COSTELLO • SANDHU

Medicine

Practical Laryngology
Practical Laryngology is an invaluable guide to laryngol-
ogy. It covers all the relevant areas in the field, from basic
science to disorders and diseases to in-clinic procedures

PRACTICAL LARYNGOLOGY
and the future of laryngology.

In an easy-to-read format, the book discusses a wide vari-

ety of topics including neurological diseases of the larynx,
swallowing disorders, laryngeal trauma, stenosis, reflux,
acute infections, inflammatory disorders, paediatrics,
benign vocal cord lesions, and dysplastic lesions.

Colour drawings, clinical photographs, and imaging sup-

port the text throughout, making it an excellent reference
to help the clinician find information quickly and easily.
Essential information is presented in a succinct and read-
able style, making it vital for higher trainees preparing for
their final exit examinations and for consultants both in gen-
eral ENT and in the subspecialty of laryngology.

Practical
This book is the ultimate guide for those wanting to learn
more about the larynx, its disorders, therapeutic interven-
tions, and other challenges that may impact patients and
their families.

K17273
Laryngology
ISBN 978-1-4441-8366-5
90000 Edited by
9 781444 183665
Declan Costello • Guri Sandhu
 Practical
Laryngology

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K17273_Book.indb 2 9/23/15 3:10 PM
 Practical
Laryngology
Edited by
Declan Costello MA, MBBS, FRCS(ORL-HNS)
Consultant ENT Surgeon and Laryngologist
Queen Elizabeth Hospital
Birmingham, UK

and

Guri Sandhu MBBS, MD, FRCS, FRCS(ORL-HNS)

Consultant ENT Surgeon
Chief of Service for Laryngology and Airway
Imperial College Healthcare NHS Trust
London, UK

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CRC Press
Taylor & Francis Group
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© 2016 by Taylor & Francis Group, LLC
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 Contents
Contributors vii
Foreword ix
Preface xi
About the editors xi
Abbreviations xiii

Chapter 1: Basic science 1

Chadwan Al Yaghchi & Martin Birchall

Chapter 2: Voice assessment in the out-patient department 11

Paul Carding & Tracy Miller

Chapter 3: The professional voice user 19

John S. Rubin

Chapter 4: Benign vocal fold lesions 27

Lindsay S. Reder & Ramon A. Franco Jr.

Chapter 5: Neurological and neuromuscular disorders of the larynx 45

Lucian Sulica

Chapter 6: Vocal fold paralysis 59

Matthew S. Broadhurst

Chapter 7: Principles of speech and language therapy 73

Christella Antoni

Chapter 8: Swallowing disorders 87

Jacqui Allen & Peter C. Belafsky

Chapter 9: Laryngeal trauma 99

Guri Sandhu & S. A. Reza Nouraei

Chapter 10: Laryngotracheal stenosis 109

Guri Sandhu & S. Mahmoud Nouraei

Chapter 11: Extra-oesophageal reflux 121

James O’Hara

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 Contents

Chapter 12: Infections of the larynx 129

Sachin Gandhi & Nick Gibbins

Chapter 13: Recurrent respiratory papillomatosis 141

Adam Donne

Chapter 14: Inflammatory disorders of the larynx 149

Ivor Kwame

Chapter 15: Dysplastic lesions of the larynx 157

Taran S. Tatla

Chapter 16: Paediatric laryngeal disorders 169

Richard J. D. Hewitt, Benjamin E. J. Hartley & Thushitha Kunanandam

Chapter 17: In-clinic procedures 179

Nancy Solowski, Greg Postma & Paul Weinberger

Chapter 18: Anaesthetic considerations in laryngology 195

Anil Patel

Chapter 19: Gender dysphoria and the larynx 201

Christella Antoni & Guri Sandhu

Chapter 20: New horizons in laryngology 213

Nick Hamilton & Martin Birchall

Index 221

vi

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 Contributors

Jacqui Allen MBChB, FRACS(ORL-HNS) Adam J. Donne PhD, FRCS(ORL-HNS)

Department of Otolaryngology Consultant Paediatric Otolaryngologist, Alder Hey
North Shore Hospital Children’s NHS Foundation Trust
University of Auckland Honorary Senior Lecturer, University of Liverpool
Auckland, New Zealand Liverpool, UK

Christella Antoni BA(Hons), MSc, MRCSLT, HCPC Ramon A. Franco Jr. MD

Consultant Speech & Language Therapist Associate Professor, Havard Medical School
Imperial College Hospitals NHS Trust Medical Director, Voice and Speech Laboratory
West London Mental Health Trust Massachusetts Eye and Ear Infirmary
Independent Practice Boston
London, UK Massachusetts, USA

Peter C. Belafsky MD, MPH, PhD Sachin Gandhi MBBS, MS(ENT)

Professor, Center for Voice and Swallowing Director Department of Laryngology
Department of Otolaryngology Head and Neck Surgery Deenanath Mangeshkar Superspeciality Hospital
University of California, Davis Pune, India
Sacramento
Nick Gibbins FRCS(ORL-HNS), MD
California, USA
Consultant ENT Surgeon
Martin Birchall MA(Hons Cantab), MB, BChir, University Hospital Lewisham
MD(Cantab), FRCS(Gen), FRCS(Otol), FRCS(ORL), Queen Elizabeth Hospital Woolwich
FMedSci Queen Mary’s Hospital Sidcup
Professor of Laryngology London, UK
University College London Nick Hamilton DOHNS, MRCS
London, UK Clinical Research Fellow
Royal National Throat, Nose and Ear Hospital  
Matthew S. Broadhurst MBBS, FRACS(­ORL-HNS)
London, UK
Laryngeal Surgery & Voice Restoration
Director, Queensland Centre for Otolaryngology & Voice Benjamin E. J. Hartley BSc, MBBS,  FRCS(ORL-HNS)
Senior Lecturer, University of Queensland Consultant Paediatric Otolaryngologist and Head &
St Lucia, Queensland, Australia Neck Surgeon
Great Ormond Street Hospital for Children
Paul Carding BA(Hons) DipCCS, PhD London, UK
Professor of Speech Pathology
National Course Coordinator in Speech Pathology Richard J. D. Hewitt BSc, FRCS(ORL-HNS)
Chair of Research Committee Consultant Paediatric Otolaryngologist, Head &
School of Allied Health/Faculty of Health Science Neck and Tracheal Surgeon
Australian National Catholic University Great Ormond Street Hospital for Children
Brisbane, Queensland, Australia London, UK
Declan Costello MA, MBBS, FRCS(ORL-HNS) Thushitha Kunanandam FRCS(ORL-HNS)
Consultant ENT Surgeon and Laryngologist Consultant Paediatric Otolaryngologist 
Queen Elizabeth Hospital Yorkhill Hospital
Birmingham, UK Glasgow, UK

vii

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 Contributors

Ivor Kwame BSc, MRCS, DOHNS John S. Rubin MD, FACS, FRCS
Honorary Specialist Registrar Co-Lead Clinician, Voice and Swallowing Disorders Unit
Departments of Ear, Nose and Throat Surgery and Renal & National Hospital for Neurology and Neurosurgery
Vascular Inflammation Lead Clinician, Voice Clinic
Imperial College Healthcare NHS Trust Royal National Throat, Nose and Ear Hospital
London, UK Consultant ENT Surgeon, University College London
Hospital Trust
Tracy Miller MSc, BSc(Hons), MRCSLT Honorary Senior Lecturer, University College London
Principal Speech and Language Therapist (Voice Disorders)
London, UK
Department of Speech, Voice and Swallowing
The Freeman Hospital Guri Sandhu MBBS, MD, FRCS, FRCS(ORL-HNS)
Newcastle upon Tyne, UK Consultant ENT Surgeon
Chief of Service for Laryngology and Airway
Reza Nouraei MA, Bchir, PhD, MRCS Imperial College Healthcare NHS Trust
Specialty Registrar in ENT Surgery, Charing Cross Hospital
London, UK
Honorary Senior Lecturer
The Ear Institute Nancy Solowski MD
University College London Laryngology/Otolaryngology
London, UK Greater Baltimore Medical Center (GBMC)
Towson,
S. Mahmoud Nouraei MD, FRCS(CTh), FETCS Maryland, USA
Department of Cardiovascular Science
Mazandaran University of Medical Sciences Lucian Sulica MD
Mazandaran Sean Parker Professor of Otolaryngology
Sari, Iran Director, The Sean Parker Institute for the Voice
Department of Otolaryngology – Head & Neck Surgery
James O’Hara FRCS Weill Cornell Medical College, New York
Consultant Otolaryngologist – Head & Neck Surgeon
New York, USA
The Freeman Hospital
Honorary Senior Clinical Lecturer, Newcastle University Taran S. Tatla BSc(Hons), MBBS, DLO, FRCS(ORL-HNS)
Newcastle upon Tyne, UK Consultant ENT – Head & Neck Surgeon
London North West Healthcare NHS Trust
Anil Patel MD, FRCA London, UK
Department of Anaesthesia
Royal National Throat, Nose and Ear Hospital Paul Weinberger MD, FACS
London, UK Assistant Professor of Otolaryngology
Center for Voice, Airway and Swallowing
Greg Postma MD Georgia Regents University, Augusta
Professor and Vice Chair
Georgia, USA
Department of Otolaryngology
Center for Voice, Swallowing and Airway Chadwan Al-Yaghchi MRCS, DOHNS
Georgia Regents University, Augusta Clinical Research Fellow
Georgia, USA Barts Cancer Institute
Queen Mary University of London
Lindsay S. Reder MD
London, UK
Assistant Professor
USC Keck School of Medicine
Department of Otolaryngology – Head & Neck Surgery
University of Southern California (Keck), Los Angeles
California USA

viii

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 Foreword
Practical Laryngology has as its editors two of our foremost the layout and printing of the book and there are superb
consultant laryngologists in the UK, both with their own high-quality illustrations and clear drawings to complement
special interests and who are at the forefront of the discipline. the text.
It is therefore no surprise that the selection of topics and the In addition to the UK authors, there are contributions
experience and knowledge of the individual contributors from the USA, Australia, New Zealand and India, and these
is excellent. Both paediatric and adult laryngology are add to the interest and overall balance of the book.
covered and in addition it covers the important pharyngeal, Having read and been involved with the writing of many
oesophageal and tracheobronchial conditions, which are so books in our discipline, I have no hesitation in stating that
important to a modern laryngology practice. I believe this to be currently the best book of its type. The
The authors of the opening three chapters on basic authors and contributors are to be congratulated and while
science, voice assessment and the professional voice user it will no doubt be bought by libraries everywhere, it would
are to be commended as they set the scene for the multiple provide an excellent addition to every individual’s bookshelf
excellent contributions that follow. Indeed, there is not a interested in our ever expanding discipline.
weak chapter in the entire book. The level of detail and the
up-to-date reference sections make this book of use even Professor David Howard
to the most experienced consultant, but equally, the clear Honorary Consultant and Senior Lecturer at Charing
presentation and layout make this an enjoyable book even Cross Hospital, Royal National Throat Nose and
for juniors in an early career in laryngology. I personally like Ear Hospital and University College London

ix

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K17273_Book.indb 10 9/23/15 3:10 PM
 Preface
The human larynx is unique in that it plays a part not only We hope that this compendium will provide the reader with
in respiration and airway protection (in common with an up-to-date reference book and a practical framework to
other mammals) but has also evolved to allow phonation approaching the problems encountered daily in the clinic.
and advanced communication. It is over one hundred and Although it is impossible to cover all areas of laryngology in
fifty years since laryngoscopy was introduced to clinical exhaustive detail, every effort has been made to discuss the
practice and the field of laryngology has evolved ever since. most common and important topics. Given the volume of
Advances in medical science and our increasing knowledge literature on head and neck cancer, laryngeal malignancies
of human physiology have influenced the patterns of are not covered; however, we have devoted a chapter to
laryngeal diagnoses and their management. Following laryngeal dysplasia, as this sits at a crossroads between benign
a period of parallel medical evolution, ‘shared-airway’ and malignant disease.
techniques have brought closer team working between the We are enormously grateful to our colleagues and friends
anaesthetist and the laryngologist. The introduction of the who have given so generously of their time and expertise,
microscope, endoscopes and lasers into surgery have allowed and also to our respective families for their patience and
for function-preserving laryngeal procedures. Within understanding during the preparation of this book.
the specialty of otolaryngology, laryngology is a rapidly We would like to dedicate this book to the next
expanding field encompassing voice, swallowing and airway, generation of laryngologists. It is our privilege to teach them
both in adults and children. and we hope to inspire others to enter this exciting field
This book is multi-authored by colleagues within the within otolaryngology.
varied specialities of laryngology, speech pathology and
anaesthesia, all of them leaders in their respective fields. Declan Costello and Guri Sandhu

About the editors

Declan Costello is a Consultant ENT Surgeon specialising voice users from stage, music and media and is ENT Surgeon
in voice disorders. With a background in singing, he has a to the Royal Society of Musicians. He has one of the largest
particular interest in vocal disorders in performers. He also practices in the world managing damaged airways and has
has a large practice in patients with vocal fold paralysis and pioneered minimally invasive techniques to restore a quality
with neurological disorders.  of life to these patients. With an enthusiasm for teaching, he
lectures and runs workshops, nationally and internationally,
Guri Sandhu is a Consultant ENT Surgeon with special interests on the management of laryngeal disorders. He is a co-founder
in voice, airway and swallowing problems. He has a large of the British Laryngological Association and Corresponding
practice managing the problems experienced by professional Fellow to the American Laryngological Association.

xi

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K17273_Book.indb 12 9/23/15 3:10 PM
 Abbreviations
AA arytenoid adduction ICU intensive care unit
ACE angiotensin-converting enzyme IFN-γ interferon-gamma
ADA adduction arytenopexy IgG4 immunoglobulin G4
AIDS acquired immunodeficiency syndrome JVC joint voice clinic
ALS amyotrophic lateral sclerosis KTP potassium titanyl phosphate (laser)
ANCA anti-neutrophil cytoplasmic antibody LCA lateral cricoarytenoid (muscle)
BTX botulinum toxin LEMG laryngeal electromyography
BVCMI bilateral vocal cord mobility impairment LMRVT Lessac–Madsen Resonant Voice Therapy
CAHA calcium hydroxylapatite LPR laryngopharyngeal reflux
CAJ cricoarytenoid joint LSVT Lee Silverman Voice Therapy
c-ANCA cytoplasmic anti-neutrophil cytoplasmic LTR laryngotracheal reconstruction
antibody LTS laryngotracheal stenosis
CAPE-V Consensus Auditory-Perceptual Evaluation Lx electrolaryngography
of Voice MDT multidisciplinary team
CD1d cluster of differentiation 1 MHC major histocompatibility complex
CIS carcinoma in situ MLB microlaryngoscopy and bronchoscopy
CMV cytomegalovirus MLTB microlaryngoscopy and tracheobronchoscopy
CN cranial nerve MMP mucous membrane pemphigoid
COPD chronic obstructive pulmonary disease MPT maximum phonation time
CP cricopharyngeal MRI magnetic resonance imaging
CPG central pattern generator MSA multiple system atrophy
CreSS Comprehensive Reflux Sympton Scale NA nucleus ambiguus
CT computed tomography NBI narrow band imaging
CTA cricothyroid approximation NTS nucleus tractus solitarius
DSI Dysphonia Severity Index OPD oropharyngeal dysphagia
EBM Evidence Based Medicine (Conference) ORL otorhinolaryngeal (surgery)
EGG electroglottography PCA posterior cricoarytenoid (muscle)
EMG electromyography PCTR partial cricotracheal resection
E-PCTR extended partial cricotracheal resection PD Parkinson’s disease
FEES functional endoscopic evaluation of PDL pulsed dye laser
swallowing PET positron emission tomography
GA Gaviscon Advance PGG photoglottography
GETS Glasgow and Edinburgh Throat Scale PPI proton pump inhibitor
GOJ gastro-oespophageal junction PR3 proteinase 3
GORD gastro-oesophageal reflux disease RCT randomised controlled trial
GPA granulomatosis with polyangiitis RFS Reflux Finding Scale
HA hyaluronic acid RLE real life experience
HFJV high-frequency jet ventilator/ventilation RLN recurrent laryngeal nerve
Hib H. influenzae type B RN rheumatoid nodule
HIV human immunodeficiency virus RRP recurrent respiratory papillomatosis
HMSN hereditary motor and sensory neuropathy RSI Reflux Symptom Index
HNR harmonic-to-noise ratio S/Z ratio ‘sssssss’/‘zzzzzzz’ ratio
HPV human papillomavirus SA (luminal) surface area
Hz Hertz SCC squamous cell carcinoma
IBM inclusion body myositis SCJ squamocolumnar junction

xiii

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 Abbreviations

SD spasmodic dysphonia UOS upper oesophageal sphincter

SGS subglottic stenosis UVFP unilateral vocal fold paralysis
SLN superior laryngeal nerve VFP vocal fold paralysis
SLT speech and language therapist VHI Voice Handicap Index
TA thyroarytenoid (muscle) VoiSS Voice Symptom Scale
TFL transnasal flexible laryngoscopy VPQ Vocal Performance Questionnaire
TNO transnasal oesophagoscope WHO World Health Organisation
TOP tracheo-oesophageal puncture

xiv

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 CHAPTER 1

Basic science
Chadwan Al Yaghchi & Martin Birchall

Vocal tract anatomy

Gross anatomy They extend anteriorly into the saccule, a tubular-shaped
pouch that lies between the vestibular fold and the inner
The larynx is located along the midline of the anterior part
plate of the thyroid cartilage.3 The saccules contain mucous
of the neck, at approximately the level of the third to sixth
glands that help lubricate the vocal folds.5
cervical vertebrae. It extends from the base of the tongue
to the trachea, and communicates posteriorly with the
Vocal folds
oropharynx and the hypopharynx.1
The larynx is subdivided into the supraglottis, glottis and The vocal folds extend from a midline point on the inner
subglottis (Figure 1.1). These subdivisions are most relevant surface of the thyroid cartilage, or the anterior commissure,
in laryngeal neoplasms, as tumours in different anatomical to the vocal process of the arytenoid cartilage. The anterior
locations behave differently. The boundary between the commissure corresponds approximately to the midway
supraglottis and glottis is widely accepted to be a horizontal point between the thyroid notch and the lower border of
line through the apex of the laryngeal ventricle. In contrast, the thyroid cartilage at the midline. The conus elasticus is
the transition from the glottis to the subglottis is more the lateral portion of the cricothyroid ligament. It extends
controversial. Various authors demarcate the transition from the anterior arch of the cricoid cartilage to the
at 10 mm below the medial free edge of the vocal fold or thyroid cartilage anteriorly and to the vocal process of the
10 mm below the apex of the laryngeal ventricle.2 arytenoid posteriorly. The thickened superior free margin
of the conus elasticus is also known as the vocal ligament.
Laryngeal inlet Running parallel and inferolateral to the vocal ligament is
the vocalis component of the thyroarytenoid muscle. The
The laryngeal inlet is the opening that connects the larynx
glottis is the space between the vocal folds. The anterior
to the pharynx. Its borders are the epiglottis anteriorly and
three-fifths of the glottis is termed the membranous vocal
superiorly, the aryepiglottic folds laterally and the mucosa
cord, or the vocal fold, whereas the posterior two-fifths
overlying the arytenoid cartilages and the interarytenoid
is termed the cartilaginous vocal cord, or the respiratory
area posteriorly. The hypopharynx extends laterally to the
glottis (Figure  1.2).6 The vocal folds are usually bulkier
laryngeal inlet to form the piriform sinuses.
and longer in adult males, resulting in a deeper voice.
Vestibular folds Note: Currently the terms vocal ‘fold’ and vocal ‘cord’ are
used synonymously by laryngologists and as yet there is no
The vestibular folds, or the false vocal cords, are bilateral consensus on terminology.
mucosal folds extending from the inner surface of the
thyroid cartilage anteriorly to the body of the arytenoid
Skeleton of the larynx
cartilage posteriorly. The body of the vestibular fold is
made by the vestibular ligament, the thickened free inferior Thyroid cartilage
margin of the quadrangular membrane. The latter is a The thyroid cartilage is formed by two quadrangular
connective tissue layer extending from the lateral aspect of laminae that join anteriorly to form the laryngeal
the epiglottis to the arytenoids.The vestibular folds contain prominence (Adam’s apple). The angle between the lamina
variable muscle structures, which are believed to contribute is more acute in adult males, hence a more  prominent
to their limited movement.3,4 Adam’s apple. They separate superiorly to form the thyroid
notch. Posteriorly, the laminae project both upwards and
Laryngeal ventricles downwards to form the superior and inferior horns. A small
The laryngeal ventricles are the spaces between the facet is located on the medial surface of the inferior horn
vestibular and vocal folds and are present bilaterally. that articulates with the cricoid cartilage.

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 Basic science

Hyoid bone,
Epiglottis
greater cornu

Aryepiglottic Thyrohyoid
Upper fold membrane
part
Epiglottic Quadrangular
tubercle membrane

Middle Laryngeal
part Vestibular fold saccule
Thyroid cartilage
Laryngeal
ventricle
Lower Vocal fold
part
Thyroarytenoid

Cricovocal Cricoid
membrane cartilage

Figure 1.1 Laryngeal subdivisions. Coronal section of the adult larynx (viewed from posteriorly) showing the supraglottis, glottis and
subglottis regions.

Epiglottis
The epiglottis is a thin, leaf-shaped fibrocartilage that lies
in the upper part of the larynx and behind both the hyoid
Menbranous vocal cord
(vocal fold)
bone and the base of the tongue. Its pointed inferior stalk
is called the petiole, and is attached to  the inner surface
of the thyroid cartilage via the thyroepiglottic ligament.
Cartilaginous vocal cord
It is anchored to the posterior surface of the hyoid bone
Arytenoid cartilage
via the hyoepiglottic ligament. Its free superior portion is
covered by mucosa, which forms the anterior border of the
Figure 1.2 Vocal cords. Schematic endoscopic view of the larynx
showing subdivisions of the vocal cord. laryngeal inlet.

