary ostia can be difficult, particularly if there is active purulent disease and a great deal of bleeding with any instrumentation in the middle meatus. Although the surgeon is advised not to continue if he or she cannot see adequately, it is unusual not to be able to gain sufficient control with local vasoconstrictors to make it possible to undertake a middle meatal antrostomy. The “lazy” way of undertaking an infundibulotomy/ middle meatal antrostomy is reserved for difficult situations when the natural ostium cannot be identified. In a minority of patients the lateral wall in the area of the uncinate process curves laterally the more posteriorly the surgeon goes so that it “fades” away and is difficult

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8  How? Operative Procedures: A Step-by-Step Safe and Logical Approach

a

b

c

d

e

f Fig. 8.20a–f  The ball probe is used to palpate so as to locate the position of the natural ostium. Only use it as a probe and direct it downward, away from the orbit.

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Infundibulotomy (Uncinectomy) ± Maxillary Sinusotomy (I, II, III) to incise in the sagittal plane or locate. A ball probe can be used to feel the posterior edge of the uncinate process. An alternative, particularly if there has been previous surgery and scar tissue makes the lateral wall featureless, it is possible to perform ballottement of the anterior and posterior fontanelles that consist solely of mucosa with a curved instrument to locate these areas of weakness. A right-angled ball probe or similar instrument can be prodded through these areas as long as they are directed laterally and inferiorly just above the level of the inferior turbinate away from the orbit and checking that the maxillary sinus is not hypoplastic. This area has no bone and the mucosa “gives” easily with little pressure. It is important to palpate where the inferior turbinate comes off the lateral wall and to point the curved sucker downward and laterally at 45° from the horizontal plane. When the area of the posterior fontanelle is identified, the sucker can be used to enter the maxillary sinus. This is best done relatively abruptly (as long as there is no evidence of a hypoplastic maxillary antrum on CT) so that mucosa on the medial wall of the maxillary sinus is punctured neatly and not torn off the medial bony wall of the antrum. The sucker is then pushed and pulled forward a little to open a false ostium that is akin to a posterior fontanelle. A back-biter is inserted in this hole, having been introduced posterior to its position, and its jaws are opened wide so as to engage both the lining of the medial wall of the maxillary sinus and the mucosa of the lateral wall of the nose. Multiple bites are then taken to widen this and to come forward and join up the maxillary ostium. The uncinate process can be taken up with these bites and, as this is a crude way of undertaking an uncinectomy along

with a middle meatal antrostomy, it can salvage a difficult situation. It is also important to join the punctured site to the natural ostia to avoid a circular motion of mucus from one ostium to the other. It is important not to come too far anteriorly, so as to avoid the nasolacrimal system, but it is important to remove the uncinate process, because to leave most of it in position above the maxillary ostium encourages the formation of polyps in this crevice. In a minority of revision cases there is so much thick osteitic bone that an anterior approach is best. This involves making an incision just anterior to the lacrimal crest and raising the mucosa posteriorly to reveal the uncinate process as it joins the lacrimal crest. The most medial lip of the lacrimal crest needs to be drilled away to improve visibility and access (Fig. 8.21a,b).

Maxillary Sinusotomy (I, II, III) First, the natural ostium is identified. In a type I sinusotomy (Fig. 8.22a,b), it is opened posteriorly to a limited extent (