Cricoid cartilage The minor cartilages of the larynx

The cricoid cartilage is the only complete cartilaginous The corniculate cartilages are two small cartilages that
ring in the human airway. The cartilage is composed of the articulate with the apex of the arytenoid cartilage. The
narrow cricoid arch anteriorly, which measures 5–7 mm club-shaped cuneiform cartilages are located within the
in height7, and a wider quadrate lamina posteriorly, which aryepiglottic fold.
measures approximately 21 mm in females and 25 mm in
males.8 At  the junction  between the lamina and the arch Hyoid bone
is a small round facet that articulates with the lower horn The hyoid bone is a horseshoe-shaped bone suspended in
of the thyroid cartilage. The superior margin of the lamina the anterior most part of the neck by the suprahyoid and
contains two smooth concave facets that articulate with the tongue muscles. It contains a quadrilateral curved central
base of the arytenoid cartilage.These are synovial joints and body and the lateral greater and lesser horns. The hyoid
therefore are susceptible to arthritis and ankylosis. bone’s anterior surface is convex with a median ridge,
whereas the  posterior surface is smooth and concave.
Arytenoid cartilages Numerous muscles, membranes and ligaments attach to the
The arytenoid cartilages are pyramidal in shape and have three hyoid bone.
surfaces, an apex and a base.They lie on the posterior aspect of
the larynx on the superior margin of the lamina of the cricoid Muscles of the larynx
cartilage.The anterior and lateral angles of the base elongate to The muscles of the larynx can be classified as extrinsic or
form the vocal and muscular processes, respectively. The vocal intrinsic muscles. The extrinsic laryngeal muscles have
ligaments attach to the vocal process, whereas the posterior and attachments outside the larynx. T
  hey include the strap muscles
lateral cricoarytenoid muscles attach to the muscular process. of the neck, the stylopharyngeus, the palatopharyngeus and the

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 Vocal tract anatomy

inferior constrictor muscles. T

  he extrinsic muscles move the Thyroarytenoid muscles
larynx as a whole and play a role in breathing and swallowing.
The thyroarytenoid muscles originate from the anterior
The origin and insertion for intrinsic muscles are
commissure tendon (or Broyle’s ligament) on the internal
confined to the larynx. Although their main functions
surface of the thyroid cartilage (Figures 1.4a–d) and
are adduction, abduction and adjusting vocal fold tension
run posteriorly to insert on the arytenoid cartilage.
(Figure 1.3), they can help modulate the laryngeal inlet as
The majority of the muscles’ fibres run lateral to the vocal
part of the airway protection mechanism.

Shortens cord and

medialises arytenoids
Arytenoid
(adductor) THYROID
CARTILAGE
Hook retracting left
TA A IA
thyroid lamina Opposes arytenoids and
laterally closes posterior commissure
LCA (adductor)

)
PCA( V
O)
Rotates vocal

A(
PC
process into lumen

Vertical belly: pulls

Oblique belly: pulls back and up (tensor)
laterally (abductor)

Figure 1.3 Actions of the laryngeal muscles. Posterior view of the relationship of the laryngeal muscles to the arytenoid cartilage.
TA, thyroarytenoid; LCA, lateral cricoarytenoid; PCA, posterior cricoarytenoid; IA, interarytenoid.

a b

c d
Figures 1.4a–d Broyle’s ligament. The anterior commissure tendon fibres can be seen inserting into cartilage. The arrangement of the
collagen fibres is well demonstrated when viewed under polarised light (d).

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 Basic science

ligament and constitute the vocalis muscle. The upper Cricoarytenoid joint
division of the muscle, which varies among individuals, runs
The cricoarytenoid joint (CAJ) is a synovial articulation
in the aryepiglottic fold, vestibular folds and lateral to the
between the base of the arytenoid cartilage and the lamina
laryngeal ventricle.
of the cricoid cartilage. The joint has a loose capsule
The primary function of the thyroarytenoid muscle is
inserting at a distance from the cartilage articulation
to shorten the vocal ligament and adjust vocal fold tension
surface margin, allowing a wider range of movement.9
during phonation. Furthermore, muscle contraction can
The arytenoid cartilage can glide forwards and backwards
rotate the arytenoid cartilage inwards to close the glottis.
over the cricoid lamina, rock medial and lateral and rotate
around its axis. The  capsule  of  the CAJ is reinforced by
Posterior cricoarytenoid muscles the posterior cricoarytenoid ligament. Despite the  name,
The posterior cricoarytenoid muscles extend upwards the majority of the ligament fibres are medial rather than
and laterally from the posterior surface of the cricoid posterior to the joint. The ligament fibres extend above the
lamina and insert on the muscular process of the arytenoid level of the articulation to insert at the arytenoid body and
cartilage.The posterior cricoarytenoid muscles are the only vocal process.9 It is believed the cricoarytenoid ligament
vocal fold abductors. The more horizontal superior part of is the major determinant of the cadaveric position of the
these muscles rotate the arytenoid cartilage laterally, thereby denervated vocal cord rather than the intrinsic muscles.10
abducting the vocal folds, whereas the vertical inferior fibres
pull the arytenoids over the upper margin of the cricoid, Membranes of the larynx
which moves them apart.
Thyrohyoid membrane
Lateral cricoarytenoid muscles The thyrohyoid membrane is a fibroelastic membrane
The lateral cricoarytenoid muscles originate from the extending from the upper border of the thyroid cartilage to
upper border of the arch of the cricoid cartilage and insert the hyoid bone. The thyrohyoid membrane is thickened in
on the muscular process of the arytenoid. They rotate the three places to form the median and the lateral thyrohyoid
arytenoid medially to close the glottis. ligaments. The thyrohyoid membrane is pierced by the
superior laryngeal vessels and the internal branch of the
superior laryngeal nerve.
Interarytenoid muscle
The interarytenoid muscle is the only unpaired intrinsic Quadrangular membranes
muscle. It runs posteriorly between the muscular processes
The quadrangular membranes extend from the lateral
of the arytenoids. Its main function is to adduct the vocal
aspect of the epiglottis inferiorly to insert on the arytenoid
folds by approximating them.
cartilage bilaterally. The membrane has two free margins:
a superior less defined margin, which forms part of the
Cricothyroid muscles aryepiglottic fold, and a thickened inferior margin, which
The cricothyroid muscles originate from the anterolateral forms the vestibular ligament.
surface of the cricoid cartilage arch.The fibres pass superior
and dorsal to insert on the oblique ridge of the thyroid Conus elasticus
cartilage. While all the other intrinsic larynx muscles The conus elasticus is a submucosal membrane that
are innervated by the recurrent laryngeal nerve, the originates from the upper border of the arch of the cricoid
cricothyroid is innervated by the external branch of the cartilage. It extends superiorly to attach to the inner plate of
superior laryngeal nerve. the thyroid cartilage anteriorly and the vocal process of the
arytenoid cartilage posteriorly.The free margin of the upper
Joints of the larynx membrane is thickened to form the vocal ligament.
Cricothyroid joint Innervation of the larynx
The inferior horn of the thyroid cartilage articulates
with  the cricoid cartilage at an encapsulated synovial Superior laryngeal nerve
joint. The cricothyroid joint allows both rotation and The superior laryngeal nerve arises from the inferior
glide movement. Contraction of the cricothyroid ganglion of the vagus nerve and contains both motor and
muscles leads to forward and downward tilting of the sensory fibres. It passes downwards and forwards along
thyroid cartilage and a simultaneous upward movement the sides of the pharynx and medial to the carotid artery.
of the cricoid. The  superior laryngeal nerve diverges into internal and

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 Vocal tract physiology

external branches. The internal branch passes between the The recurrent laryngeal nerve and the superior laryngeal
middle and inferior constrictor muscles, and then enters nerves communicate at a variety of sites in the larynx. The
the larynx by piercing the thyrohyoid membrane with the best described of these is Galen’s anastomosis, between
superior laryngeal artery. In the larynx, this nerve divides the posterior branch of the recurrent laryngeal nerve and
into an ascending branch, which supplies the piriform the dorsal branch of the internal superior laryngeal nerve.
sinus mucosa, and a descending branch, which supplies the Other sites of anastomosis are the interarytenoid plexus, the
supraglottic area. The external branch continues on the cricoid anastomosis and the communicating nerve between
external surface of the larynx, beneath the sternothyroid the external superior laryngeal nerve and the recurrent
muscle. It  provides the motor innervation for the laryngeal nerve.12
cricothyroid muscle. It occasionally provides a supply to the
thyroarytenoid muscle and other intrinsic laryngeal muscles, Blood supply to the larynx
albeit mainly proprioception. The superior laryngeal nerve
The laryngeal blood supply is derived mainly from the
receives a branch from the superior sympathetic ganglion
superior and inferior laryngeal arteries, which originate
on each side of the upper neck.
from the corresponding superior and inferior thyroid
Of surgical importance is the close proximity between
arteries.The superior laryngeal artery runs over and pierces
the superior laryngeal nerve and the superior thyroid
the thyrohyoid membrane as it enters the larynx, along
artery, which makes it susceptible to injury during
with the internal branch of the superior laryngeal nerve.
thyroidectomy.11 Damage to the external branch can lead to
The inferior laryngeal artery runs along and enters the
cricothyroid muscle paralysis, which will limit the patient’s
larynx with the recurrent laryngeal nerve.The cricothyroid
ability to raise the pitch of the voice. Damage to the internal
artery, a variable branch of the superior thyroid artery,
branch leads to sensory loss in the supraglottic area, which
runs horizontally over the cricothyroid membrane and
increases the risk of aspiration.
contributes to the laryngeal blood supply. Venous drainage
Recurrent laryngeal nerve occurs via the superior and inferior laryngeal veins that run
parallel to their corresponding arteries.
The right recurrent laryngeal nerve originates from the
vagus at the level of the right subclavian artery, and passes
below and behind the artery. On the left side, it originates Lymphatic drainage of the larynx
from the vagus in the chest and passes around the aortic The free edge of the vocal cords has no lymphatic vessels;
arch. Both the right and left recurrent laryngeal nerves however, the supraglottic and subglottic regions have
travel upwards towards the larynx, running along the a rich lymphatic network with distinct patterns. The
tracheoesophageal groove. The nerves enter the larynx superior surface of the vocal cords has several lymphatic
with the inferior laryngeal artery immediately behind the vessels running parallel to the free margin of the cord,
cricothyroid articulation. The nerve gives two, or more, draining the lymph towards the posterior commissure
branches just before or after it enters the larynx. The nerve and then to the supraglottic and subglottic lymphatic
carries sensory fibres supplying the subglottic region and networks. The inferior surface of the cord and the
motor fibres innervating all the intrinsic laryngeal muscles, subglottic region have a rich lymphatic network with a
excluding the cricothyroid. number of large collecting lymphatic vessels. The lymph
The recurrent laryngeal nerve has a close but variable drainage from this network is found to communicate
anatomical relationship with the inferior thyroid artery, with the subglottic network inferiorly and with the
which puts it at risk during thyroidectomy. The nerve can supraglottic network via the anterior and posterior
pass in front, behind or between this artery’s branches. commissures.13,14

Vocal tract physiology

Basic functions interrupted out-breath. This preserves the ability to cough
should ingested material  enter the airway. A cough is the
The human larynx serves three main functions: airway
explosive release of a forced out-breath from a tightly closed
protection, respiration and phonation. Acting as a
glottis that relaxes.The cough can therefore be employed at
sphincter, the larynx prevents food, liquids and saliva from
any time to expel material from the airway.
entering  the trachea.This is achieved via posterior reflection
During the respiratory cycle, the glottis operates to
of the epiglottis to close the laryngeal inlet, closure of the
optimise respiratory function. During quiet breathing
true and false cords and cessation of respiration during an

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 Basic science

the vocal folds are maintained in the paramedian position The laryngeal protective reflex takes precedence
with limited subtle movements. Minor inspiratory vocal over other upper airway tract functions. It remains intact
cord lateralisation and expiratory medialisation movements while performing voluntary voicing and respiratory tasks,
are thought to help maintain positive pressure in the alveoli including forced inhalation, humming, phonation and
during passive breathing. Increased respiratory demand voluntary glottic closure.17
leads to vocal fold abduction and a subsequent increase
in the glottis cross-sectional diameter, which reduces air Phonation
turbulence.4
Speech production is one of the most complex functions of
The role of the larynx in phonation is discussed later in
the human larynx. It results from vibrating the vocal folds,
this chapter.
which produces a fundamental tone called the fundamental
Laryngeal reflex frequency. The fundamental frequency is the number of
times the vocal folds open and close per second.This sound
Afferent system produced by the vocal folds is modified by the rest of the
Sensory nerve fibres supplying the supraglottis and superior vocal tract to produce speech.
glottis are derived from the internal branch of the superior
laryngeal nerve.The area below the vocal folds is innervated The vocal tract
by the recurrent laryngeal nerve. The sensory innervation There are various components of the vocal tract:
in the larynx is at its highest density in the laryngeal inlet,
which is consistent with its primary function of airway ●● Activator. The lungs and respiratory muscles produce
protection. airflow through the vocal folds, causing them to vibrate.
●● Generator.The vocal folds act as vibrators.
Efferent system ●● Resonator. The voice signal produced by the vocal
folds is modulated within the various pharyngeal and
The recurrent laryngeal nerve innervates all the intrinsic
supraglottic cavities. The resonating frequency of these
laryngeal muscles, except for the cricothyroid muscle,
cavities can be adjusted by a change in their three-
which is innervated by the external division of the superior
dimensional shape.
laryngeal nerve. Motor innervation for these muscles
●● Articulator. The palate, tongue, teeth and lips can
originates in the medullary nucleus ambiguus.
further modulate the voice signal to produce speech.
Protective reflex
Stimulating the upper respiratory tract evokes a strong
Myoelastic-aerodynamic and body-cover
glottic adduction reflex. Most of the afferent impulses for theories of phonation
this reflex travel from the respiratory tract to the brainstem The phonation process begins with the laryngeal muscles
via the internal branch of the superior laryngeal nerve. closing the glottis and placing the vocal folds under
Efferent impulses are then sent via the recurrent laryngeal appropriate longitudinal tension. When exhalation starts,
nerve to close the glottis.The entire reflex, from respiratory pressure builds up in the subglottic area until it reaches a
stimulation to glottis closure, has a 25 ms latency, which critical phonation threshold pressure. At that point, the
suggests that this brainstem reflex is multisynaptic.15,16 subglottic air pressure (aerodynamic forces) exceeds glottic
Unlike many animals, humans lack a crossed adductor closure (myoelastic) forces, and air is allowed to escape
reflex mechanism. This indicates that stimulating one between the vocal folds. The  vocal folds start to open in
superior laryngeal nerve does not activate the contralateral a posterior to anterior direction to allow air through the
adductor muscles. Therefore, unilateral superior laryngeal cords and reduce the subglottic pressure. The vocal folds
nerve palsy might lead to aspiration, despite an intact then begin to approximate, posterior to anterior. The vocal
recurrent laryngeal nerve function. folds myoelastic forces are enhanced by the Bernoulli effect,
Bilateral stimulation of the superior laryngeal nerve in which airflow through a narrow channel exerts negative
leads to closure of the three muscular tiers of the laryngeal pressure on the channel walls. The vocal folds close fully
sphincter. The first tier is the superior division of the until the subglottic pressure reaches the threshold for the
thyroarytenoid muscle within the aryepiglottic folds, next cycle.
whereas the second tier is the thyroarytenoid within the false In a coronal section of the vocal folds, the mucosal wave
vocal folds. T  he  protection results primarily from closing starts inferiorly and propagates superiorly towards the
the third tier, the inferior division of the thyroarytenoid in upper margin of the vocal folds. When the cycle begins,
the true vocal folds. the two vocal folds are completely closed, but as subglottic

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 Histology of the larynx

pressure increases, the lower margins of the folds begin ●● Mass per unit length. The fundamental frequency of
to separate. The separation moves superiorly and air is vocal fold vibration is inversely proportional to its mass.
released once the upper margins separate. Due to a pressure Longitudinal stretching of the vocal folds via cricothyroid
drop, elastic recoil of the cords and the Bernoulli effect, contraction reduces the fold’s mass per unit length,
the mucosal margins begin to approximate until they close thus increasing the vibration frequency. In contrast,
at the lower margin. The closure moves superiorly to the thyroarytenoid muscle contraction increases the mass per
upper margin, and the glottis closes fully to begin another unit length and decreases the fundamental frequency.
cycle (Figure 2.2). ●● Stiffness. Vocal fold tension plays an important role in
The body-cover model of voice generation suggests two the control of fundamental frequency. It is affected by
layers with different structural qualities: a loose cover of the vocal fold’s contractile forces and tissue elasticity.
mucosa and the superficial layer of lamina propria (forming Adjusting the vocal fold tension via muscle contraction
the cover) vibrating over a vocal ligament (intermediate and changes the vibration rate.
deep lamina propria) and thyroarytenoid muscle (body).18 ●● Viscosity. The ease with which a cover can slide over a
The cover is loose, pliable and non-contractile, whereas body is inversely related to the viscosity of the system.
the body is stiff and has an active contractile ability. Several Thus, hydrating the vocal folds reduces viscosity and
factors affect fundamental frequency: improves the voice quality.

Histology of the larynx

Epithelium and submucosal glands The gelatinous superficial layer of the lamina propria
is mostly acellular and composed of extracellular matrix
The larynx represents the junction between the upper
proteins, water, collagen clusters of the basal membrane,
aerodigestive tract and the lower respiratory tract. Similarly,
reticular fibres and straight or coiled elastin fibres arranged
the laryngeal mucosa represents a transitional area between
in a longitudinal fashion. The epidermal-lamina propria
the stratified squamous epithelium and the pseudostratified
junction is an area of a particular importance for normal
columnar respiratory epithelium.
phonatory function. The basal cells of the epidermis rest
The lingual surface, the upper half of the laryngeal surface
on the basement membrane. Anchoring looped collagen
of the epiglottis and the aryepiglottic folds are covered with
fibres extend from the lamina densa zone of the basement
stratified squamous epithelium. The remaining larynx is
membrane into the superficial layer of the lamina propria,
lined with pseudostratified respiratory mucosa, except for
and back, and insert into the basement membrane. These
the vocal folds, which maintain their squamous epithelium.
anchoring loops intertwine with the thicker longtudinal
The latter is an area of ‘wear and tear’ due to constant
fibres of the lamina propria, forming a woven network of
contact with the contralateral vocal fold during phonation,
fibres.19,20
hence the more resistant epithelium.
The submucosal laryngeal glands are complex, arborised
structures composed of a series of mucous tubules that drain
into common collector ducts.19 They are mainly present
in the lamina propria of the laryngeal mucosa, with the
exception of the laryngeal surface of the epiglottis where
Superficial
they extend deeper. The free edges of the vocal folds lack Intermediate
any submucosal gland, and they depend on the laryngeal Deep
vestibule glands for their surface lubrication.
Muscularis Epithelium
Lamina propria
The structure of the vocal fold’s lamina propria is important
for phonation and the quality of the voice sound produced.
It allows the loose superficial mucosal layers to vibrate freely
over the stiffer, deeper layers of the vocal ligament and the
thyroarytenoid muscle. The lamina propria is arranged
into three layers: the superficial layer (Reinke’s space), the
intermediate layer and the deep layer. As already stated, the
latter two form the vocal ligament (Figure 1.5). Figure 1.5 Microstructure of the vocal cord lamina propria.

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 Basic science

The intermediate layer contains thicker collagen and elastin Macula flavae

fibres running parallel to the free edge of the vocal  fold.
The anterior and posterior macula flavae are unique
The deep layer of the lamina propria is composed of tightly
histological structures, measuring 1 × 1 × 1 mm, located
arranged collagen fibres and coiled elastin. In addition it
at both ends of the vocal folds.They are composed of high-
contains glycoproteins and glycosaminoglycan. The collagen
density fibroblasts in activated phase, collagen and elastin
fibres arrangement allows the vocal folds to resist longitudinal
fibres. They are believed to be responsible for the synthesis
forces during phonation while permitting mucosal vibration
of the fibrous component of the vocal folds. Their role is
in the lateral plane.
most prominent in the new born larynx.21

Immunology of the larynx

The larynx plays an important immunological role because The other unique feature of laryngeal mucosa is the
of its location as a crossroad between the respiratory and presence of MHC class II molecules, which are involved
gastrointestinal systems and as a junction between the in presenting an exogenous antigen to T helper cells.
immunoglobulin A-dominated upper airway and the MHC class II molecules are typically expressed only on
immunoglobulin G-dominated lower airway. In addition, ‘professional’ antigen presenting cells such as dendritic cells
it is the narrowest part of the entire airway and the point and macrophages. While this expression has been shown in
of greatest airflow turbulence. This turbulence exposes the the laryngeal mucosa of healthy individuals, in-vitro grown
laryngeal epithelium to a constant barrage of potentially laryngeal epithelial cells do not express MHC class  II
immunogenic, foreign materials. molecules unless they are stimulated with interferon-
In addition to its role as a physical barrier, the laryngeal gamma (IFN-γ). The mechanism of in-vivo stimulation and
epithelium has unique immunological characteristics.22 the role of MHC class II expression, however, are not fully
Major histocompatibility complex (MHC) class I molecules understood. It is believed that these molecules contribute
are present on all nucleated cells in the human body. Each to immune tolerance to inhaled antigens in the absence
of these molecules contains a fraction of an intracellular of co-stimulatory molecules, although this remains largely
protein called an epitope. These are mostly ‘normal’ self- speculative.
proteins that are constantly built and broken down within Virtually all types of immune cells have been identified
the cell. In addition, they present ‘abnormal’ proteins in the larynx and are distributed throughout the mucosa
resulting from intracellular infection and tumourigenesis. and lamina propria. The exception is the highly organised
In the laryngeal mucosa, MHC class I molecule expression lymphoid collections, which are similar to Peyer’s patches and
decreases towards the lumen. In contrast, levels of β2 are located predominantly in the supraglottic area. Dendritic
microglobulin, a protein essential for forming functional cells have been heavily investigated owing to the roles they
MHC class I complex molecules, do not follow the same play in antigen presentation and immune response initiation.
pattern. This discrepancy led to the discovery of the non- Dense populations of dendritic cells exist in the larynx,
classical MHC class I molecule cluster of differentiation mainly around the basal membrane where dendrites extend
1 (CD1d) on the laryngeal epithelium. The distribution of through the mucosal layers. Helper and cytotoxic T  cells
CD1d along the laryngeal epithelium appears to follow an are concentrated in the lamina propria and the MHC class
opposite gradient from lumen to deep.The function of such I-rich deeper layer of the epithelium.This distribution seems
an arrangement is not fully understood. While the deep logical, as these T cells recognise antigens presented by the
MHC class I-rich compartment plays a role in detecting MHC class molecules. Insults to laryngeal mucosa, such as
viral infection, the role of CD1d in immune regulation tobacco smoking and laryngopharyngeal reflux, change the
remains a subject of debate. immunological composition and function of the mucosa.

Airway biodynamics
During inspiration, air passes through several complex Airflow
cavities from the nose (or mouth) to the pharynx, and it
Airflow rate is defined as the amount of fluid moved in
enters the trachea via the glottis. Airflow through these areas
one second. This is different to airflow velocity, which
is highly irregular due to their complicated anatomy. Once
is the  distance a fluid travels in one second. According to
in the trachea, the airflow becomes more laminar.

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 References

the equation, airflow velocity = airflow rate/cross-sectional or cross-sectional area of the tube, the less air resistance is
area of the tube, the relationship between flow rate and flow encountered.23
velocity is related to the airway diameter. Airflow occurs In reality, the trachea is a complex structure, as three-
when there is a pressure difference between one point and quarters of its diameter is composed of flexible cartilaginous
the other.Airflow typically follows one of two main patterns: rings and one-quarter is composed of the trachealis muscle.
During inspiration, the intrathoracic, tracheobronchial
●● Laminar flow. In this pattern, air flows in layers with the lumen normally expands due to an increased intraluminal
central layer running faster than the peripheral layer. pressure and an increasingly negative intrapleural pressure,
In laminar flow, the relationship between flow rate and which reduces airflow resistance. The posterior wall
driving pressure is linear. This indicates that an increase normally bulges out under these circumstances; however, the
in driving pressure will lead to a proportional increase in trachealis muscle contraction prevents excessive expansion.
airflow. The opposite pattern takes place during expiration – the
●● Turbulent flow. The air runs in a random pattern within trachealis muscle bulges inwards, narrowing the airway.
the airway, with both axial and radial flow. The latter In  the case of forced expiration, trachealis contraction
exerts constant pressure on the walls of the airway and prevents excessive invagination and protects the airway.
consumes energy. Therefore, a higher driving pressure is These pressure changes are in the opposite direction in the
required to maintain flow rate. case of the cervical trachea.

Airway resistance Lung tissue resistance

The trachea can be readily described as a flexible tube. The As it expands, lung tissue offers resistance related to lung
luminal surface area (SA) of the tube is related to the square volume.At a high lung volume, the alveoli are more distended
of the radius (SA = πr2), therefore a small change in the and the elastic recoil of their walls is higher. In the lungs, the
radius leads to a big change in SA. According to the Venturi airway is surrounded and attached to alveoli. As lung volume
Equation, airflow velocity is directly related to the SA, and increases, the tension in the alveoli also increases and pulls
a reduction in the SA will lead to an increased velocity the attached airway outwards to increase its diameter while
and turbulence of the air stream. Furthermore, resistance reducing resistance. In smaller lung volumes, the elastic recoil
to airflow is inversely related to the radius of the tube to of the alveoli is decreased and the airway is narrower, which
the fourth power. In other words, the greater the radius results in an increased airway resistance.

References
1 Standring S (2008) Gray’s Anatomy: The Anatomical 8 Eckel HE, Sittel C, Zorowka P et al. (1884) Dimensions
Basis of Clinical Practice, 40th edn. Churchill Livingston, of the laryngeal framework in adults. Surg Radiol Anat
London. 16:31–316.
2 Virk JS, Sandhu G (2012) Where is the glottis? Clin 9 Pastor LM, Ferran A, Calvo A et al. (1994)
Otolaryngol 37:253–254. Morphological and histochemical study of human
3 Kothby MN, Kirchner JA, Kahane JC et al. (1991) submucosal laryngeal glands. Anat Rec 239:453–467.
Histo-anatomical structure of the human laryngeal 10 England RJA, Wilde AD, McIiwain JC (1996)
ventricle. Acta Otolaryngol 111:396–402. The posterior cricoarytenoid ligaments and their
4 Reidenbach MM (1998) The muscular tissue of the relationship to the cadaveric position of the vocal
vestibular folds of the larynx. Eur Arch Otorhinolaryngol cord. Clin Otolaryngol 21:425–428.
225:365–367. 11 Cernea CR, Ferras AR, Nishio S et al. (1992) Surgical
5 Prades JM, Dumollard JM,Timoshinko AP et al. (2000) anatomy of the external branch of the superior
Descriptive anatomy of the cricoarytenoid articulation laryngeal nerve. Head Neck 14:380–383.
application to articular dynamics in carcinology. Surg 12 Sulica L, Blitzer A (2006) (eds.) Vocal Cord Paralysis.
Radiol Anat 22:277–282. Springer, Berlin.
6 Berkovitz BKB, Hickey SA, Moxham BJ (2000). 13 Liu YH, Xu SC, Tu LL et al. (2006) A rich lymphatic
Anatomy of the larynx. In: Diseases of the Larynx. network exists in the inferior surface of the vocal
(ed. A Ferlito) Arnold, London, pp. 25–44. cords. Surg Radiol Anat 28:125–128.
7 Janfaza P, Nadol JB, Galla R et al. (2001) Surgical 14 McCllouch T, V  an Daele D, Cicci MR (2011)
Anatomy of the Head and Neck. Lippincott Williams & Otolaryngology head and neck surgery: an integrative
Wilkins, Philadelphia. view of the larynx. Head Neck 33:S46–S53.

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 Basic science

15 Czibulka A, Ross DA, Sasaki CT (2000) Laryngeal 20 Gray SD,Ringnatari SS,Harding P (1994) Morphologic
physiology. In: Diseases of the Larynx. (ed. A  Ferlito) ultra structure of anchoring fibres in the normal vocal
Arnold, London, pp. 51–58. fold basement membrane. J Voice 8:48–52.
16 Suzuki M, Sasaki CT (1977) The effect of various 21 Sato K, Hirano M (1995) Histologic investigation of
sensory stimuli on reflex laryngeal adduction. Ann the macula flava of the human vocal fold. Ann Otol
Otol 86:30–36. Rhinol Laryngol 104:138–143.
17 Henriquez VM, Schulz GM, Bielamowicz S et al. 22 Thibeault S, Rees L, Pazmany L et al. (2009) At the
(2007) Laryngeal reflex responses are not modulated crossroads: mucosal immunology of the larynx. Mucosal
during human voice and respiratory tasks. J Physiol Immunol 2:122–128.
585:779–789. 23 Spector JG (2000) Laryngeal stenosis. In: Diseases of the
18 Titze IR, Jiang J, Drucker DG (1988) Preliminaries Larynx. (ed. A Ferlito) Arnold, London, pp. 397–428.
to the body-cover theory of pitch control. J Voice
1:314–319.
19 Ishii K, Zhai WG, Akita M et al. (1996) Ultrastructure
of the lamina propria of the human vocal fold. Acta
Otolaryngol (Stock) 116:778–782.

10

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 CHAPTER 2
Voice assessment in the out-patient
department
Paul Carding & Tracy Miller

Introduction
A successful voice assessment determines the cause, the auditory evaluation and measurements of vocal function
severity and the prognosis of the problem and enables the and vocal physiology. It is time-consuming and cannot be
planning of the most appropriate treatment programme. fully achieved in a ‘routine’ out-patient appointment. Given
Voice assessment is multidimensional; it requires history the complexity of many voice disorders, it usually requires
taking, observation, clinical examination of the structures, a multiprofessional approach.

Voice case history

A thorough case history is essential for the clinical team and provide a valuable baseline against which one can judge
patient to understand the nature of the voice problem, the the success of intervention.6 Perhaps most crucially, the
possible causes and the reasons for its persistence. Questions patient description provides valuable information about
about the patient’s medical history, social behaviours, their insight, awareness and knowledge of their own voice
lifestyle, vocal demands and stressors are essential to problem.
determine areas that might require further exploration.
Case history formats vary by centre and by clinician to Onset of the problem
accommodate clinician preference and patient needs. Some Details of events around the time of onset can be
clinicians may use a series of formal (set) interview questions diagnostically valuable. This information may relate to
and some will administer questionnaires prior to or during a viral infection acting as a trigger and may point to a
assessment.1 Questionnaires exist for specific vocal disorders reduction in general wellbeing. Sudden onset dysphonia/
such as spasmodic dysphonia and paradoxical vocal cord aphonia or difficult life events leading up to the onset of the
dysfunction2, which, of course, can only be administered dysphonia may be suggestive of a functional (non-organic)
post diagnosis. Specific questionnaires of patient groups (e.g. dysphonia linked to psychological distress. Gradual onset is
singers or teachers3) also exist. They are usually designed more common in hyperfunctional and organic dysphonia.
to elicit detailed information pertaining to the patient’s Co-occurring onset of dysphagia, dysarthria or dysphasia
occupation or work demands. will indicate a possible neurological aetiology.
Whatever the format, the areas discussed below should
be covered. Vocal variability
Dysphonia often varies with voice use and rest, time
Patient description of the problem of day and emotional and stress factors. Dysphonia/
How the patient describes the specific nature of their aphonia interspersed with normal voice may suggest a
voice problem can provide essential diagnostic and psychogenic aetiology. A voice that returns to normal with
therapeutic information. Terms such as ‘hoarse’ or rest is indicative of a hyperfunctional dysphonia5, whereas
‘rough’ may be indicative of mucosal changes or muscle normal voice would not be expected in organic pathology.
tension dysphonia; ‘breathy’ or ‘weak’ may be related to In patients who report poor voice on awakening, one
the glottic closure problems seen in vocal cord palsy or possible explanation may be acid reflux.3 It is always
neurological conditions, as well as in the hyperfunctional unwise to assume that the voice the patient presents with
or psychogenic dysphonias, and vocal fatigue may in the clinic is necessarily typical of the voice at other
indicate vocal hyperfunction.4,5 Self-reporting may also times.7

11

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 Voice assessment in the out-patient department

Throat symptoms which they work/play and how well they care for the
voice (e.g.  smoking/alcohol intake, shouting/raising of
Vocal tract discomfort is common in dysphonia. Throat
the voice/singing, hydration levels) are all valuable.
aching, tension, tightness and effort are often related to
muscle  tension8, while soreness, burning and irritation
are more frequently inflammatory symptoms of mucosal General health
changes.8 The Vocal Tract Discomfort Scale is available to Many medical conditions affect the voice including asthma,
quantify the severity and frequency of throat symptoms.9 This chronic obstructive pulmonary disease (COPD), reflux,
tool may also be useful in determining those patients who hypo/hyperthyroidism and inflammatory diseases such
may benefit from laryngeal manipulation or manual therapy.10 as rheumatoid arthritis. A simple symptom checklist helps
in relating voice changes to systemic disease and general
Vocal demands health problems. Likewise, a list of medications helps predict
The case history should also assess the demands that the adverse side-effects on the voice (e.g. bronchodilators and
patient is placing on the voice including questions on medications that may cause coughing or dryness of the
the amount and type of voice use in the patient’s work, mucosa). The case history should also strive to identify
home and social life. Information on the environment in possible psychological distress.

Observation (posture, breathing, palpation)

Informal patient observation is on-going throughout the the  abdomen. Shallow breathing involving the upper
assessment. It helps form the clinical diagnosis and develop chest could indicate asthma or COPD, or excessive
a treatment plan. muscular tension, leading to reduced subglottic pressure
and less effective vocal fold function.4 Close observation
General observation should indicate how frequently the patient inhales
The patient’s general appearance is a sign of health and during conversation, whether the patient is running out
wellbeing, mood and energy. Certain neurological signs of air before completing their sentence and excessive
may be visible: reduced facial expression and/or tremor upper chest and shoulder movements. Listening to the
(possibly suggestive of Parkinson’s disease), facial weakness or patient’s breathing can help identify respiratory disorders
asymmetry (neurological disorders affecting motor function) or disorders at the laryngeal level, such as vocal cord
or involuntary movements (dystonia). Vocal habits such as paralysis, mass lesions, paradoxical vocal cord movement
continuous throat clearing or coughing are also informative. and stridor.
Posture
Inappropriate posture and head/neck positions affect Muscular tension
breathing and voice support from the internal and external The clinician should note excessive, or reduced, tension
laryngeal muscles.11,12 Poor posture contributes to many in the jaw and temporomandibular joints, facial muscles
voice disorders, and correcting posture has been an element and the extrinsic and intrinsic laryngeal muscles. Palpation
of voice therapy for many years (Alexander technique, for evaluation and treatment of muscle tension dysphonia
Feldenkrais technique).4,11 is common in many clinics. A wide literature describes
how muscular tension abnormalities can influence voice
Breath support production. There are a number of diagnostic, assessment
Good breath support provides power to the voice. and treatment protocols relating to muscular tension and
The most efficient, natural breathing is supported in common palpation sites.4,9,13–15

Formal auditory perceptual evaluation

Perceptual auditory evaluation is the expert listener’s evaluation is generally considered the foundation of voice
judgement of voice quality. In most cases this means the assessment; a patient seeks treatment because of the way
semi-objective assessment of deviation from what is their voice sounds, and essentially judges the success of the
considered normal by patient and clinician. Perceptual intervention by improvements in that sound.16

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 Patient questionnaires

A formal perceptual evaluation tool reduces the GRBAS

excessive use of descriptive terms that are a feature of self-
GRBAS is a quick, reliable and robust tool for the
reporting to a more succinct and systematic description
perceptual rating of dysphonic voices. It is most reliable
of the voice that can be communicated to other
when used by experienced voice clinicians after detailed
professionals and to the patient. To examine the voice
training.19–22 It is the most widely used rating scale and is
in a number of contexts (e.g. free conversation, reading
considered the minimum standard of perceptual evaluation
out loud) prolonged vowel phonation and set phrases are
in the UK.16 GRBAS is a 4-point scale of 0 (normal)
recommended. Discrepancies in voice quality between
to 3 (extreme) for five parameters. Grade (G) represents
these tasks can be diagnostically and therapeutically
the overall severity of the dysphonia; Roughness (R) is
revealing. An experienced and skilled clinician can use
the psychoacoustic impression of irregular vocal cord
perceptual auditory evaluation to help identify features
vibration, perceived as hoarseness or harshness; Breathiness
of an underlying vocal cord problem. This tool may also
(B) is the perception of air leakage through the glottis;
alert the team to potential misdiagnosis (or at least justify
Asthenia (A) is the impression of weak voice, which lacks
additional endoscopic evaluation). A full understanding
energy and strength at the level of the glottis; and Strain (S)
and analysis of voice quality can also inform treatment
is the psychoacoustic impression of laryngeal effort. As an
(especially for the voice pathologist/therapist). Perceptual
example, a patient with reduced laryngeal closure due to
auditory evaluation can also provide a valid, reliable and
vocal cord palsy may present with a GRBAS evaluation
sensitive measure of voice change following intervention
of G2R1B2A2S1, indicating a weakness at the glottis
by surgery, medical therapy or voice therapy.6
resulting in moderate breathiness with some laryngeal
Perceptual evaluation scales are chosen according to
strain to compensate.
purpose. A quick and easy tool such as GRBAS17 is ideal
for an ENT clinic, but a slightly more detailed evaluation Consensus Auditory-Perceptual Evaluation
may be found by using Consensus Auditory-Perceptual
Evaluation of    Voice (CAPE-V).18 It is important to of Voice
note that these perceptual rating scales define and CAPE-V was developed from a consensus meeting
grade deviations away from ‘normal’; they are unable to sponsored by the American Speech–Language–Hearing
differentiate between individual voices that would fall Association in 2002. V
  isual analogue scales are used to assess
within the broad category of ‘within normal limits’ for the six vocal parameters considered the most commonly
the speaker’s age, sex and cultural background. It is also used and easily understood. These are: Grade, Roughness,
important to remember that voice quality ratings always Breathiness and Strain (from GRBAS), with the addition of
use an ‘overall’ severity rating and then a rating of specific Pitch and Loudness to assess appropriate pitch and volume
auditory voice quality characteristics (e.g.  ‘breathiness’). and their respective ranges. Other voice features can be
Very specific voice qualities or characteristics (e.g. voice noted as appropriate; these may include resonance, vocal
tremor) or a more detailed auditory analysis may be stamina/fatigue and vocal quality for vegetative tasks such
required in a different environment (e.g. highly specialist as coughing, laughing or crying.
clinic, research or theatre/drama).

Patient questionnaires
Having a voice disorder can severely affect a patient’s daily Vocal Performance Questionnaire
activities, emotions and social life. By understanding the
The VPQ is a 12-item scale to address the physical, social
impact of the dysphonia on an individual’s quality of life,
and emotional aspects of the voice problem.26 It provides
clinicians can understand why they have sought help and
a total score of 12 (no impairment) to 60 (most severe
can plan appropriate patient-focused treatment. Validated
impairment) with no subscales. It has been shown to have
Quality of Life tools also provide useful patient-reported
good validity and test–retest reliability and hence is a useful
outcome measures for treatment, and are widely cited in
tool for voice outcome following intervention.25
the literature. They have established validity, reliability and
sensitivity to change.23–25 In the UK, the Vocal Performance
Questionnaire (VPQ), the Voice Handicap Index (VHI) Voice Handicap Index
and  the Voice Symptom Scale (VoiSS) are the  most The VHI is a 30-item scale, grouped into three domains:
commonly used. functional, emotional and physical aspects of the voice

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 Voice assessment in the out-patient department

disorder.27 A questionnaire was developed and validated.27 Voice Symptom Scale

It was later suggested that the domains were not statistically
The VoiSS is a 30-item scale with a total score and three
independent and hence a short-form 10-item VHI was
content domains: impairment, physical symptoms and
developed.28,29 The performance characteristics of the
emotional response.31 It is considered the most rigorously
VHI-10 were compared with the VPQ.30 They concluded
developed, evaluated and psychometrically robust measure
that both are short, convenient, internally consistent,
for self-assessment of voice quality. It is especially appropriate
unidimensional tools for measuring the severity of a voice
where a more detailed self-reported outcome is required and/
disorder (as perceived by the patient). Either questionnaire is
or where throat symptoms (i.e. soreness, pain) are of interest
highly appropriate in a busy ENT clinic.
alongside voice handicap and disability.

Laryngeal endoscopy and stroboscopy

Laryngoscopic examination is essential for diagnostic as coughing, sniffing and Valsalva can be observed. There
and treatment planning purposes.5 Laryngeal endoscopy are several examination and documentation protocols
is performed for two important reasons: to examine available.4,33 Finally, live flexible endoscopy visual feedback
the vibratory behaviour of the sound source (the vocal is both prognostically valuable and therapeutically effective
folds), and to study the shape and behaviour of the for many patients.34
resonating spaces of the supraglottic tract.4 By observing By contrast, rigid endoscopy is performed by inserting a
the phonatory and resonatory structures under various rigid metal tube transorally. This results in the transmission
conditions, critical diagnostic, prognostic and treatment- of high-intensity light and can produce a highly magnified
shaping information can be obtained.32 Voice production image of the laryngeal structures. The quality of this image
requires very fine control and therefore a vocal disorder enables identification of subtle laryngeal anomalies.32 The
is an extremely sensitive indicator of possible disease. main disadvantage of rigid endscopy is that the procedure
Consequently, the exclusion of disease remains of interferes with the production of natural speech and voice
paramount importance to the laryngologist. However, production and is restricted to evaluation of phonatory
endoscopy is also essential for understanding aberrant function during isolated vowels only.
phonatory physiology and this is the primary concern of
the speech-voice pathologist. Stroboscopy
Stroboscopy has become established as an essential adjunct
Flexible and rigid endoscopy to endoscopic examination of the vocal folds. It allows
Indirect laryngoscopy using a mirror may reveal mass lesions examination of the vibratory movements of the vocal folds
and other gross anatomical abnormalities. It is of historic and provides a basis for making judgements on the integrity
importance but barely justifiable given the availability of the vocal fold body–cover relationship.32 Good quality
and quality of the alternatives that allow far more detailed voice requires regular (periodic) vibration of the vocal folds
assessment. There is debate about the relative merits of and integrity of the vibratory margin of the fold itself.3
flexible versus rigid endoscopy. Flexible endoscopy allows A  diagrammatic representation of the vocal fold vibratory
transnasal laryngeal visualisation. This approach avoids the cycle is illustrated in Figure 2.1. Stroboscopic lighting
problems of the gag reflex and disturbs the supraglottic close to the vocal frequency generates aliased (pseudo-slow
tract less.4 The technique allows for the examination of motion) images of the vocal folds and allows evaluation of
phonatory function during connected speech, singing and the wave activity of the leading edges of the folds during
other vocal and vegetative tasks. voicing. These vibrations are far too rapid for the eye to
Flexible fibreoptic laryngoscopy using continuous light detect under continuous light. Rigid endoscopy has been the
enables prolonged and detailed examination of the laryngeal preferred means of capturing stroboscopic images because of
structures (including the aryepiglottic folds, ventricular the greater amount of light and the highly magnified images.
folds, arytenoids and true vocal folds) and supraglottic However, flexible endoscopes are now produced with a
structures (including the hypopharyngeal, pharyngeal, miniature digital camera at the distal tip (the so-called ‘chip
oral nasal and palatal structures). The examination is on the tip’ flexible endoscopes).This development, alongside
performed at rest and during dynamic voice tasks. It is advances in fibreoptic technology, has meant that flexible
clearly important to examine the very tasks that the patient endoscopic stroboscopy is reaching a comparable quality to
reports as problematic. Other diagnostic manoeuvres such rigid endoscopic images.

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 Laryngeal endoscopy and stroboscopy

1 6

2 7

8
3

4 9

5 10

Figure 2.1 Diagrammatic representation of a single vibration of the vocal folds (called ‘the vocal fold vibratory cycle’ or ‘the glottal cycle’).
The cycle begins by the adduction of vocal folds (point 1) and subglottal pressure begins to build up. This eventually reaches a point where
the subglottal pressure overpowers fold resistance just enough for the vocal folds to start to blow open (point 2). A consequence of the
open phase (points 3–7) is that subglottal pressure reduces again and the vocal fold resistance overpowers the airflow. This signals the start
of the closing phase (point 8) as the folds move toward each other. Once the glottis is closed, the subglottal pressure begins to build up
again to start the next entire glottal cycle (point 10). The speed quotient can be defined as the ratio of the durations of the opening phase
to the closing phase. The open quotient can be defined as the ratio of the duration of the open period to the duration of the entire cycle.
During the closed phase the vocal folds absorb the impact of their collision. The more ‘elastic’ and compliant the vocal folds are, the more
they are able to absorb the impact.

Boehme and Gross35 described the added diagnostic value light; there is a reliance on the extraction of a fundamental
of stroboscopy. Definitions of standard terminology used frequency for synchronisation of the stroboscopic light.
in stroboscopy is given by Mathieson.5 Several authors3,35 Therefore, examination of severely dysphonic (aperiodic)
identify key stroboscopic features that require qualitative voices is not possible.5,37
analysis: (a) symmetry of mucosal waveform movement, Furthermore, stroboscopy only gives the illusion of
(b) periodicity of mucosal waveform movement, (c) glottic continuous motion. Some information (e.g. intermittent
closure pattern, (d) the amplitude of mucosal waveform or irregular activity) is lost.4,5 Other visual examination
vibration and (e) the presence of non-vibrating portions. techniques such as ultra-high-speed photography, narrow
There are several documentation protocols that exist for band imaging and laryngeal videokymography have been
practicing voice clinicians.4,17,35,36 developed3,37, but are not yet available routinely in a clinical
There are disadvantages to stroboscopy. The evaluation setting. High-speed (digital) photography holds enormous
is subjective, dependent upon examiner experience and potential for the study of vocal behaviour. This technique
training; inter- and intra-rater reliability is often not reported is not dependent on tracking the fundamental frequency of
in the literature. Hirano and Bless36 recommend a digital the vocal output and is capable of capturing subtle vibratory
image training programme to develop stroboscopic evaluation features that are not often apparent in traditional stroboscopic
skills.35 Most significantly, the voice waveform must be motion. In addition, this new technology can reveal key vocal
reasonably periodic in order to trigger the stroboscopic dynamics during phonatory onset and offset.32

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 Voice assessment in the out-patient department

Instrumental measures
In voice therapy,‘instrumental measures’ are indices of physical relationship has yet to be proved convincingly but lack
properties of voice production including airflow, pressure and of evidence has not encumbered their extensive use in the
sound waveform. Many instrumental measures have been research literature. Jitter (pitch perturbation) is a measure of
applied to laryngeal function and vocal output. Only the the cycle-to-cycle involuntary variations in the frequency of
most important measures will be reviewed, since they rarely the vocal note. Shimmer (amplitude perturbation) is a similar
feature in routine voice assessment. Instrumental techniques measure of irregularity in amplitude. Harmonic-to-noise ratio
have been widely used as outcome measures in the published (HNR) expresses the relative amounts of periodic (regular
literature, but the justification has often been poorly argued and repetitive) and aperiodic (irregular and non-repetitive)
and there are problems concerning reliability, validity and components in the sound signal. Pathological voices tend to
applicability.23 Some key measures are described below. exhibit higher jitter, shimmer and HNR than normal voices.
Multi-parameter indices are also used. The Dysphonia
Simple aerodynamic assessments of core Severity Index (DSI)40 is compiled from: highest frequency
phonatory ability and capacity (F0-High in hertz), lowest intensity (I-Low in decibels),
These include maximum phonation time (MPT) and S/Z maximum phonation time (MPT in seconds) and jitter (%).
ratio.The MPT is the maximum time (in seconds) for which The DSI ranges from +5 (perceptually normal) to –5
a person can sustain a vowel sound (usually ‘ah’ as in ‘art’) (severely dysphonic). A correlation exists between the DSI
produced on one breath at comfortable pitch and loudness. and the VHI score.
Typically, the best of three attempts is used as a measure of Historically, sound recording and processing has required
glottic efficiency. A maximum phonation time of 26–35 dedicated and expensive hardware and software (e.g.
seconds in males and 15–25 seconds in females is considered KayPENTAX Computerized Speech Lab, CSL), but the
normal.5 An abnormally low MPT is often found in laryngeal consumer home recording market means that professional
paralysis and could be considered as an appropriate outcome quality hardware is cheap, and software (notably Audacity
measure following therapy or surgical intervention.17 and Praat) is now free.
The S/Z ratio is the length of time the patient can hold the Sound source signal processing has limited clinical
‘sssssssssss’ in comparison with the ‘zzzzzzzzzz’ sound. The application, primarily due to the unclear relationship
normal ratio is 1:1, but subjects with laryngeal pathology can with perceptual impression. However, there remain other
typically phonate ‘zzzzzzzz’ for a shorter time than ‘ssssssss’.38 problems of measurement reliability; small changes in
procedure can give vastly different results in the same
Complex aerodynamic assessment measures patient.41,42 Perhaps most significantly, Titze43 and others
These include: phonatory airflow (measurement of steady have stressed that acoustic analysis is best applied to periodic
and peak airflows during connected speech); phonatory or nearly periodic (Type I) signals of near-normal voices,
air pressure (measurement of air pressure below the vocal which rather limits their value in the voice clinic.
folds); and phonation threshold pressure (minimum level of
lung pressure required to sustain vocal fold oscillation at a Electrolaryngography/electroglottography
specific pitch). Electrolaryngography (Lx) is a non-invasive technique
Airflow and volume can be measured by spirometry, that records the contact between the vocal folds during
a key tool of the respiratory physiologist. Instrumentation to phonation.39,44,45 Two electrodes are placed either side of
measure air pressure per se is readily available, but phonation the larynx and a small electrical current is passed between
threshold (subglottal) pressure is difficult to measure directly them. This technique is valuable in providing micro level
and is usually estimated by intraoral pressure at the time detail of the cycle-to-cycle behaviour of the vocal folds
phonation stops. during voicing.4 The output, often known as the Lx
waveform, identifies the closing, closed and open phases of
Sound source signal processing the vibratory cycle. This cycle is illustrated in Figure 2.2.
This measures cycle-to-cycle parameters from the acoustic The degree of vocal fold contact is represented by the
waveform.These techniques typically measure the irregularity amplitude of the waveform, and reduced amplitude can be
(or aperiodicity) of the vocal note on the premise that this indicative of poor vocal cord contact in pathological voices.
irregularity correlates with dysphonia.39 Ostensibly, aperiodic Fundamental frequency can be measured during production
components are introduced by irregular or asymmetric of a single note as well as during connected speech and
adduction (closing) of the vocal folds; they impair the clarity irregularity (%) of this is commonly used as a graphic
of the vocal note and are perceived as ‘hoarseness’. This exact indicator of disordered voice.

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 References

B airway’s modulation of the source waveform. However,

surface electrodes are not without problems, particularly
interference from electrical noise.39 In photoglottography
(PGG), a light is shone through the glottis whose intensity
relates to the open area of the vocal fold.46 Combined EGG
and PGG might provide maximum information, but this
A A1
technique has not been adopted in clinical practice.
15 MS
Figure 2.2 Features of a normal electrolarynography waveform Electromyography
over 15 milliseconds of time. Point A represents the start of the Electromyography (EMG) is a technique that uses a
closing phase of the vocal folds (i.e. when they first begin to needle or hooked wire electrodes, which are inserted
make contact). Point B represents the point of maximum (full) into four pairs of laryngeal muscles: the thyroarytenoid,
contact of the vocal folds. Point A1 represents the start of the the lateral cricoarytenoid, the posterior cricoarytenoid
next vibratory cycle. Therefore, A to B represents the closing
and the cricothyroid.47 The patient performs a variety
phase of the vocal folds and B to A1 represents the opening phase
of vocal tasks. The electromyograms are assessed by
of the vocal folds. Both the opening and closing phases appear
to be smooth (i.e. not ‘jerky’ or interrupted). The closing phase listening and viewing the waveform to document
is very quick, as the vocal folds ‘snap shut’. The opening phase is insertion activity, spontaneous activity, recruitment and
significantly longer than the closing phase. In a steady state vowel waveform morphology.47 EMG provides information
production, each cycle of vibration will look very similar. about the integrity of the superior and recurrent
laryngeal nerves and the muscles that they innervate.47
Some clinicians prefer electroglottography (EGG) to It is rather invasive by comparison with most of the other
sound source signal processing because it avoids the upper tests described here.

Conclusion
Most voice disorders are complex and diagnosis needs to with the multi-dimensional nature of voice disorders so
be based on the results of detailed assessment, taking into that they can be aware of any limitations in their assessment
account many factors as described in this chapter. It can and refer on to specialist voice clinics, if needed, to ensure a
often be difficult to carry out all relevant assessments in the highly informed diagnosis is made.
busy, routine ENT clinic, but clinicians should be familiar

References
1 Martin S, Lockhart M (2005) VIP: Voice Impact Profile. 9 Mathieson L, Hirani SP, Epstein R et al. (2009)
Speechmark Publishing, Bicester. Laryngeal manual therapy: a preliminary study
2 Koschkee DL, Rammage L (1997) Voice Care in the to examine its treatment effects in the management of
Medical Setting. Singular Publishing, San Diego. muscle tension dysphonia. J Voice 23:353–366.
3 Sataloff RT (2005) Clinical Assessment of Voice. Plural 10 Lieberman J, Rubin J, Harris T M et al. (2005) Laryngeal
Publishing, San Diego. manipulation. In: Treatment of Voice Disorders. (ed. RT
4 Harris T, Harris S, Rubin JS et al. (1998) In: The Sataloff) Plural Publishing, San Diego, pp. 115–132.
Voice  Clinic Handbook. Whurr Publishers, London, 11 Koojiman PGC, deJong FICRS, Oudes MJ et al. (2005)
Chapter 13. Muscular tension and body posture in relation to voice
5 Mathieson L (2001) The Voice and its Disorders, 6th edn. handicap and voice quality in teachers with persistent
Whurr Publishers, London. voice complaints. Folia Phoniatr Logop 57:134–147.
6 Carding PN (2000) Evaluating Voice Therapy: Measuring 12 Lagier A, Vaugoyeau M, Ghio A et al. (2010)
the Effectiveness of Treatment.Whurr Publishing, London. Coordination between posture and phonation in
7 Jones SM, Carding PN, Drinnan MJ (2006) Exploring vocal effort behavior. Folia Phoniatr Logop 62:195–202.
the relationship between severity of dysphonia and 13 Aronson AE (1990) Clinical Voice Disorders, 3rd edn.
voice-related quality of life. Clin Otolaryngol 5: 411–417. Thieme, New York.
8 Mathieson L (1993) Vocal tract discomfort in 14 Roy N, Leeper HA (1993) Effects of the manual
hyperfunctional dysphonia. J Voice 2:40–48. laryngeal musculoskeletal tension reduction technique

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 Voice assessment in the out-patient department

as a treatment for functional voice disorders: perceptual 30 Deary IJ, Webb A, Mackenzie K et al. (2004) Short,
and acoustic measures. J Voice 7:242–249. self-report voice symptom scales: psychometric
15 Roy N, Nissen S, Dromey C et al. (2009) Articulatory characteristics of the voice handicap index-10 and
changes in muscle tension dysphonia: evidence of vowel the vocal performance questionnaire. Otolaryngol Head
space expansion following manual circumlaryngeal Neck Surg 131:232–235.
therapy. J Commun Disord 42:124–135. 31 Deary IJ, Wilson JA, Carding PN et al. (2003) VoiSS:
16 Carding PN, Carlson E, Epstein R et al. (2000) Formal a  patient-derived Voice Symptom Scale. J  Psychosom
perceptual evaluation of voice quality in the United Res 54:483–489.
Kingdom. Log Phon Vocol 25:133–138. 32 Aronson AE, Bless DM (2009) Clinical Voice Disorders,
17 Hirano M (1981) Clinical Examination of Voice. 4th edn. Thieme, New York.
Springer-Verlag, New York. 33 Poburka BJ (1999) A new stroboscopy rating form.
18 Consensus Auditory-Perceptual Evaluation of Voice J Voice 13:403–413.
(CAPE-V) (2002) ASHA Special Interest Division  3, 34 Rattenbury H, Carding PN, Finn P (2004) Evaluating
Voice and Voice Disorders. www.asha.org the effectiveness and efficiency of voice therapy using
19 DeBodt M, Wuyts FL,Van de Heyning PH et al. (1997) transnasal flexible laryngoscopy. J Voice 18:522–533.
Test-retest study of the GRBAS scale: influence of 35 Boehme G, Gross M (2005) Stroboscopy. Whurr
experience and professional background on perceptual Publishers, London.
ratings of voice quality. J Voice 11:74–80. 36 Hirano M,Bless DM (1993) Videostroboscopic Examination
20 Dejonckere PH, Obbens C, Leeper HA et al. (1993) of the Larynx. Singular Publishing, San Diego.
Perceptual evaluation of dysphonia: reliability and 37 Svec J, Schutte H (1996) Videokymography: high-speed
relevance. Folia Phoniatr Logop 45:76–83. line scanning of vocal fold vibration. J Voice 10:201–205.
21 Chan KMK, Yiu EML (2006) A comparison of two 38 Eckel FC, Boone DR (1981) The S/Z ratio as an
perceptual voice evaluation training programs for indicator of laryngeal pathology. J Speech Hear Disord
naïve listeners. J Voice 20:229–241. 46:147–149.
22 Eadie TL, Baylor CR (2006) The effect of training 39 Baken RJ, Orlikoff RF (1999) Clinical Measurement of
on inexperienced listeners’ judgments of dysphonic Speech and Voice, 2nd edn. Singular Publishing, New York.
voices. J Voice 20:527–544. 40 Wuyts FL, De Bodt MS, Molenberghs G et al.
23 Carding PN, Wilson JA, MacKenzie K et al. (2009) (2000) The dysphonia severity index: an objective
Measuring voice outcomes: state of the science review. measure of voice quality based on a multi-parameter
J Laryngol Otol 123:823–829. approach. J Speech Lang Hear Res 40:796–809.
24 Steen IN, Mackenzie K, Carding PN et al. (2008) 41 Brockmann M, Drinnan MJ, Storck C et al. (2011)
Optimising outcome assessment in voice intervention, Reliable jitter and shimmer measurements in voice
II: sensitivity to change of self-reported and observer- clinics: the relevance of vowel, gender, vocal intensity,
rated measures. J Laryngol Otol 122:46–51. and fundamental frequency effects in a typical clinical
25 Webb AL, Carding PN, Deary IJ et al. (2007) Optimising task. J Voice 25:44–53.
outcome assessment of voice interventions, I: reliability 42 Brockmann M, Storck C, Carding PN et al. (2008)
and validity of three self-reported scales. J  Laryngol Voice loudness and gender effects on jitter and shimmer
Otol 121:763–767. in healthy adults. J Speech Lang Hear Res 51:1152–1160.
26 Carding PN, Horsley I, Docherty G (1999) A study 43 Titze IR (1995) Workshop on Acoustic Voice Analysis:
of the effectiveness of voice therapy in the treatment Summary Statement. National Centre of Voice and
of 45 patients with non-organic dysphonia. J Voice Speech, Denver.
13:72–104. 44 Fourcin A, Abberton E (1971) The first application of a
27 Jacobsen B, Johnson A, Grywalski C et al. (1997) The new laryngograph. Med Biol Illus 21:172–183.
Vocal Handicap Index (VHI). Am J Speech Lang Pathol 45 Rothenberg M, Mashie JJ (1998) Monitoring vocal
6:66–70. fold adduction through vocal fold contact area. J Speech
28 Wilson JA, Webb A, Carding PN et al. (2004) The Hearing Res 31:338–351.
Voice Symptom Scale (VoiSS) and the Vocal Handicap 46 Murty GE, Carding PN, Lancaster P (1991) An
Index (VHI): a comparison of structure and content. outpatient clinic system for glottographic measurement
Clin Otolaryngol 29:169–174. of vocal fold vibration. Br J Disord Commun 26:115–123.
29 Rosen C, Murry T, Zina A et al. (2000) VHI change 47 Sataloff RT, Mandel S, Heman-Ackah Y et al. (2005)
following treatment of voice disorders. J Voice 14: Laryngeal Electromyography, 2nd edn. Plural Publishing,
619–623. San Diego.

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 CHAPTER 3

The professional voice user

John S. Rubin

Overview
This chapter reviews care of the professional voice user. telephone operators, receptionists, salespeople, stock and
Clearly, the first question to be addressed is: who can be bond traders, also fulfill the definition. Furthermore, any
considered as a professional voice user? It has been suggested individuals studying to join into these professions should be
that this group would include anyone who uses their voice included.1 This demonstrates that professional voice users
as a primary means of occupational communication.1 encompass a large proportion of society. It is extraordinary
Specifically, this could include: how we, as a society at large, take our voices for granted,
and how much psychological as well as physical damage we
●● The requirement for occupational communication by
suffer when our voices stop being available as and when
means of the voice.
required.This will be expanded on later in the chapter.
●● The production of a desirable and dependable vocal
Even among ‘elite’ voice users, performance requirements
sound carrying its own message, often requiring subtle
vary enormously. Examples might include:
pitch, tonal and volume modifications.
●● Classical performance in which purity and clarity (and
If this definition is accepted, it becomes evident that a
often power) of the sound are of major importance.
fairly large proportion of the workforce can be included
●● Pop/rap/rock/blues in which vocal colourisation attains
within it. Some have separated out a group of ‘elite vocal
far greater importance.
performers’.2,3 However, in this chapter it is preferable
●● The acting and broadcasting voice in which the vocal
to maintain the broader perspective. Thus singers, actors,
persona and emotional montage often take on a life of
broadcasters, announcers, public speakers, politicians and
their own.
talk show hosts may immediately come to mind. However,
other groups of occupations, for example call centre Of course, underpinning all of these performance styles
workers, teachers, sports coaches, exercise and aerobics are adequate breath support, posture and, in many cases,
instructors, clergy, lay preachers, barristers and trial lawyers, excellent microphone and amplifier utilisation.

Anatomy and physiology of the voice

As the discussion proceeds on professional voice users, it of expiration. On this basis, the abdominal wall musculature
is necessary to characterise the vocal organ. It is important plays a substantial role. The innermost layers are of particular
that the entire body is considered. That said, the vocal tract importance. The intercostal muscles are also of importance,
is generally divided into power source, true vocal folds and especially when sustaining a long or powerful sound.4–9
resonators. Almost any pulmonary pathology can affect the efficiency
of expiration and thereby impact on the power source. This
Power source could vary from post-viral cough, asthma, bronchitis, chronic
The critical issue when discussing the power source is the obstructive pulmonary disease and emphysema through
development and maintenance of a column of air under cystic fibrosis, asbestosis and pneumoconiosis through cancer
pressure, which is presented to the subglottis and glottis. of the lung. Similarly, pathology affecting the abdominal
Whereas the diaphragm is the essential muscle for the act musculature (for example diastasis recti due to pregnancy)
of inspiration, expiration – and in particular controlled and pathology affecting the rib cage (for example pectus
expiration – is necessary for vocalisation. In this model, the excavatum, kyphoscoliosis) can affect the power source.
relaxing diaphragm interacts with the muscles of expiration Ageing also has a direct affect on the power source. Costal
as well as with the natural elastic recoil implicit in the act cartilages calcify with age and pulmonary function declines.10

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 The professional voice user

True vocal folds completeness of vocal fold closure or the mucus that
lubricates the vocal folds may impact on the voice.
The length of the true vocal folds varies in adult humans
from approximately 15–18 mm in females and 20–22 mm
in males.11 As Scherer points out11,12, they can only vibrate Resonators
together and create sound when held relatively close In an isolated larynx, the sound created by vibrations of the
together, in approximately 10–15% of their adductory and vocal folds is heard as a ‘buzz’, the fundamental frequency
abductory range. Pitch is predominantly determined by the of which is determined by the number of vibrations per
stretch placed on the vocal folds by the intrinsic laryngeal seconds (in hertz [Hz]).This ‘buzz’ is rich in harmonics and
musculature. Power of the voice is more dependent on overtones. As this sound passes upwards through the moist
factors such as subglottic pressure.13–17 While the vocal folds structures of the pharynx and oral (and nasal) cavities, it is
can vibrate many hundreds of times per second, adult males modified by these structures. Different frequencies of the
in conversational speech tend to vary the vibrations therein sound are damped (absorbed) and others are amplified
from 75 to 450 times per second (Hertz) and adult females (reflected) to give peaks of certain frequencies known
from 130 to 520 times per second.18,19 In cyclical vocal fold as formants. This is a dynamic process (with changes in
vibrations, closure of the vocal folds relies on elastic recoil the shape of the larynx, pharynx and oral cavity causing
and the Bernoulli effect. the altered resonant frequencies), and is fundamental to the
Bernoulli noted that when a stream of air passes creation of understandable speech.27 It is often stated16 that
between two surfaces, there is a negative pressure the first region of amplified energy (the first formant) tends
between those surfaces; hence, they tend to be pulled to be located somewhere around 500 Hz in men (and about
together. Thus, air passing between the vocal folds 10–15% higher in women). The position of the posterior
generates negative pressure and tends to pull them third of the tongue plays a major role in this. Other formants
together, causing glottic closure. Further refinements of of amplified energy often occur at approximately 1,500 Hz
this model include work by such scientists as Colton16,20, and 2,500 Hz corresponding to some degree to the position
Scherer11, Titze14,15,21–23, Baken18,24, Hollien 25 and of the middle and tip of tongue respectively.8,27 The
others. Recently, it has become clearer that Euclidean adult male vocal tract is approximately 17 cm in length.26
mathematics is not sufficient to explain vocal fold Obviously, alterations of the vocal tract, for example those
function and the field of non-linear dynamics has been brought about by surgery on the pharynx or tongue, can
invoked to a greater or lesser degree. 26 impact on the resonators and the resultant sound. Recently,
As a general rule, anything that affects the stiffness studies utilising functional MRI have proved to be of
or elasticity of the vocal folds, the regularity and/or substantial benefit to the understanding of this process.28,29

Vocal difficulties in performers

Students are particularly prone to vocal difficulties, and it is utilisation of health services.31 Higher stress levels at the
instructive to examine some of the issues they encounter: workplace promote illnesses such as sleeping problems,
it is common, for example, that students of the performing eating disorders, anxiety and depression.32 Stress at work
arts often have many commitments at any given time. has been associated with a variety of health-related issues
Many are away from home having to fend for themselves including hypertension and coronary artery disease33 and
for the first time. At the same time they find themselves in back and upper extremity musculoskeletal disease.34
a busy schedule learning singing, acting and dance, with Stress has a considerable impact on the voice. Changes in
issues relating to posture and breath support all at the emotions can have rapid effect on the autonomic nervous
same time. Of course there are new friendships to make system, yielding rapid swings in secretion, muscle motility
and social events to attend. These young adults often have and acidity. It has been known for over 30 years35–37 that
difficulties with time management, and will require help emotional stress can lead to contraction of the intrinsic and
in learning to prioritise their different work and social extrinsic laryngeal musculature.
commitments. Of course there are many other ‘stressors’ that can lead
A common denominator found in almost all students to voice problems. Viral upper respiratory tract illnesses
as well as other professional voice users is stress.30 Stress are commonplace. Sequelae can include bronchitis,
can be associated with psychophysiological dysfunction. sinusitis, acute laryngitis and cough. Post-viral illness with
About one-third of workers report high levels of stress, prolonged cough is also not uncommon and can lead to
and workers who experience stress demonstrate higher mucosal changes at the level of the true vocal folds as well as

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 Vocal difficulties in performers

perilaryngeal muscle maladaptation. Tonsillitis is prevalent Systemic issues affecting the voice
in young adults, as is glandular fever.
Many underlying illnesses can impact on the voice. Thyroid
Throat irritation can be brought about through a variety
axis disorders, eating disorders and hormonal disorders are but
of mechanisms. Approximately 20–25% of the western
a few. Neurological voice disorders should never be forgotten
world suffers with allergy, allergic rhinitis and/or asthma.
by the practising laryngologist. Conditions such as myasthenia
Information relating to the effects of allergy on the voice
gravis may have voice problems as a first manifestation. Some
is still in its infancy38–42 but it does appear that it can play
forms of Parkinsonism can also present with voice issues.Vocal
a role in voice problems, as can some of the medications
cord paralysis or paresis can be a presenting sign of underlying
prescribed (see below).
disorders as diverse as lung cancer, mediastinal lymphoma,
Cigarette smoking is still relatively common amongst
sarcoidosis, acromegaly or it could be a sequela of a viral upper
young adults. It is an important role of the laryngologist to
respiratory illness. Many other neurological illnesses have
review the short- and long-term side-effects at some length.
voice speech and swallowing issues at some point during their
Many young people do not find long-term risk such as lung
course.49–52 These are discussed in Chapter 5 (Neurological
cancer sufficiently worrisome to stop smoking and indeed
and neuromuscular disorders of the larynx).
many seem to use cigarette smoking as a form of weight
Musculoskeletal problems are commonplace. They
control. The likely risks of skin damage and wrinkling and
range from muscular sprains to road traffic injuries. Even
of reflux related to smoking often seem to be more cogent.
exercise can cause voice problems due to vocal grunting
A number of drama schools now formally or informally
when lifting weights or vocal dryness when preparing for
require their students to undertake a pact not to smoke,
marathons.6,53,54
and this is most helpful. Laryngologists should work closely
with primary care doctors to encourage smoking cessation, Stress and the voice
and performers should be counselled to attend smoking-
There are many potential external stressors that students
cessation clinics.
frequently face. These vary widely from problems at home
Alcohol and controlled substances become more available
or with friends to problems in a production, for example
to the young adult when away from home and can have
from over-rehearsing, from special effects, from singing
direct and indirect effects on the voice. Laryngopharyngeal
requirements or stage screaming. There may also be voice
reflux is extremely commonplace in the western world and
abuse outside of performing (working in call centres,
appears to be particularly problematic among professional
waitressing or working in noisy environments).
voice users, perhaps due to the increased use of the
abdominal musculature implicit to supporting subglottal
Caring for the professional voice user –
pressure.43–46
the voice clinic team
Medications affecting the voice A diagnostic and therapeutic team should include a
Many medications have potential vocal side-effects. Dryness laryngologist, a speech and language therapist (SLT),
of the voice and vocal tract can be caused by: decongestants; a physiotherapist and a psychotherapist. The clinic should
antihistamines; many of the anti-depressive medications; also have ready access to voice coaches and singing teachers.
a number of other medications prescribed for psychological The laryngologist needs to act like a sleuth. He/she needs
disorders (e.g. anticholinergics); and inhaled steroids for to ascertain:
asthma.
●● The overall state of the performer.
A number of medications, including calcium channel
●● The specific state of the performer’s vocal tract.
blockers, can increase reflux. Another group of medications
●● The performer’s requirements for this performance.
that could prove problematic to the professional voice
●● Any specific demands for this role.
user (from the standpoint of potential vocal bruising
●● The performer’s schedule.
or haemorrhage) include those with the side-effect of
●● The performer’s training experience both in singing and
platelet dysfunction/anticoagulation. Aspirin and non-
speaking (and possibly in dance).
steroidal anti-inflammatories are regularly prescribed as
are, in older performers with heart issues, warfarin and The SLT has a major role in ‘listening’. It would be
clopidogrel. The risks and benefits of stopping any of these anticipated that the SLT would perform perceptual and
medications must be carefully considered on a case-by-case acoustic analysis. Most will also undertake some type of
basis, often in direct communication with the primary care quality of life questionnaire. Many will have had training in
doctor, cardiologist, rheumatologist or other prescribing counselling.The patients will regularly discuss psychological
physician.47,48 and emotive issues with the SLT that they will not have

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 The professional voice user

discussed with the laryngologist. Recently, more and more there has been an acute haemorrhage. Voice rest is also
SLTs are becoming adept at laryngeal manual therapy.55–59 prescribed by some laryngologists when previous
The physiotherapist is an extremely valued member of pathology has become aggravated. Even after surgery,
the voice team.Their role is to perform a systemic and site- opinions vary relating to voice rest, from none to upwards
specific review of the musculoskeletal system as it pertains of 3 weeks. However, a balance must be struck between
to the patient’s voicing problem. It has previously been adequate rest to allow recovery from injury and over-
determined that a large percentage of patients presenting to resting leading to weakening of the intrinsic and extrinsic
the voice clinic have musculoskeletal elements relating to laryngeal muscles.
the voice problem. The laryngologist can learn to ascertain
a number of these but the physiotherapist has a substantial Corticosteroids
role is managing the underlying problem.54–56 As with voice rest, opinions in the laryngological
The psychiatrist or psychotherapist is an extremely helpful community vary widely relating to the use and dosages
asset to the voice clinic. Patients presenting with voice of steroids in patients presenting with hoarseness. There
problems do not have a greater degree of psychiatric disease is considerable potential for abuse of corticosteroids by
than the general population.30,60–64 That said, Rosen et al.65 professional voice users, and education as to side-effects is
and Aronson35–37 have observed that voice is ‘part’ of the paramount. Side-effects can include adrenal suppression
individual and has an essential role in communication of and immunosuppression, elevation of blood sugar, bone
‘self ’. Thus there is among professional voice users a special density loss and ‘steroid psychosis’ amongst others.1,4
potential for psychological impact. Rosen goes on to note Nonetheless, a brief course of oral or intramuscular steroid
that self-alienation can occur when ‘our’ voice is no longer can be performance-saving; typically, this has minimal
‘us’. Psychosocial determinants do appear to have some side-effects and has a role in the armamentarium of the
impact on presentation; in House’s study66 over 50% of laryngologist. Corticosteroids will cross the placental barrier
individuals experienced an ‘event’ that they could not speak and will also be present in breast milk, and they are known
out about compared with 16% of controls. to have teratogenic potential; thus particular precaution
Rubin and Greenberg have developed a psychodynamic is necessary in women who are either pregnant or breast
model that can be helpful. In this model, an event occurs feeding. Under those circumstances they should only be
triggering dysphonia. It may be organic or psychological prescribed following a frank discussion with the patient
in nature but leads to dysphonia. The dysphonia then and in consultation with the patient’s primary health care
has emotional/physical consequences (e.g. anxiety, fear, physician and/or obstetrician.1
musculoskeletal issues) and the situation becomes reinforcing
in nature.67 Greenberg concurs with House that the underlying Performance cancellation
problem may have been exacerbated by the individual’s Physicians and other paramedical personnel caring for
inability to discuss it. He feels that just the act of discussing the professional voice users will not infrequently find themselves
problem often helps the patients unburden themselves. Rubin in the position of needing to offer an opinion on the
feels that personal empowerment is important to recovery, advisability of performing. This is rarely a straightforward
even if the underlying issue is never discovered.67 On this basis, problem and often requires a multidisciplinary discussion
speech therapy is also of great importance. with the patient, his or her musical director and the speech
It is crucial to incorporate the patient’s opinion into the therapist. The patient’s overall wellbeing is paramount, as
team’s analysis of the problem. For example, an unpublished are the risk/benefits of cancelling a given performance/
study by Rubin and Epstein on sequential patients with voice performances. Most voice teams would consider an acute-
problems presenting to the voice clinic demonstrated that the onset vocal fold haemorrhage as a definite indication
patients regularly perceived the severity of their voice problem for cancellation. Other medical problems tend to be less
(as determined using the Voice Activity and Participation clear-cut. In general, the more time available for medical
Profile68) to be severe, while the objective and subjective management (weeks, versus days, versus hours) the greater
analysis performed by the speech therapist demonstrated it to the likelihood of successful short-term management of the
be mild to moderate on acoustic and perceptual examination.69 presenting problem.

Voice rest Useful advice

When should voice rest be ‘prescribed’ for the professional The development of good vocal habits is necessary for a
voice user? There is no unanimity in the field. Most long and fruitful career as a professional voice user. This
laryngologists believe that voice rest is indicated if is true for all, but particularly applicable for the student

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 References

or young performer with no previous formal training. exercise is a beneficial aspect of self-health. The larynx
The  importance of stable and regular sleep and eating consists of muscles that benefit from regular use. Many
patterns should be emphasised. Dietary advice should be experts recommend both regular warm up and cool
offered, suggesting at least three meals should be eaten during down exercises of the voice. When using the voice, it is
the day with a healthy balance between the various food important to recognise the potential for vocal overuse in
groups and, if possible, several hours should elapse between noisy environments such as restaurants, cars and planes, and
the last meal and bedtime. Vocal hygiene, including advice to generally practise self-awareness when exercising the
about hydration, should ideally consist of approximately voice.70
2 litres of water sipped (not gulped) throughout the day (it When considering exercise regimens, it is important
is notable that gulping water too quickly can actually cause for the voice professional to recognise that the abdominal
reflux, and drinking excessive amounts of water can lead to muscles are enormous in comparison with those of
hyponatraemia). the larynx and also deserve regular exercise. The type of
Time management, as has already been suggested, appears exercise undertaken is up to the individual, but any high-
to be a key problem for students as well as professional voice impact exercise programmes would benefit from discussion
users throughout their careers. ‘Mindfulness’ and finding with an expert. Involvement in mind-body programmes
an adequate amount of time for oneself is important for a such as yoga, Alexander, Feldenkrais or Pilates seem to be
healthy state of mind and body. Incorporation of regular beneficial.

References
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Logop 59(6):286–296. 13 Hollien H, Coleman RF (1970) Laryngeal correlates
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19 Gould WJ (1991) Caring for the vocal professional. 35 Aronson A (1990) Clinical Voice Disorders, 3rd edn.
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21 Titze I, Durham P (1986) Passive mechanisms 38 Randhawa PS, Nouraei S, Mansuri S et al. (2010)
influencing fundamental frequency control. In: Allergic laryngitis as a cause of dysphonia: a preliminary
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T Baer, C Sasaki, K Harris). College-Hill Press, 39 Cohn JR, Spiegel JR, Hawkshaw M et al. (1997) Allergy.
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Science. Singular Publishing, San Diego. The  role of allergy in the etiogenesis of laryngeal
24 Baken RJ (1996) Clinical Measurement of Speech and mucosal lesions. Acta Otolaryngol (Stockh) 527(Suppl):
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25 Hollien H, Colton R (1969) Four laminagraphic 41 Karayiwasam H, Lloyd SW, Rotiroti G et al. (2014)
studies of vocal fold thickness. Folia Phoniatr 21: Corticosteroid therapy in otolaryngology. In: Diagnosis
179–198. and Treatment of Voice Disorders, 4th edn (eds. JS Rubin,
26 Baken RJ (2006) Dynamical disorders of voice: RT Sataloff, GK Korovin) Plural Publishing,
a chaotic perspective on vocal irregularities. In: San Diego.
Diagnosis and Treatment of Voice Disorders, 3rd edn. (eds. 42 Randhawa PS, Mansuri S, Rubin JS (2010) Is
JS Rubin, RT Sataloff, GK Korovin) Plural Publishing, dysphonia due to allergic laryngitis being misdiagnosed
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27 Sundberg J (1997) Vocal tract resonance. In: Professional 35(1):1–5.
Voice: The Science and Art of Clinical Care, 2nd edn. 43 Koufman JA,Wright SC Jr. (2006) Laryngopharyngeal
(ed.  RT Sataloff) Singular Publishing, San Diego, reflux and voice disorders. In: Diagnosis and Treatment of
pp. 167–184. Voice Disorders, 3d edn. (eds. JS Rubin, RT Sataloff, GK
28 Echternach M, Sundberg J, Markl M et al. (2010) Korovin) Plural Publishing, San Diego, pp. 419–430.
Professional opera tenors’ vocal tract configurations 44 Sataloff RT, Castell DO, Katz PO et al. (1999) Reflux
in registers. Folia Phoniatr Logop 62(6):278–287. Laryngitis and Related Disorders. Singular Publishing,
29 Lowell SY, Kelley RT, Colton RH et al. (2012) Position San Diego, pp. 55–67.
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dysphonia. Laryngoscope 122:370–377. Pepsin detection in patients with laryngopharyngeal
30 Sataloff RT (1991) Stress, anxiety, and psychogenic reflux before and after fundoplication. Surg Endosc
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Clinical Care. (ed. RT Sataloff) Raven Press, New York, 46 Sataloff RT, Spiegel JR (1991) Care of the professional
pp. 195–200. voice. Otolaryngol Clin North Am 24:1093–1124.
31 NIOSH (1999) Stress at Work. US National Institute 47 Harris TM, Rubin JS (2006) Medications and the
for Occupational Safety and Health, DHHS (NIOSH) voice. In: Diagnosis and Treatment of Voice Disorders, 3d
Publication, Number 99–101. edn. (eds. JS Rubin, RT Sataloff, GK Korovin) Plural
32 Schultz D, Schultz SE (2010). Psychology and Work Publishing, San Diego, pp. 549–560.
Today. Prentice Hall, New York, pp. 91–94. 48 Lavy JA, Wood G, Rubin JS et al. (2000) Dysphonia
33 Prim, D (2005) What workplace stress research is telling associated with inhaled steroids. J Voice 14:581–588.
technical communication. Tech Comm 52:449–455. 49 Sataloff RT, Mandel S, Rosen DC (1997) Neurologic
34 Sauter S, Hurrell J, Murphy J et al. (1997) Psychosocial disorders affecting the voice in performance. In:
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50 Rubin AD, Sataloff RT (2007) Vocal fold paresis and 61 Ginsberg BI, Wallack JJ, Srain JJ et al. (1988) Defining
paralysis. Otolaryngol Clin North Am 40(5):1109–1131. the psychiatric role in spastic dysphonia. Gen Hosp
51 Rubin JS, Epstein R, Shields K (2014) Neurological Psychiat 10(2):132–137.
voice disorders. In: Laryngology Otorhinolaryngology  – 62 Liu C-Y, Yu J-M, Wang N-M et al. (1988) Emotional
Head and Neck Surgery Series. (Series eds. MV Kirtane, symptoms are secondary to the voice disorder in
CE de Siuza; Volume ed. AK Bhattacharrya) Thieme patients with spasmodic dysphonia. Gen Hosp Psychiat
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52 Costello D, Rubin JS Movement disorders of the 63 Schalen L, Andersson K (1992) Differential diagnosis
larynx. In: Scott–Brown’s Otorhinolaryngology, Head and and treatment of psychogenic voice disorder. Clin
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CRC Press, Oxford. In press. 64 Murry T, Cannito MP, Woodson GE (1994) Spasmodic
53 Koufman J, Blalock O (1991) Functional voice dysphonia. Emotional status and botulinum toxin
disorders. Otolaryngol Clin North Am 24:1059–1073. treatment. Arch Otolaryngol Head Neck Surg 120:310–316.
54 Rubin JS, Blake E, Mathieson L (2007) Musculoskeletal 65 Rosen DC, Sataloff RT (1997) Psychological aspects
patterns in patients with voice disorders. J  Voice of voice disorders. In: Professional Voice: The Science and
21(4):477–484. Art of Clinical Care. 2nd edn. (ed. RT Sataloff) Singular
55 Roy N, Leeper HA (1993) Effects of the manual Publishing, San Diego, pp. 305–318.
laryngeal musculoskeletal tension reduction technique 66 House AO, Andrews HB (1988) Life events and
as a treatment for functional voice disorders: perceptual difficulties preceding the onset of functional dysphonia.
and acoustic measures. J Voice 7:242–249. J Psychosom Res 32:311–319.
56 Roy N, Bless DM, Heisey D et al. (1997) Manual 67 Rubin JS, Greenberg M (2002) Psychogenic voice
circumlaryngeal therapy for functional dysphonia: disorders in performers: a psychodynamic model.
an evaluation of short- and long-term treatment J Voice 16(4):544–548.
outcomes. J Voice 11:321–331. 68 Ma EPM, Yiu EML (2001) Voice activity and
57 Mathieson L, Hirani, SP, Epstein R et al. (2009) participation profile: assessing the impact of voice
Laryngeal manual therapy: a preliminary study to disorders on daily activities. J Speech Lang Hear Res
examine its treatment effects in the management of 44:511–524.
muscle tension dysphonia. J. Voice 23:353–366. 69 Epstein R, Stewart L, Rubin JS (2005) Who’s reality
58 Mathieson L (2001) The evidence for laryngeal is it anyways? The interrelationships of objective
manual therapies in the treatment of muscle tension and perceptual evaluations and the patient’s own
dysphonia. Curr Opin Otolaryngol Head Neck Surg perspective in a sequential series of voice patients seen
19:171–176. in one voice center. (Unpublished data)
59 Mathieson L (2001) Greene and Mathieson’s The Voice 70 Carroll LM (2005) The role of the voice specialist
and Its Disorders, 6th edn. Whurr Publishers, London. in the non-medical management of benign voice
60 Carpenter B (1993) Psychological aspects of vocal fold disorders. In: Diagnosis and Treatment of Voice Disorders,
surgery. In: Voice Surgery. (eds. WJ Gould, RT Sataloff, 3d edn. (eds. JS Rubin, RT Sataloff, GK  Korovin)
JR Spiegel) Mosby, St. Louis, pp. 339–343. Plural Publishing, San Diego, pp. 585–607.

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 CHAPTER 4

Benign vocal fold lesions

Lindsay S. Reder & Ramon A. Franco Jr.

Introduction
Benign vocal fold lesions are the most common lesions a year due to hoarseness. The economic impact of this
found in the larynx and are responsible for dysphonia that hoarseness has been estimated to be about £136,000,000
leads to a decrease in quality of life and loss of professional ($200,000,000) per year, making it imperative that
productivity. It has been estimated that approximately 7% physicians understand the nature of these lesions and how
(about 22 million people) miss at least one day of work best to treat them.

Vocal fold nodules

Aetiology/pathogenesis epithelial thickening and, when well formed, become what
is commonly called a nodule.1,2 Continued modelling of
Vocal fold nodules are the most common benign lesions of
vocal folds and the effect of trauma and resultant mass lesions
the vocal folds.They are more frequent in boys and women
has shown the relationship between high vocal demands,
and are commonly diagnosed in those with heavy voice
lack of training and inadequate hydration as risk factors for
use, either professionally or socially. Classically, vocal fold
the production of vocal fold nodules. This model showed a
nodules are described as bilateral and are usually relatively
direct relationship between the driving force of voicing and
symmetric. Symptoms of vocal fold nodules, including
an inverse relationship between cover depth, thus suggesting
effortful phonation, inconsistent voice quality and harsh or
that increased volume and decreased vocal fold cover depth
breathy hoarseness, are related to the lesions’ impairment
(i.e. lack of warming up and poor hydration) may lead to the
of the mucosal wave and/or closure. Voice quality is often
development of these fibrovascular lesions.3 These theories
described as husky, harsh or breathy. Larger lesions will often
may also be the basis for using voice therapy as the initial
lead to a lower than expected pitch. Singers may experience
management strategy in the treatment of nodules.
difficulties with their high notes, especially when singing
softly, with new-onset inconsistency of notes. Additionally,
speaking and singing generally become more effortful. Clinical findings
The term nodule, like polyp, is a morphological Laryngeal examination should include flexible laryngoscopy
description of the lesion’s appearance rather than a and rigid or flexible stroboscopy and voicing at different
histological description. The pathophysiology of nodules is frequencies; however, evaluation at the modal frequency is
multifactorial, but the endpoint is subepithelial deposition of imperative for proper strobe interpretation of the mucosal
scar in the mid-musculomembranous region. These lesions wave. Examination will show bilateral masses at the
are described as fibrovascular, representing scar in the area medial surface of the middle of the membranous vocal
of the basement membrane zone. Several institutions have fold (Figure  4.1a). There may be associated increased
developed models to evaluate the biomechanical factors vascularity over the superior and/or medial surfaces of
that lead to scar formation in this area. Early modelling the vocal folds, highlighting the increased forces needed
suggests that during normal phonation, mechanical stress to overcome the laryngeal inefficiency from the persistent
is highest at the tendinous attachments and lowest at the gaps (Figure 4.1b). Moderate and large nodules will often
mid-fold region. Conversely, during hyperfunctional inhibit full glottic closure, accounting for many of the voice
speech, there is increased stress in the mid-membranous symptoms. Small nodules may only be visualised at high
vocal fold, and these speech types may therefore lead to frequency on stroboscopic examination. Additionally, the
nodules (and polyps). It has been postulated that mechanical height of the nodule and its placement in a cephalocaudal
trauma causes disruption of the epithelial attachments and direction will affect the degree of glottic insufficiency.When
simultaneous haemorrhage and oedema in the subepithelial the nodules are sufficiently large, the closure of the glottis
space.This injury, when chronic in nature, may then lead to is often described as hourglass with anterior and posterior

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 Benign vocal fold lesions

Figure 4.1a The classic appearance of vocal nodules as seen on a Figure 4.1b Vocal fold nodules cause laryngeal inefficiency by
halogen light flexible distal-chip examination. There are bilateral allowing air to escape during phonation through the persistent
fibrovascular masses situated in the mid-musculomembranous anterior and posterior gaps. Because of the pressure leak, more
region of the vocal folds. Note the accumulation of mucus over the subglottal driving pressure is necessary to achieve a loud voice.
lesions due to the airway forces generated around these lesions. The increased vascularity is testament to these sustained elevated
The lesions are typically, but not always, symmetric in size and airway forces.
located at the same location on the vocal fold.

the mainstay of symptomatic treatment because the large

majority of symptoms will respond to appropriate therapy
and improved voicing techniques with minimal chance of
irreversible sequelae. Some argue that lack of response to
voice therapy should alert the practitioner to the possibility
that the lesion may not be a nodule, but this argument is
controversial. Voice therapy focuses on modifying the way
the voice is produced. Therapy often includes techniques
aimed at relieving muscle tension, such as vocal hygiene,
direct facilitation, relaxation and respiration.5 Some believe
that therapy does not significantly alter or eliminate the
nodules because they are fibrovascular lesions. There is a
reversible component, usually present in the form of oedema
from the high collision forces from the phonotrauma,
which can be reduced through the use of improved voicing
techniques.
Figure 4.1c During stroboscopic evaluation, sustained high- Lesions that are recalcitrant, recurrent or do not respond
frequency phonation will usually result in the classic hourglass- to therapy may be responsive to surgery, intralesional
shaped glottal closure pattern due to the premature contact in injections or chemically induced hypofunction. Surgical
the mid-portion of the membranous vocal folds. treatments for nodules were begun well before Hirano6
described the multilayered substructure of the vocal folds
glottic gaps (Figure 4.1c). Surrounding Reinke’s oedema and the importance of the superficial lamina propria layer to
may aid in glottic closure, but the closed phase may be normal voice production. Historically, surgery for nodules
shortened. The mucosal wave should be relatively normal, consisted of vocal fold stripping, a technique that called
with minimal or no impairment of the vibratory properties.4 for ‘grabbing’ vocal fold mucosa and an indiscriminate and
uncontrolled tearing of the cover of the vocal fold in the
Management region of the lesion. Although the lesion was removed, so
In the treatment algorithm, the clinician should consider too was plenty of viable and pliable normal mucosa. This
starting with the least invasive treatment and advance to led to adynamic segments along the valving surface of the
the most aggressive as required. Voice therapy has become vocal folds, increased vocal effort from the aerodynamic

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 Vocal fold polyps

inefficiency (from the lack of closure) and generally allow healing of the surgical site and the patient beginning
unhappy, chronically-hoarse patients. Aware of the to speak under the supervision of a voice-trained speech
importance of the mucosa to voice, phonomicrosurgical pathologist.
interventions attempt to remove the lesions with little More recently, other techniques, including
damage to surrounding mucosa by using incisions close radiophonosurgery and angiolytic lasers, have been
to the lesion. As little dissection as necessary is undertaken reported; however, the use of these two techniques is not
and one should avoid placing incisions on the medial edge yet widely accepted. Adjuvant therapies such as intralesional
of the vocal folds whenever possible. The risks of resecting steroid injections and chemical denervation of the laryngeal
nodules (which are epithelial scar) include inducing adductors with botulinum toxin (BTX) have also been
further scar formation, stiffness of the vibratory surface and described.7–10 Intralesional steroid injections have the
deficiency of the vocal fold leading to glottic insufficiency. added theoretical advantage that they are known to soften
Most surgeons who resect large and symptomatic nodules and reduce the amount of collagen in scars in other parts
that have proven recalcitrant to therapy will remove both of the body (skin). Most of the morbidities associated with
at the same time, taking care not to extend the incisions traditional phonomicrosurgical techniques are related to
into the anterior commissure region. Voice rest of varying surgical incisions. Steroid injections avoid these and may
lengths from none to 2 weeks is typically instituted to potentially reduce the nodule size and associated symptoms.

Vocal fold polyps

Vocal fold polyps take several different forms, including the Clinical findings
isolated, unilateral epithelial lesion often associated with
Laryngeal examination will reveal either a stalked or a
vocal overuse and the bilateral or diffuse polyps of polypoid
sessile lesion, usually on the medial edge of the vocal fold
corditis/degeneration. The pathophysiology, diagnosis and
(Figure 4.2a).The lesion will frequently be associated with
management will be discussed separately.
a feeding vessel, varix or ectasia, or a network of vessels
Unilateral vocal fold polyps (Figure 4.2b). There may be contralateral reactive changes
and scar formation opposing the polyp due to the repetitive
striking forces (Figure 4.2c) The mucosal wave may be
Aetiology/pathogenesis intact or diminished depending on the hyalinisation and
Unilateral vocal fold polyps are seen mostly in adults, more size of the lesion. The size and pliability of the polyp will
often in men, and typically in patients who overuse or
misuse their voice. They have been associated with speech
that includes hard glottal stops and intermittent loud
voicing. They may be pedunculated or broad-based and
can be haemorrhagic or non-haemorrhagic, although this
may simply represent the stage at which the same lesion is
visualised by the clinician. The pathophysiology of polyps
is believed to involve damage to the microcirculation
(i.e. injury to a capillary) in the superficial lamina propria
layer with subsequent escape of blood, local oedema and
reorganisation with hyalinised stroma.11–13 Haemorrhagic
polyps may be associated with a larger feeding vessel or
varix. Histological examination reveals a lesion that is
largely acellular, with evidence for fibrosis and thickened
epithelium over the superficial lamina propria and increased
vascularity in a stromal matrix. Immunohistochemistry
studies reveal clustered fibronectin and disruption of the
Figure 4.2a Polyps are differentiated from nodules mainly by
laminar pattern, suggesting diffuse injury in the region of the unilateral nature of the lesion. Histologically it is difficult to
the polyp.14 It has been widely accepted, however, that the separate nodules from polyps. This unilateral polyp is based along
histological differentiation of polyps from nodules may the medial edge of the right true vocal fold. The fine vascular
prove difficult for the pathologist since they both represent component contributes to the reddish hue that is seen through
fibrovascular lesions. the polyp.

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 Benign vocal fold lesions

involves phonosurgical techniques with or without a

microflap. Recently, angiolytic lasers (585-nm pulsed dye
laser [PDL] or a 532-nm pulsed potassium titanyl phosphate
[KTP] laser) have been employed to ablate vessels that are
involved with the lesion without significant epithelial or
superficial lamina propria injury. In order to avoid recurrence
of polyps, it is strongly recommended that patients
participate in voice therapy, prior to surgery, to address the
behavioural concerns that may have led to the development
of the lesion.

Laryngeal polyps associated with

polypoid corditis
Figure 4.2b When the polyp has a large vessel network it is
classified as a haemorrhagic polyp. This large sessile haemorrhagic
Aetiology/pathogenesis
polyp extends away from the medial edge, encompassing the Laryngeal polyps associated with polypoid corditis, also
superior aspect of the left vocal fold. During resection the feeding known as polypoid degeneration or Reinke’s oedema, are a
vessels should be visualised and treated either with an angiolytic different entity. Polypoid corditis is seen almost exclusively
laser (such as a 585 nm PDL or a 532 nm pulsed KTP laser) or in chronic smokers and historically has been incorrectly
removed using phonomicrosurgical techniques. described as a condition only seen in women.11 The husky
and deep voice that accompanies this disorder may be less
acceptable in women than men and therefore medical
attention is sought more frequently by women. Reinke’s
oedema has also been reported in patients with chronic
exposure to occupational irritants and those with acid
reflux. The diffuse polypoid changes in the subepithelial
space is thought to be oedema caused by venous stasis and
vascular congestion, as well as stimulated overproduction
of the native constituents of the superficial lamina propria
(glycosaminoglycans). Symptoms can range from difficulties
phonating to airway obstruction from large ball-valving
lesions.

Clinical findings
Evaluation of the larynx reveals diffuse polypoid changes
of the true vocal folds that may not be symmetric. The
polypoid changes are superiorly-based as opposed to
Figure 4.2c Although polyps tend to be unilateral, repeated the medially-based, phonotraumatic haemorrhagic-type
contact with the opposite vocal fold can lead to the formation of polyp (Figure 4.3a). There may also be involvement of
a reactive fibrovascular lesion (like a nodule). supraglottic structures, but the voice symptoms are related
to the extent of the true vocal fold changes. Because the
changes are frequently over the superior and lateral aspect
determine if there is going to be incomplete glottic closure of the vocal folds, the polyp may not interfere with the
and resultant harshness or breathiness to the voice quality. valving surface of the vocal fold and may not affect
the  mucosal wave or closure. Large lesions may appear
Management to have a stalk that allows these polyps to move in and
Treatment of laryngeal polyps usually involves surgery out of the glottic aperture with respiration, often getting
and voice therapy, although a small proportion of polyps drawn down between the vocal folds during inspiration
may resolve, with regression of the vascular or edematous and expelled during phonation or exhalation. These
component, without surgical intervention. Surgical treatment lesions may cause stridor at rest and may become so large

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 Vocal fold cysts

Figure 4.3a Polypoid corditis, also known as Reinke’s oedema,

mainly involves the superior surfaces of the vocal folds bilaterally.
There is overproduction of superficial lamina propria in response Figure 4.3b Surgical intervention is typically reserved for those
to chemical exposure such as cigarette smoke. This image was patients who have quit smoking or for those who have airway
taken during inspiration when the excess superior vocal folds are obstruction. This intraoperative photo reveals extensive polypoid
pulled medially, obliterating the glottic aperture. changes that gave this patient night-time sleep apnoea, dysphonia
and dyspnoea.

they lead to frank airway obstruction, sleep apnoea and cold techniques, raising a microflap on the superior surface
dyspnoea on exertion or at rest (Figure 4.3b). and removing the redundant/oedematous tissue either with
microinstruments or a small laryngeal suction. Excess mucosa
Management can then be carefully resected to create close apposition
The first step in treating polypoid corditis is smoking of the mucosal edges without overlapping them. Care is
cessation. Some surgeons reserve surgical management to taken to preserve medial surface superficial lamina propria
those with airway obstructive symptoms; however, surgical and epithelium to avoid leaving the patient with glottal
treatment for voice improvement is also warranted if the insufficiency. Additionally, restraint is used near the anterior
offending irritant is effectively eradicated. The surgeon is commissure to avoid webbing. Many suggest leaving some
urged to be conservative when surgically resecting the lesion, polypoid disease behind in order to safeguard sufficient
as overresection of the polypoid tissue can lead to long- glottic closure and preserve a mucosal wave. Other techniques
lasting dysphonia from glottic insufficiency. Historically, that have been described include using a microdebrider in
polypoid changes were managed with vocal fold stripping, place of laryngeal suction and the use of an angiolytic laser
an uncontrolled tearing of mucosa (potentially down to the (i.e. PDL or KTP) to treat the lesions and allow involution
vocal ligament) that often resulted in adynamic segments of the oedema with removal of the microcirculation. The
with severe dysphonia or aphonia. Some suggest treating one laser procedure can be performed in the office setting in an
side at a time, with a healing interval between surgeries to awake patient, using topical anaesthesia, or in the operating
evaluate the voice outcomes15 or to avoid anterior glottic room under general anaesthesia in conjunction with
web formation. Surgery usually employs microsurgery with phonomicrosurgery techniques.

Vocal fold cysts

Aetiology/pathogenesis epidermoid cysts and pseudocysts. Mucous retention
cysts are thought to arise when a mucous gland duct is
Vocal fold cysts are intracordal lesions (subepithelial)
obstructed causing retention of secretions (Figure 4.4a).
within the superficial lamina propria that may extend
The relationship between the genesis of these cysts
from the epithelium down to the vocal ligament. They
and voice use has not been well documented. On the
come in several varieties, namely mucous retention cysts,

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 Benign vocal fold lesions

Figure 4.4a The large mucous retention cyst can be seen occupying Figure 4.4b Epidermoid cysts are filled with keratinaceous debris
the medial edge of the left vocal fold. Mucous cysts are typically a giving them a whitish appearance. Because of the keratin, they
shade of yellow and tend to be pliable. Resection is predicated on tend to be much harder and lack the pliability found in the mucous
removal of the entire cyst lining. cysts.

other hand, epidermoid cysts contain keratinaceous debris striking zone, but careful analysis may reveal a mass lesion
(Figure 4.4b).They are seen in a similar cohort of patients on one side and reactive scarring changes on the opposite
as vocal fold nodules and polyps and are believed to be vocal fold. The mucosal wave may be diminished over the
at least partly due to vocal misuse and phonotrauma. The cyst, especially if it extends to the vocal ligament.4 However,
hypotheses to explain the development of epidermoid this may be variable depending on cyst size, vocal effort and
cysts state that either an epithelial rest is buried in the the amount of viable mucosa overlying the cyst. Diagnosis
subepithelial tissue during development, or epithelium of the cyst is often not made until examination under
becomes deposited in the subepithelial layer when there magnification in the operating room, when an encapsulated
is mucosal damage and healing from vocal abuse. Keratin lesion is discovered on creation of a microflap.
collects in the cyst and may rupture, causing egress of
keratinaceous debris. With time the deflated cyst collects Management
more debris, causing fluctuating dysphonia, the severity Treatment is multidisciplinary and similar to that for
of which is directly related to the amount of debris. epithelial lesions, often requiring voice therapy targeting
If the rupture leaves a small opening for debris to escape behavioural use of the voice in addition to microsurgical
intermittently, this may be referred to as an open cyst. If the removal of the lesion.Although these lesions will not resolve
rupture leaves an opening that is as large as the cyst itself, with therapy or voice rest alone, sometimes the lesions can
it may leave an empty pocket that manifests as a sulcus.11 remain stable over an extended period of time, making
Alternatively, the cyst can remain stable in size and not non-surgical treatment an option in some patients who are
rupture and present simply as a subepithelial mass. resistant to surgery. Surgery may leave an area devoid of bulk
and can lead to glottic insufficiency. Generally, a microflap
Clinical findings can be raised, the encapsulated cyst removed and the flap
Voice symptoms are variable and often depend on the size of laid back down to preserve the overlying epithelium and
the lesion and any contralateral reactive change. Laryngeal superficial lamina propria. In this way, the hope is that
findings will also vary depending on the size of the lesion. minimal scarring will occur at the site and improvement in
Stroboscopy will often reveal a unilateral lesion in the the voice can be expected.

Vocal fold pseudocysts

Aetiology/pathogenesis defined as a unilateral localised area of Reinke’s oedema,
often occurring in the mid-portion of the medial edge
Vocal fold pseudocysts have historically been poorly
of the vocal fold (Figure 4.4c). Koufman and Belafsky16
understood. Recently, a pseudocyst of the vocal fold has been

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 Vocal process granulomas

and effortful attempts to obtain glottal closure leads to

microvascular and epithelial injury (similar to that theorised
to occur in the development of nodules). However, when a
‘podule’ develops on one side only, it continues to absorb
the burden of continued subglottal forces more than the
other side due to its increased mass and compliance. In this
way, it may protect the contralateral side from developing a
similar or reactive lesion.16

Clinical findings
Voice symptoms such as breathy dysphonia, vocal fatigue
and strain are as likely to be related to the vocal fold paresis
and secondary hyperfunction than to the pseudocyst itself.

Management
Figure 4.4c There is a large posterior pseudocyst along the left Several treatment options have been presented including
vocal fold. The pseudocyst is a localised swelling of Reinke’s space observation and voice therapy. Unloading of the
(superficial lamina propia). Curiously, the left vocal fold also compensatory hyperfunction may, however, make the
contains an epidermoid cyst anterior to the pseudocyst. voice worse. In  their series, Koufman and Belafsky16
described various surgical treatments including resection
designated this entity a ‘paresis podule’ due to its frequent alone, laryngoplasty/lipoinjection alone or resection plus
occurrence in association with a unilateral vocal fold paresis. medialisation. They noted that in most patients choosing
The hypothesis behind its development is that asymmetric resection alone, the condition recurred.

Vocal process granulomas

Aetiology/pathogenesis
Posterior glottic granulomas, most commonly known
as vocal process granulomas, are usually seen in the area
overlying the vocal process of the arytenoid, but can also
be seen arising on the supraglottic arytenoid. They have
been known by many names, including contact ulcer,
contact granuloma, post-intubation granuloma and vocal
fold granuloma. It is generally accepted that granulomas
in this area represent an exaggerated form of the healing
process whereby the granuloma forms to try to protect the
injured area at its base to allow the area to heal. They may
be sessile or based on a narrow stalk. They can grow to be
quite large (Figure 4.5a) and therefore impinge on the
airway and voicing mechanism. Teflon-induced vocal fold
granulomas are a separate entity and will be discussed later
in this section.
Vocal process granulomas occur in two subsets of patients,
those with and those without intubation trauma. Intubation-
Figure 4.5a Granulomas typically do not grow large enough to
related (sometimes referred to as reparative) granulomas
obstruct the airway but, as can be seen here, they can become
can occur with both short- and long-term intubation. In quite large. The yellow hue is due to the breakdown of blood within
patients who develop granulomas after a short intubation the granuloma. Throughout a normal day, the vocal processes are
(i.e. only for the length of a surgery), the pathophysiology exposed to a tremendous number of collisions during phonation
is thought be a result of mucosal injury from the placement and deglutition, decreasing the chances that the granuloma will
of the endotracheal tube or manipulation of the tube in-situ shrink in size.

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 Benign vocal fold lesions

(i.e. coughing against the tube). In extended intubation, the

granuloma may be the product of pressure necrosis on the
vocal process. In patients without a history of intubation,
the cause is often related to mechanical and/or chemical
trauma. Granulomas of this type are also seen in patients with
phonotraumatic behaviour (i.e. chronic cough and chronic
throat clearing) and in patients who have acid reflux that
travels proximally to the laryngopharynx. There is presumed
to be a mechanical injury to the vocal process mucosa, which
does not heal well given the chronicity of the offending
behaviour, as well as irritation from acid. A third theory
suggests that glottic insufficiency (from any cause) may be the
inciting event that establishes compensation by hyperfunction
of the laryngeal musculature and leads to increased pressure
on the vocal processes of the arytenoids.17,18 In their series,
Carroll and colleagues found glottic insufficiency in 53% of Figure 4.5b Arytenoid process granulomas can take many forms
patients with a vocal process granuloma.They concluded that depending on the forces acting on them. Although ­unilateral well-
formed lesions predominate, bilateral lesions are not ­uncommon.
not only is glottic insufficiency a common finding in patients
The granulomas depicted here are depressed or cup-shaped.
with granulomas, but they also postulate that recalcitrant,
recurrent and difficult to treat granulomas may be the result
of unrecognised glottic insufficiency.18

Clinical findings
Presenting symptoms are similar, regardless of the cause.
Complaints include unilateral localised discomfort,
odynophagia, hoarseness and globus, and some patients may be
relatively asymptomatic. Patients may give a history of chronic
cough, throat clearing, heartburn or gastro-oesophageal
reflux disease. Voice complaints may be due to laryngeal
hyperfunction or to glottic insufficiency if the granuloma is
large.
Laryngeal examination reveals a smooth lesion that may be
pale or pink and usually unilateral. Lying over the vocal process
of the arytenoid, the lesion may appear shallow and ulcerated
(Figure 4.5b) or large and heaped-up (­Figure 4.5c). The
Figure 4.5c The abundant vascular supply in this unilateral
larger granulomas are often broad-based but may also be arytenoid process granuloma gives it a pink/red hue. Acute areas
pedunculated. The posterior glottis may show other signs of haemorrhage and superficial networks of vessels can be seen
of inflammation such as oedema and erythema. When throughout the base and the apex of the lesion.
granulomas resolve, they often leave a vascular ‘tattoo’, a dark
spot at the base of where they originated. to weaken the adduction of the vocal folds.18,19 Doses
vary widely and are surgeon-dependent. Additionally,
Management intralesional steroid injection has been described, as has
Treatment should escalate from conservative management angiolytic laser treatment either in the office setting or
to surgery only in cases of long-term persistence, airway the operating room.9,20,21 Finally, phonosurgery can be
obstruction or suspicion of malignancy. Conservative performed to remove the lesion and injection of Botox®
management generally entails acid reduction and voice (onabotulinumtoxinA) or steroid can be performed at the
therapy. Acid reflux treatment is generally with twice- same setting. It has been reported that a large majority (up to
daily proton-pump inhibitor therapy and consideration 92% in one study) of granulomas that are surgically removed
for an H2-blocker or other acid neutraliser. Voice therapy will recur, especially if the underlying cause has not been
is focused on vocal hygiene and decreasing traumatic adequately addressed. As  such, laryngopharyngeal reflux,
behaviours. Adjunct procedures that have been described phonotraumatic behaviours and, perhaps, an unrecognised
include using BTX either unilaterally or bilaterally in order glottic insufficiency need to be addressed simultaneously.

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 Vocal fold sulcus and scar

Teflon granulomas
Aetiology/pathogenesis subglottis. There is often an inflammatory reaction leading
to erythema and oedema of the surrounding vocal fold.
Teflon® (polytetrafluoroethylene) was the mainstay for
Depending on how superficial the lesion is, stroboscopy
augmentation laryngoplasty for nearly three decades, but fell
may reveal alterations in mucosal wave properties and phase
out of favour in the 1980s due to increasing complications
symmetry. The voice can have a lower than expected pitch
including overinjection and delayed granuloma formation.
and have at least some roughness and strain.
The use of Teflon for augmentation has been discontinued in
most centres as alternative injection materials and improved
framework surgery techniques have been developed. In Management
addition to presenting as laryngeal granulomas, reports have Treatment of Teflon granulomas is difficult and options
described cases of ‘teflonomas’ outside of the larynx including range from observation to surgical intervention, either
in the thyroid gland and strap muscles. Additionally, when open or endoscopic. It has been well documented that
evaluated radiographically, Teflon can be misinterpreted these patients often require multiple surgical procedures
as a malignancy on several imaging modalities including and voice outcomes are not always better after removal of
CT, MRI and PET. On  histopathology  the granuloma the Teflon due to scarring and glottic insufficiency. Open
is consistent with a foreign body granuloma reaction. approaches include a lateral thyrotomy technique that
Evaluation of lesions that were removed early post injection allows for reconstruction at the same setting. In a technique
showed an inflammatory infiltrate, and postmortem studies described by Billente et al.,23 a lateral laryngotomy is
of human larynges as well as multiple animal studies performed for removal of the submucosal Teflon and
showed giant cells and collagen fibrils as a matrix for the surrounding granuloma, and the defect is then repaired
Teflon particles enveloped within a fibrous casing. It has using a strap muscle and/or silastic implant medialisation.
been postulated that the foreign body reaction and intense Endoscopic approaches attempt to spare mucosa while
inflammatory response that happens are due to reactivity avoiding the morbidity of the external incision. This has
with the thyroarytenoid muscle.22 been described using both cold techniques and CO2 laser.
Surgery proves difficult as the Teflon and the reactive
Clinical findings changes involve the thyroarytenoid muscle diffusely and
The most common presenting symptom in patients with a complete extirpation is often near impossible. Additionally,
Teflon granuloma is hoarseness, although there are reports removal of the granuloma typically results in recurrence of
of patients with a neck mass instead of, or in addition to, the glottic insufficiency that the Teflon was initially meant
dysphonia. It can also cause dyspnoea if the granuloma to correct, and the remaining vocal fold will undoubtedly
is large, extends into the subglottis or causes vocal fold be scarred. Reconstruction can be done at the same time
fixation. Teflon granulomas usually present as a submucosal as the resection with injection augmentation, or it can be
mass of the vocal fold that may extend toward the supra- or delayed until the vocal fold has healed.

Vocal fold sulcus and scar

Aetiology/pathogenesis ●● Type III (sometimes referred to as IIb), or sulcus vocalis,
is thought to arise from a ruptured cyst and goes at least
Sulcus vocalis is a linear groove along the free edge of the
to the vocal ligament and may actually invade into the
vocal fold that represents a significant loss of the superficial
thyroarytenoid muscle; it is sometimes referred to as
lamina propria layer.24,25 This focal loss leads to mucosal
pouch or pocket sulcus (Figures 4.6b, 4.6c).
stiffness and can cause significant dysphonia. Three types of
vocal fold sulcus have been described26:
The incidence of vocal fold sulcus has been difficult to
●● Type I, or physiological sulcus, is characterised by elucidate given the difficulty in diagnosis in the clinical
superficial atrophy but relatively intact lamina propria setting. Historical postmortem studies found an incidence
(Figure 4.6a). rate of sulcus of 0.4–2.5%27,28; however, two more recent
●● Type II (sometimes referred to as IIa), or sulcus vergeture, cadaver studies found a 36–39% rate.29,30 The reason for this
extends through the superficial lamina propria and large difference was thought to be due to methodological
almost to the vocal ligament (Figure 4.6b). differences whereby the original studies were more gross

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 Benign vocal fold lesions

Figure 4.6a There is loss of the superficial lamina propria layer Figure 4.6b This image contains an example of both a Type II sulcus
with the resultant linear depression seen from the anterior on the left true vocal fold (right side of the image) and a Type III
junction of the true vocal folds to just anterior to the vocal sulcus over the superomedial aspect of the mid-posterior right
processes bilaterally in the Type I sulcus. There is typically lateral true vocal fold (left side of the image). There is more extensive
cricoarytenoid (LCA) muscle hyperfunction seen in these cases ‘wearing away’ of the superficial lamina propria along the medial
as the larynx works hard to bring the vocal processes together to left true vocal fold, down to the vocal ligament, with a substantial
make up for the lack of firm glottic closure. In this image there mucosal wave deficit in that region. The Type III sulcus, or pocket
is close approximation of the arytenoid bodies due to the LCA sulcus, can be seen as a slit-like opening that represents the
muscle hyperfunction. opening to epithelial invagination down to the vocal ligament or
muscle layers. The vocal processes are prominently displayed and
form an indentation into the glottic airway from the LCA muscle
hyperfunction.

Figure 4.6c The same larynx as in Figure 4.6b seen during active

abduction. Note how the Type II sulcus on the left true vocal fold
appears as a white linear streak, compared with the excavated
appearance in 4.6b. The arytenoid bodies are also not rotated, as
Figure 4.6d There is substantial scar bridging the area from the
in Figure 4.6b, where there is prominence on the vocal processes
right arytenoid (left part of the image) to the anterior commissure.
bilaterally from the LCA muscle hyperfunction.
Note the radial bands of scar going laterally as well as in an antero-
evaluations and the current studies were performed on posterior direction. A scar like this does not vibrate well, and leads to
whole-mount vocal folds. The aetiology of sulcus has diminished voice quality, stamina and volume from glottic air leaking.
not been well defined. Type I sulcus is thought to occur
from the natural ageing process but can be accelerated by an acquired process, and the deeper types are postulated
increased voice use. The cause of Types II and III has been to be the end result of a ruptured epidermoid cyst.24
debated; theories include congenital mucosal bridges versus Vocal fold scar (Figure 4.6d) can occur in the absence of

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 Vocal fold sulcus and scar

Table 4.1  Glottic scar types characterised by degree of glottic insufficiency31

Type I Mild to moderate glottic insufficiency and reduced vibrations of the vocal folds. The scar involves
the mucosal and submucosal levels of the vocal fold
Type II Anterior moderate glottic insufficiency, seen around the anterior commissure region. The scar involves
the vocalis muscle. No mucosal wave is seen along the anterior vocal fold edges
Type III Considerable glottic insufficiency. The scar is adherent to the inner perichondrium of the thyroid
cartilage. The defect extends up to the supraglottic region; twisted arytenoids may be noticed
Type IV Considerable glottic insufficiency. Web formation at the anterior commissure region. Bilaterally reduced
mucosal wave of the vocal folds

a pathological  sulcus. Benninger and colleagues31 defined

several causes of vocal fold scar including traumatic,
neoplastic, iatrogenic, inflammatory and miscellaneous.
Arens and Remacle32 divided scar into four types depending
on the severity of glottic insufficiency (Table 4.1).
All types of sulcus and scar can lead to mild to severe
dysphonia from the disturbance in mucosal wave properties
and the spindle-shaped glottic insufficiency that is
customary. The pathophysiology of dysphonia takes into
consideration the bowing of the vocal folds, thus leading to
glottic insufficiency, stiffness of the focal fold due to adhesion
of the epithelium to vocal ligament and compensatory
hyperfunction of the supraglottic structures (secondary
muscle tension dysphonia). Patients may experience poor
vocal control and vocal fatigue in addition to aberrations
in voice quality. There are changes to the viscoelastic and Figure 4.6e There is a large pocket sulcus along the medial edge of
vibratory properties of the vocal folds with scar and sulcus. the right true vocal fold (left half of the image), which is partially
filled with trapped keratinaceous debris that has not made its
Objective acoustic and aerodynamic analysis substantiates
way through the open mouth of the Type III sulcus. There is very
rough, strained and breathy voice quality and generally typically a network of large vessels that accompanies the pocket
shows a higher than expected fundamental frequency, sulcus over the superior surface ipsilaterally.
increased jitter and shimmer, and decreased noise-to-
harmonic ratio. Aerodynamics will vary depending on the
amount of breathiness versus strained quality; decreased closure that may not be visible with white light or halogen
mean airflow rate and increased peak air pressure can be light. Laryngeal stroboscopy will show disruption of the
shown if they are strained or increased airflow if they have mucosal wave (adynamic segments) in the area of scar or
more of a breathy voice quality. sulcus, and may show phase asymmetry, closure disparity
and glottic gap. It is also possible that the diagnosis is not
Clinical findings made until examination in the operating room with
Laryngeal examination will show a spectrum of findings microscopic assistance. A pocket sulcus, which has a narrow
depending on the location, size and type of sulcus. There aperture, may fill with keratin and look like a cyst; these
may be an obvious bowing of the vocal fold(s) that is are often associated with a large vessel situated lateral to
visible  with indirect laryngoscopy and halogen light. the area of stiffness (Figure 4.6e). The medial edge of the
In these sulcus cases the classic configuration of the larynx vocal fold may look more translucent or ‘thin’ in the case
is spindle-shaped, where the vocal processes converge with of physiological sulcus, or may look more dense or white if
a gap between the membranous vocal folds (Figure 4.6a). there is dense scar.
The vocal folds may, however, look normal until assessed
with stroboscopy. Stroboscopic examination is imperative Management
in the diagnosis of sulcus and scar. Stroboscopy allows Treatment options vary depending on the type of sulcus
for detection of the free edge vibratory asymmetries, or scar and the degree of symptoms that the patient is
submucosal scars and lesions, and information about glottic experiencing. Many patients will choose to be observed

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 Benign vocal fold lesions

or partake in voice therapy alone. The results from voice been described with alloplastic and autologous materials.
therapy are not well established, but for patients with early, Alloplastic fillers, such as calcium hydroxylapetite (Radiesse
physiological sulcus, it may improve their voice symptoms, Voice®) and polydimethylsiloxane particles (Vox Implant®),
at least temporarily. Local intralesional injection of have regulatory approval for use in many juridisctions for
corticosteroids may have a role in diminution of scar, but vocal fold augmentation. Although not approved for this
it does not address the loss of bulk along the medial edges. indication, some surgeons use other temporary alloplastic
Although a dedicated study looking specifically at this has fillers that are hyaluronic acid based (Restylane®, Perlane®,
not been carried out, preliminary data show that steroid Juvederm®). Injection augmentation with autologous fat
injections may prove beneficial for softening the vibratory and fascia has also been described, and is performed in a
surface of the scarred area.33 This is a technique frequently way similar to the technique used for other types of glottic
practiced at the time of phonosurgery to attempt prophylaxis insufficiency. Caution should be taken when considering
against iatrogenic scar. Surgical management includes augmentation without treatment of the scar, as medialising
augmentation/medialisation, incision and undermining two stiff mucosal edges may not improve the dysphonia
of the scar, and resection of the sulcus. Bouchayer and and can actually cause the strain to be amplified. External
colleagues24 described their technique of resection, which medialisation, or thyroplasty type I, can also be performed to
starts with hydrodissection with a steroid injection to open remedy the glottic insufficiency that accompanies sulcus or
the lips of the sulcus (Figure 4.6f ). A  mucosal incision scar. Techniques using a solid implant, Gore-Tex or muscle
is then made on the superior surface of the vocal fold and transposition have all been described.25,34 Epithelial freeing
the sulcus is carefully dissected from the underlying vocal or undermining can be performed through a microflap
ligament and an elliptical incision used to remove the sulcus, technique, which may sometimes be closed with fibrin glue
leaving healthy adjacent tissue and mucosal margins to close or sutures. Epithelial undermining is often combined with
without a depression.24 Occasionally, a small amount of an augmentation to overcome the glottic gap.34 Finally,
undermining of the margins may be necessary. Detachment Sataloff 35 has described his preliminary outcomes using
at the bottom of the pouch often proves difficult as there fat  implantation after elevating the scar, with promising
can be infiltration of the vocal ligament. Augmentation has results.
Recently, techniques using angiolytic lasers, mucosal
slicing techniques and mucosal grafting have been
described to attempt restoration of a mucosal wave.
Regardless of the technique, if mucosal wave reappears, it
can take up to 6–12 months. The PDL has been studied in
the dermatological literature for treatment of cutaneous
scar, and Mortensen and colleagues36 have evaluated the
usefulness of PDL in the treatment of vocal fold scar, either
iatrogenic or radiation induced. In their prospective pilot
study comprising three PDL treatments per patient spaced
1 month apart, 10 out of 11 patients reported subjective
improvement in voice 6 months post treatment. Acoustic
and aerodynamic outcomes also improved, and blinded
review of the stroboscopic examinations revealed an
improvement in post-treatment appearance compared with
pre-treatment. Mucosal grafting has been described  for
cases where the amount of scar and/or tissue loss is too
Figure 4.6f The pocket sulcus can be examined well in the much to overcome with resection and/or augmentation
operating room using instruments that can probe the depth of alone. Historically, this had been done via a laryngofissure,
penetration. In this patient the medial aspect of the left true vocal but recently has been described endoscopically. The
fold has a pocket sulcus that extends down to the vocal ligament
procedure entails de-epithelialisation of the area to be
(Type III sulcus). Surgical resection of the mouth of the lesion with
all of the epithelial surfaces allows the edges to seal together and
grafted and use of harvested buccal mucosa that has been
improves vocal quality in many patients. The most significant sutured to a silastic sheet. The mucosa–silastic graft is
improvement is in the stability of the voice, since epithelium then sutured endoscopically using a Lichtenberger needle
will no longer be trapped and create a mass that varies with carrier, which is passed out through the skin of the neck
the amount of trapped epithelium. and secured over a bolster.34

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 Benign tumours

Benign tumours
Laryngeal papillomatosis
Aetiology/pathogenesis
Recurrent respiratory papillomatosis (RRP) will be
covered in detail in a separate chapter. Briefly, RRP is a
benign epithelial tumour caused by human papillomavirus
(HPV), usually types 6 and 11, that affects approximately
4 per 100,000 children and 2 per 100,000 adults. Although
the condition is rare, it is the most common benign tumour
that is managed by otolaryngologists.11 The adult-onset
variant is generally considered to be less aggressive than
the juvenile-onset type; however, disease burden can still be
great in adults.Although quite uncommon, there is evidence
that RRP can transform into squamous cell carcinoma, so
long-term follow up is warranted.
Figure 4.7a There is a single moderately-sized exophytic focus of
papilloma along the medial edge of the left true vocal fold creating
Clinical findings severe dysphonia. Although the lesion appears solitary, genetic
Laryngeal RRP generally presents with hoarseness, which testing of surrounding ‘normal’ vocal fold epithelium reveals the
may be somewhat insidious in onset. A  papilloma that presence of human papillomavirus DNA, meaning the entire larynx
is large or involving the subglottis may also present with is infected even when there is only a single, or even no, lesion
dyspnoea, but this is less common in adults than in children. currently identified.
Laryngeal examination will reveal papillomatous lesions that
can be exophytic or flat (Figure 4.7a), and can be singular
in location or diffuse. On close examination, it is possible to
see the red pinpoint dots within the lesions, signifying the
blood vessels within the papilloma (Figure 4.7b).

Management
Treatment of laryngeal papillomatosis, similar to other
chronic disorders that affect the vocal folds, should match
the aggressiveness of the disease. Since HPV cannot be
cured through surgical treatments, it is important to avoid
techniques that inflict damage, since even normal appearing
epithelium will have evidence of viral DNA. It is almost
inevitable that papillomas will recur, so treatment should
be symptom based and conservative, aiming to preserve as
much normal anatomy as possible. The current treatment
Figure 4.7b In this image multiple sessile and exophytic lesions
paradigm combines medical management with surgery.
can be seen in the same larynx. The anterior and superior aspect
Medical therapies have varied efficacy in the literature, but of the left true vocal fold is affected, while the majority of the right
are often used as an adjunct.These include supplementation true vocal fold appears unaffected. The red stippled appearance
with indole-3-carbinol and treatment with interferon. of the lesions gives away that these are lesions from a human
Intralesional injection with cidofovir has been used for papillomavirus infection.
some time and has proven to be the most effective adjuvant
to surgery. Unfortunately, the injection schedule and dosing controlled studies comparing bevacizumab to cidofovir are
differs between centres37, making true comparisons difficult. warranted.38,39 Surgical management of papillomatosis aims
Recently, use of intralesional bevacizumab has been used to treat only those areas affected by papilloma and not harm
in an uncontrolled manner in small numbers of patients; unaffected structures to avoid causing permanent damage

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 Benign vocal fold lesions

such as scar, web and stenosis. Cold instrumentation or confused with squamous cell carcinoma on first assessment.
careful removal with a microdebrider has been described. Histologically, granular cell tumours are polymorphic
The use of lasers has seen a shift from use of the CO2 and the cells can be spindle-shaped to polygonal. There is
laser (which is still frequently used in the supraglottis) to abundant pale, eosinophilic, granular cytoplasm and the
the angiolytic lasers such as the PDL and the KTP laser. nuclei are hyperchromatic.42,43 The location of these lesions
Angiolytic lasers are used to treat the feeding blood vessels. is most commonly in the true vocal fold and usually in the
They are not ablative lasers like the CO2, and inflict much posterior one-third of the vocal fold. It has been described
less damage to the epithelium and surrounding structures. in supraglottic locations, including the arytenoid and false
They also create a cleavage plane at the basement membrane vocal fold, and has been reported in the subglottis and
of the epithelium, therefore allowing removal of the diseased postcricoid regions.43
epithelium while preserving the deeper superficial lamina
propria and vocal ligament.40,41 Clinical findings
RRP is discussed in more detail in Chapter 13 Granular cell tumours may present with dysphonia, cough,
(Recurrent respiratory papillomatosis). dysphagia, odynophagia, otalgia, stridor and haemoptysis44,
but if not impeding glottic closure and vibration
Granular cell tumours (i.e. in a supraglottic subsite) they may be discovered
incidentally. Laryngeal examination will demonstrate a
Aetiology/pathogenesis pink or pale submucosal mass in the mid-posterior vocal
Granular cell tumours are rare neurogenic tumours, 50% fold and differentiation of this from other submucosal
of which occur in the head and neck. While the most lesions (i.e. a vocal fold cyst) may be difficult on indirect
common head and neck site is the tongue, up to 10% of laryngoscopy. Generally, diagnosis is made after excision and
these tumours occur in the larynx and most frequently histopathological examination. Patients often have more
involve the true vocal folds. A very small number (<2%) than one granular cell tumour in different sites in the body,
have been reported to be malignant. The exact cell lineage either synchronously or metachronously. It is estimated that
of these lesions is poorly understood, but they are felt to the risk of a second granular cell tumour is 4–10%.44 While
be derived from undifferentiated mesenchymal or Schwann the recurrence rate is low, estimated at 2–5%45, complete
cells. With immunohistochemistry they stain positive for excision is recommended when feasible.
S-100, neuron specific enolase, myelin-specific protein and
other antibodies frequently seen in neural tissues, and are Management
usually negative when stained for epithelial markers.42 The Treatment is largely surgical, as there is no known medical
cause of granular cell tumours is also poorly understood. therapy and these tumours have proven to be radio-resistant.
Although several aetiologies have been proposed, their Lesions that involve the vocal folds are usually amenable
rarity precludes exact identification. Grossly, the lesions are to direct microlaryngoscopy and phonosurgical resection
well circumscribed but non-encapsulated. The majority of using cold techniques or laser. Follow-up is warranted given
them show pseudoepitheliomatous hyperplasia and may be the small risk of malignancy and recurrence.

Rheumatological and immunological conditions causing vocal

fold lesions
of antibodies by the bone marrow that cannot be broken
Amyloidosis down in the normal fashion and are therefore deposited
in extracellular locations. The secondary form is caused
Aetiology/pathogenesis by chronic infectious and inflammatory diseases.
Amyloidosis is the extracellular accumulation of Amyloid deposits are characterised histopathologically by
abnormal fibrillar proteins; it can be localised or systemic. amorphous eosinophilic deposits on haematoxylin and
Amyloidosis is categorised into primary (localised or eosin stain and apple-green birefringence when stained
systemic), secondary (localised or systemic), related to with Congo Red.The most common location for localised
multiple myeloma, hereditary and haemodialysis related. amyloid in the head and neck is the larynx46–50, although
The cause for primary amyloidosis remains poorly systemic amyloid is often associated with deposits in the
understood, but the  pathogenesis includes production tongue base. Amyloidosis in the larynx constitutes less

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 Rheumatological and immunological conditions causing vocal fold lesions

than 1% of benign lesions found in the larynx in historical found the vocal fold lesions were on the inferior surface and
studies, although its rarity makes it difficult to study. It most opted to treat the worse side initially, taking the mucosal
commonly affects the supraglottis and the true vocal folds and subepithelial lesion down to the thyroarytenoid muscle.
but has also been reported in the subglottis and trachea. Surgery for the contralateral vocal fold was undertaken
only if, after several months, there was still a great deal of
Clinical findings dysphagia or stroboscopy perturbation. Amyloid lesions
Presenting symptoms are usually related to size and location are known to recur, so conservative and staged surgery is
and include hoarseness, dyspnoea, dysphagia and cough.There recommended, especially for lesions on the true vocal folds
can be asymptomatic lesions, but in general, if the lesions affect and near or involving the anterior commissure.
the true vocal folds, dysphonia will be present. Laryngeal
examination is variable, but vocal fold lesions are submucosal
and are described as granular or rough in appearance and have Rheumatoid nodules
a yellow, pink or red hue (Figure 4.8).Amyloid deposits can be
nodular or diffuse, but are generally of the nodular type in the Aetiology/pathogenesis
larynx.48 They can occur on the superior, inferior or medial Rheumatoid nodules (RNs) are small submucosal lesions
portions of the vocal fold. Stroboscopy may reveal impairment that are sometimes observed with autoimmune diseases;
of the mucosal wave and glottic closure depending on the most commonly these nodules are seen in rheumatoid
location and size of the lesion(s). arthritis, but have also been reported in cases of systemic
lupus erythematosus.They are also known as bamboo nodes
Management or bamboo nodules due to their appearance on laryngoscopy
Treatment is based on symptoms. Localised glottic amyloid (Figure 4.9). RNs are considered to be less morbid than
is best treated with microscopic direct laryngoscopy and some of the other laryngeal manifestations of autoimmune
excision, but large obstructive supraglottic lesions may diseases, such as laryngeal stenosis and cricoarytenoid joint
require an external/laryngofissure approach.46 Adjuvant fixation; however, they can cause significant dysphonia and
and medical treatments such as radiation, chemotherapy impact quality of life. The incidence of RNs is difficult to
and intralesional injection of steroids have not shown great discern, as they seem to be quite rarely reported and no
efficacy.49 The CO2 laser is often used, depending on the large studies have focused purely on this question. Laryngeal
location of the lesion. In their series, Dedo and Izdebski51 manifestations of rheumatoid arthritis in some form are,

Figure 4.8 Amyloid deposits are submucosal; they can be Figure 4.9 Rheumatoid nodules are nearly always situated over
diffusely present throughout the larynx or can form focal the superior surfaces of the vocal folds. Their appearance can
masses. The left false vocal fold is grossly enlarged from the vary with the level of activity of the rheumatoid disease, and at
submucosal amyloid, but careful inspection reveals multiple times rheumatoid nodules can have a central yellow body with
foci with a yellow–tan appearance over the right vocal process a halo of erythema indicating active inflammation. Treatment
and anterior right false vocal fold, which also represent amyloid of the primary rheumatological problem is imperative. Surgical
deposits. Surgical resection is the treatment of choice for intervention should be considered as a last resort since rheumatoid
symptomatic patients. nodules can re-form after complete surgical resection. They are
the local manifestation of the systemic inflammatory condition.

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 Benign vocal fold lesions

however, noted in up to 80% of patients on postmortem convex appearing bands at the mid-membranous vocal
examination.52–54 The pathogenesis of RNs is not fully fold (Figure 4.9).532 They are frequently bilateral, but
understood, but elsewhere in the body they are known to may not be exactly opposing each other. Stroboscopy may
occur at sites of repeated trauma or injury. Given this, it reveal premature contact and anterior and/or posterior
makes sense that RNs of the vocal folds are found at the glottic gap.
striking zone, or mid portion of the fold. Histopathology of
vocal fold RNs has shown a necrotic centre surrounded by Management
palisading histiocytes with a third outer layer of fibrosis.52 Treatment generally follows a conservative path. Resection
This is a similar finding to subcutaneous RNs. can be performed using a microflap technique; however,
there is a high likelihood of recurrence, so preoperative
Clinical findings counselling is important. There have been no studies
The most common presenting symptom is dysphonia dedicated to oral or intralesional steroid injections for these
characterised by change in pitch, poor vocal control or a lesions, so the outcomes from steroid treatment are not
rough or raspy quality; however, globus is also occasionally known.Voice therapy should always be considered, and may
reported. Laryngeal examination reveals lesions transverse allow the patient to avoid secondary hyperfunction and
to the long axis of the vocal fold with yellowish-white maintain vocal hygiene.

References
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and hyperfunctional dysphonia: implications for with a vocal nodule. Arch Otolaryngol Head Neck Surg
the pathogenesis of vocal nodules. Ann Otol Rhinol 137(10):1011–1016.
Laryngol 107(7):603–610. 11 Bastian RW (2010) Benign vocal fold mucosal
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19 Damrose E, Damrose J (2008) Botulinum toxin as 35 Sataloff RT, Spiegel JR, Hawkshaw M et al. (1997)
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31 Benninger MS, Alessi D, Archer S et al. (1996) Vocal 810–814.
fold scarring: current concepts and management. 46 Kennedy TL, Patel NM (2000) Surgical manage-
Otolaryngol Head Neck Surg 115(5):474–482. ment of localized amyloidosis. Laryngoscope 110(6):
32 Arens C, Remacle M (2010) Scarred larynx. In: Surgery 918–923.
of Larynx and Trachea. (eds. M Remacle, HE  Eckel) 47 Hazenberg AJC, Dikkers FG, Hawkins PN et al. (2009)
Springer, Berlin, pp. 171–176. Laryngeal presentation of systemic apolipoprotein
33 Mortensen M, Woo P (2006) Office steroid injections A-I-derived amyloidosis. Laryngoscope 119:608–615.
of the larynx. Laryngoscope 116:1735–1739. 48 Penner CR, Susan M (2006) Head and neck
34 Friedrich G, Dikkers FG, Arens C et al. (2013) Vocal amyloidosis: a clinicopathologic study of 15 cases.
fold scars: current concepts and future directions. Oral Oncol 42:421–429.
Consensus report of the Phonosurgery Committee 49 Pribitkin E, Friedman O, Hara BO et al. (2003)
of the European Laryngological Society. Eur Arch Amyloidosis of the upper aerodigestive tract.
Otorhinolaryngol 270:2491–2507. Laryngoscope 113:2095–2101.

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 Benign vocal fold lesions

50 Mitrani M, Biller HF (1985) Laryngeal amyloidosis. 53 Beirith SC, Marcio C, Ikino Y (2013) Laryngeal
Laryngoscope 95:1346–1347. involvement in rheumatoid arthritis. Braz
51 Dedo HH, Izdebski K (2004) Laryngeal amyloidosis J Otorhinolaryngol 79(2):233–238.
in 10 patients. Laryngoscope 114:1742–1746. 54 Speyer I, Heijnen AM (2008) Prevalence and relative
52 Woo P, Mendelsohn J, Humphrey D (1995) risk of dysphonia in rheumatoid arthritis. J  Voice
Rheumatoid nodules of the larynx. J Laryngol Otol 22(2):232–237.
113:147–150.

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 CHAPTER 5

Neurological and neuromuscular disorders

of the larynx
Lucian Sulica

Introduction
The larynx is a biological valve located at the junction of expiratory airflow, depends on a still more sophisticated
the respiratory and digestive tracts. Its evolutionary origins interaction between afferent and efferent neural systems
lie in the need to protect the lungs of amphibious organisms to produce precise and finely-modulated glottic closure.
from water, and airway protection remains its most Therefore, it should come as no surprise that the larynx
important biological task. For this, it depends on a sensitive is exquisitely sensitive to neurological derangements,
neural system that responds to a wide variety of stimuli, and is involved in a wide variety of neurological disorders.
both mechanical and chemical, to trigger laryngeal closure. In fact, compromise of laryngeal function – alterations in
Its function as a phonatory organ, which arose because its respiration, deglutition and phonation – may sometimes be
position atop the trachea gave it a unique ability to regulate the earliest sign of such disease.

Neurolaryngological evaluation
Although the fundamentals – careful history taking and This need not be exhaustive and time-consuming; a cranial
thorough examination – remain the same, the task of nerve (CN) examination should already be a routine part of
neurolaryngological diagnosis differs in several important the otolaryngological assessment, and an assessment of strength,
ways from the standard laryngeal evaluation. rigidity, tremor and coordination in the upper extremities
First, because neurological disorders are by definition and an evaluation of gait adds considerable information in
disorders of laryngeal motion, examination must be dynamic exchange for only minutes of time. Special note should be
and performed across a variety of laryngeal tasks; sustained made of articulatory difficulties, often confused with voice
phonation alone frequently will not reveal all the relevant disorders by patients and their physicians, and velopharyngeal
findings. The spasms of spasmodic dysphonia (SD), for insufficiency, which frequently occurs together with vocal fold
instance, may only be evident in connected speech. Subtle dysfunction in the context of neurological illness.
cases of paresis may remain obscure until repetitive motion Fourth, for many neurological diseases, particularly
has fatigued the laryngeal muscles. An extended examination movement disorders, there is no known biological marker,
also helps to distinguish innocent asymmetries in laryngeal so there is no definitive laboratory or radiological study to
motion from significant findings, which are typically more confirm diagnosis. Spasmodic dysphonia, essential tremor
consistent. Sensory abnormalities may go unappreciated until a and Parkinson’s disease are all cases in point. Diagnosis rests
swallowing trial is undertaken.Tasks that may be helpful in the on judicious interpretation of the features of the clinical
assessment include quiet and forceful expiration, swallowing, examination. This redoubles the importance of this element
sustained and connected speech, rapid alternating tasks and of the evaluation.
occasionally singing and other special forms of phonation. Laryngeal electromyography (LEMG) continues to
Second, the larynx is best examined using a flexible occupy an ill-defined place in the evaluation of neurological
endoscope, since rigid peroral endoscopy or mirror laryngeal disorders. It is important to understand that, apart
examination renders many laryngeal tasks other than from amyotrophic lateral sclerosis, in which EMG (typically
sustained phonation impossible, and forces the patient into of the tongue) may be diagnostic, EMG findings are not
a non-physiological posture, which may mask characteristic definitive. Nevertheless, LEMG can be extremely helpful in
laryngeal findings. (1) identifying laryngeal pareses that are part of a systemic
Third, because neurological disease often is not restricted neurological disorder, (2) distinguishing these from innocent
to the larynx, a broader neurological assessment is essential. asymmetries of laryngeal motion and (3)  characterising

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 Neurological and neuromuscular disorders of the larynx

Figure 5.1 This EMG recording of the thyroarytenoid muscle of a patient with essential voice tremor during sustained /i/ phonation
clearly reveals the perfectly rhythmic waxing and waning activation of the muscle typical of tremor, in this case at a rate of 5 Hz.
Normally, muscle activation should be continuous during this activity (each horizontal division = 100 msec; each vertical
division =100 μVolts).

laryngeal motions, as in tremor (Figure  5.1). The utility those disorders which the otolaryngologist must recognise
and limitations of LEMG are beyond the scope of this because patients may present without antecedent diagnosis
discussion – the reader is directed to specialty texts for or with erroneous diagnosis, and those in which adept
further discussion. otolaryngologic management may achieve meaningful
The inventory of neurological disease reviewed in improvement for the patient, or conversely, uninformed
this chapter is not exhaustive. The author has focused on intervention may create difficulties.

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

Movement disorders
Parkinson’s disease Clinical findings
Asymmetry in the physical examination is typical; the most
Aetiology/pathogenesis common presenting symptom is unilateral extremity tremor.
Cogwheel rigidity describes a ratchet-like sensation felt
Parkinson’s disease (PD) is a progressive neurodegenerative
during passive flexion/extension of the upper limb or neck.
illness characterised by four cardinal signs: resting tremor,
Bradykinesia refers to slowness of voluntary movement.
cogwheel rigidity, bradykinesia and impaired postural reflexes.
When this affects the muscles of facial expression, it yields
At least two must be present for the diagnosis to be entertained.
a characteristic lack of facial affect described in the medical
Most commonly, PD is idiopathic, although there are
literature  as ‘mask-like’. The integrity of postural reflexes
postencephalitic, drug-induced (following metaclopramide,
can be easily evaluated by asking the patient to walk three
neuroleptics and other dopamine antagonists) and traumatic
or four paces and turn 180 degrees. Affected patients will
variants (as in boxers).

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 Movement disorders

not be able to pivot, but instead will take several steps to enthusiasm for vocal fold augmentation to remedy the
rotate their body. observed glottic insufficiency18,19 has been tempered by
an understanding for the broader range of abnormalities
Management involved in Parkinson hypophonia. Deep brain stimulation
The underlying pathology is neuronal loss in the substantia has been shown to be most effective in tremor suppression,
nigra and consequent loss of dopamine in the basal ganglia. but evidence for practical voice and speech benefit from
The mainstay of treatment remains dopamine replacement, this procedure remains equivocal.
augmented by agents to boost transit of levodopa across The most effective intervention, apart from systemic
the blood–brain barrier and other dopamine receptor medication, may be behavioural therapy. Lee Silverman
agonists that have been developed in recent years. The aim Voice Therapy (LSVT) is an intensive course of behavioural
is symptomatic relief, and the underlying disease remains therapy that aims to increase phonatory effort to overcome
relentlessly progressive. Stimulation of deep brain nuclei the impaired self-perception of loudness, and which appears
by means of a surgically implanted electrode is gaining to result in improved neuromuscular control of the entire
popularity in incapacitating cases of parkinsonism that resist upper aerodigestive tract. The mechanism for this effect
medical management. remains unclear. Benefit has been demonstrated in placebo-
controlled trials and appears to be sustained over time.20–23

Parkinson hypophonia
The characteristic low-intensity monotone voice of patients
Multiple system atrophy
with PD has been termed Parkinson hypophonia. The Multiple system atrophy (MSA) is a neurodegenerative
laryngoscopic correlates of Parkinson hypophonia include syndrome that features parkinsonism and autonomic and
vocal fold bowing (spindle-shaped glottic insufficiency; cerebellar dysfunction. When symptoms of autonomic
Figures 5.2a, b), vocal fold bradykinesia and tremor.5–7 dysfunction – typically postural hypotension – are
These laryngeal abnormalities usually co-exist with oral- prominent, it is known as Shy–Drager syndrome. When
motor articulatory difficulties and poor respiratory function cerebellar dysfunction – gait ataxia, severe intention
and coordination, both reflections of underlying rigidity and tremor and dysarthria – predominates, it is known as
bradykinesia. These are not infrequently accompanied by olivopontocerebellar atrophy. Many cases are initially
cognitive dysfunction.8–12 In addition, underestimation of diagnosed as PD until the appearance of additional
own-speech volume is a perceptual anomaly that has been symptoms makes the nature of the disease clear. MSA is
found consistently in patients with Parkinson hypophonia, and usually lethal, with a mean survival of 8–10 years.24
may be a critical derangement in this type of dysphonia.13,14 Laryngeal problems may contribute to the mortality of
MSA – night-time respiratory dysfunction appears to be a
Management leading cause of death. Nocturnal stridor is present in some
Standard medical treatment with levodopa generally 13% of patients, and is a poor prognostic sign.24,25 Both
improves speech and voice difficulties in PD.15–17 Early bilateral VFP and paradoxical vocal fold adduction during

a   b
Figures 5.2a, b Poor phonatory glottal closure is shown in this 56-year-old man with Parkinson’s disease. Glottic insufficiency is exacerbated
by early vocal fold atrophy. Symptoms were typical of Parkinson hypophonia and the patient improved with voice therapy.

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 Neurological and neuromuscular disorders of the larynx

inspiration have been amply documented in MSA and weakness lasting several days, followed by a months long
appear to account for this symptom.26–31 Early identification plateau of somewhat milder weakening that constitutes
of either of these abnormalities followed by tracheostomy the principal therapeutic effect. The breathy dysphonia
may prevent or delay some deaths24,32, although there is that usually follows adductor muscle injection is a clinical
evidence that central respiratory dysfunction is substantial manifestation of this pattern; the initial effect of the toxin
in these patients, independent of the laryngeal findings.33 causes some glottic insufficiency. In general, the two phases
Of additional concern is misdiagnosis of patients with MSA, of toxin effect are proportional. In the case of adductor
which may prompt the otolaryngologist to consider vocal SD, for example, the duration of breathiness can usually
fold medialisation, as in PD, which is likely to exacerbate be shortened by sacrificing the duration of therapeutic
respiratory problems, possibly to a life-threatening degree. effect. Naturally, patients want to minimise the frequency
of injections, but each will have a different tolerance for
a breathy voice. Dyspnoea is the equivalent early effect
Spasmodic dysphonia (focal in abductor SD, because the posterior cricoarytenoid is
­laryngeal dystonia) being weakened. The potential for dyspnoea imposes an
important limitation in BTX treatment of abductor SD,
Aetiology/pathogenesis and probably for this reason, results are less satisfactory
than for adductor SD.35
SD is a form of dystonia, a chronic neurologicalal disorder
There is no specific anti-dystonia pharmacological
of central motor processing characterised by task-specific,
agent. Drugs are prescribed empirically, and unfortunately
action-induced muscle spasms. In the vast majority of cases,
their utility is often limited by significant central nervous
SD affects connected speech, although there are rare cases of
system side-effects such as sedation and memory loss.
breathing dystonia. SD typically begins in the mid-30s and
Voice therapy is sometimes useful in an adjunctive role,
is more common in women (63%).34 Approximately eight
but does not yield marked improvement by itself.35 Like
out of ten affected individuals have adductor SD, which
other types of dystonia, adductor SD has been treated
causes inappropriate glottal closure, producing characteristic
surgically. The underlying principle is the same as that of
harshness, strain and strangled breaks in connected
BTX treatment: denervation. Yet, when this is performed
speech. Abductor SD, in contrast, causes inappropriate
surgically, a disappointingly large number of patients
glottal opening that produces hypophonia and breathy
have had recurrence of their symptoms after a period of
breaks. Because of compensatory manoeuvres or mixed
time.36,37 Reasoning that recurrence of symptoms is due
dystonic features, voice patterns encountered clinically
to reinnervation, for which there exists abundant EMG
may not always be typical or easy to discern. However, the
evidence, even after excision of a segment or recurrent
classification of SD into abductor and adductor types is
nerve, Berke38 has proposed a selective distal denervation
central to botulinum toxin (BTX) treatment.
of the adductor branches of the recurrent nerve, with
immediate reinnervation using a non-laryngeal nerve.
Clinical findings/diagnosis
Long-term data regarding this procedure are accruing.
Diagnosis is based on a careful history and examination of Currently, the author believes that surgery should be
the glottis during a variety of laryngeal tasks. Clues in the reserved for the rare patient who does not benefit from or
history include deterioration of voice quality under stress or cannot tolerate BTX.
on the telephone, and improvement with sedatives such as
alcohol or benzodiazepines. Some patients find that certain
tactile or proprioceptive manoeuvres – so-called ‘sensory Essential tremor
tricks’, like chewing or supporting the head – can improve
speech.The mechanism for this is not known. Aetiology/pathogenesis
Essential tremor is an age-related disease of involuntary
Management movement. In many instances the disease is familial and it
The standard treatment for SD is EMG-guided can be inherited in an autosomal dominant fashion; the
transcutaneous BTX injection of the hyperactive remainder of cases appear to be sporadic.39–43 Absence of
muscles  – thyroarytenoid-lateral cricoarytenoid muscle a family history of tremor does not preclude a diagnosis of
complex in adductor SD and posterior cricoarytenoid essential tremor.
muscle in abductor SD. This offers symptom control for The phonatory apparatus may be involved in 25–30%
the period of toxin effect, usually 3 months or more. BTX of patients with essential tremor.44 Voice tremor may be
treatment results in an initial period of marked muscle the only manifestation of essential tremor45, but usually

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 Movement disorders

it is associated with tremor in other parts of the body, in more than half of patients (16 of 28) treated in an open
including the upper extremities or head. Essential tremor, trial54, results not supported by a subsequent blinded
when it affects the voice, is usually not restricted to the investigation.55 A case of effective treatment with gabapentin
intrinsic muscles of the larynx; extrinsic laryngeal muscles, has been reported.56 These few reports notwithstanding,
pharyngeal and palatal muscles, the muscles of articulatory pharmacological treatment of voice tremor has been sparsely
structures, as well as muscles of the diaphragm, chest wall studied; further investigation is called for.
and abdomen, which affect phonatory expiration, are often BTX treatment of essential voice tremor is predicated
variably involved.46–48 The term ‘essential voice tremor’ on the assumption that vocal fold tremor and resulting
thus describes the clinical situation better and is more apt inappropriate glottal aperture account for the greater part
than ‘essential laryngeal tremor’. of the symptoms of essential tremor of the phonatory tract.
Generally, BTX is injected into one or both thyroarytenoid
Clinical findings muscles51,57–60 in the manner of the treatment of adductor
Because of the broad involvement of different muscle SD and in comparable doses (Table 5.1). According to
groups, a patient with essential voice tremor may present patient self-perception of vocal quality, BTX injections were
with variability in frequency as well as (or in place  of) useful in 67–80% of cases. Acoustic measures documented
intensity. Most often, though, patients complain of intensity benefit less often, leading investigators to hypothesise
fluctuations associated with a perception of increased that much of the perceived improvement resulted from
phonatory effort. Symptoms are usually present across all decreased phonatory effort.
phonatory activity. Patients with essential voice tremor
generally report slowly worsening symptoms over
months to years. Voicing worsens with anxiety or stress, Tics and Giles de la Tourette’s
and is especially troublesome under more demanding ­syndrome
acoustic conditions, such as speaking against background
noise, addressing a classroom or conference, or using the Aetiology/pathogenesis
telephone.49,50 In common with other manifestations of
Tics are abrupt, purposeless movements or vocalisations
essential tremor, alcohol may effect voice improvement.
that interrupt normal motor activity. Motor tics can
Similar features are found in SD which can be a source of
assume almost any form, from simple twitches or blinking
diagnostic confusion.
to complex patterned motions like grimacing or hand
gestures. Vocal tics can also be simple, such as grunting, or
Diagnosis complex, such as meaningful phrases. In the context of
Diagnosis of essential tremor is clinical. Rhythmic, otolaryngology practice, tics should remain a consideration
oscillatory motion of the palate, pharynx and/or vocal in cases of particularly persistent throat clearing or
folds at the characteristic rate of 4–10 Hz is diagnostic. coughing.Tics are usually suppressible to some degree, and
Vocal fold tremor is bilateral and grossly  symmetric. occur along a broad clinical spectrum from mild and barely
Tremor may be present across all laryngeal tasks, including noticeable to severely disruptive and thus crippling to the
quiet respiration as well as phonation. If both history and patient in his daily activity. Often, they are associated with
examination are characteristic, further investigation is behavioural abnormalities such as obsessive compulsive
unnecessary. If findings are atypical or ambiguous, and disorder or attention deficit hyperactivity disorder. Gilles
especially if onset of symptoms is rapid, it is prudent de la Tourette’s syndrome is diagnosed when multiple
to consult a neurologist. Ruling out thyrotoxicosis motor tics and at least one vocal tic are present for at least
and drug-induced tremor – in the otolaryngological 1 year, beginning under the age of 21. Coprolalia, the best
pharmacopoeia, adrenergic decongestants are the most known feature of Gilles de la Tourette syndrome, is rare,
common source – will prevent an unnecessary referral. occurring in less than 10% of cases.

Management Management
First-line treatment of essential tremor is pharmacological. Treatment is aimed at controlling symptoms. Dopamine
Propranolol and primidone are the mainstays of treatment, antagonists (haloperidol, clozapine and others) appear
with proven efficacy in controlled clinical trials.51 However, to be especially effective. Unilateral and bilateral BTX
neither has been shown to improve voice tremor in studies of injections of the thyroarytenoid muscles, as for adductor
small numbers of patients.52,53 Methazolamide, a carbonic- SD, have been successful in controlling vocal tics,
anhydrase inhibitor, appeared to improve vocal symptoms including coprolalia.61–64

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 Neurological and neuromuscular disorders of the larynx

Table 5.1  Botulinum toxin treatment of essential voice tremor: summary of studies (From Sulica L, Louis E [2006] Essential voice tremor.
In: Textbook of Laryngology. [eds. AL Merati, SA Bielamowicz] Plural Publishing, San Diego, pp. 245–253.)

Outcome
Number Patient Blinded
of Muscles subjective perceptual Acoustic
Study Type of study subjects injected Dose used evaluation evaluation analysis
Hertegard Open trial 15 Bilateral TA, 0.6–5 U per 10 of 15 (67%) Significant mean Significant
et al.57 occasionally side (TA) reported benefit improvement on decrease of F0
thyrohyoid & VAS & F0 variation
cricothyroid
Warrick Open trial with 10 Bilateral TA 2.5 U per 8 of 10 (80%) No statistically No statistically
et al.58,59 crossover (unilateral side wished to be significant significant
vs. bilateral injection) Unilateral TA 15 U treated again improvement change

Koller et al.51 Open trial ? Bilateral TA 1.0–2.5 U Significant mean Not reported Not reported
per side improvement on
0-to-100 scale of
function
Adler et al.60 Dose-randomised 13 Bilateral TA 1.25 U, 2.5 Significant mean Significant mean Significant
open trial U or 3.75 U improvement on improvement on mean
per side 5-point tremor 5-point tremor improvement in
severity scale severity scale F0 variation
U = units of botulinum toxin type A; TA= thyroarytenoid; VAS = 100 mm visual analogue scale; F0 = fundamental frequency.

Motor neuron disorders

function, which appears relatively well preserved even in
Amyotrophic lateral sclerosis advanced disease.66 Vocal fold movement abnormalities are
occasionally seen, but do not appear to be central to dysphagia
Aetiology/pathogenesis in ALS.67,68 However, velopharygneal insufficiency from
Amyotrophic lateral sclerosis (ALS) is a degenerative disorder palatal weakness is relatively common and may benefit from a
of unknown cause that affects both upper and lower motor prosthesis or a palatal adhesion procedure.
neurons. Loss of the former results in hyperreflexia and
spasticity, and loss of the latter results in weakness and muscle Management
wasting.The disease typically becomes apparent after the age of The primary disease process remains untreatable, and
50, and slightly more men than women are affected. Patients interventions are usually supportive and symptomatic.Timely
may present to the otolaryngologist with dysarthria, typically placement of a gastrostomy tube prevents malnutrition and
caused by tongue muscle involvement. Tongue fasciculations minimises the risk of aspiration. Optimally, gastrostomy tube
are distinctive and virtually pathognomonic. Relentlessly placement, like the creation of a tracheostomy for ventilatory
progressive ALS has a 50% mortality at 4 years, usually related support, is discussed with the patient and family as part of
to respiratory muscle weakness.65 end-of-life planning, well in advance of clinical need.

Clinical findings
Drooling may occur early in the course of the disease, and
Poliomyelitis and post-polio
affected patients may benefit from anticholinergic medication. ­syndrome
Dysphagia is a common complaint in mid- to late-stage disease
secondary to involvement of bulbar motor neurons.The deficit Poliomyelitis is a viral disease that resolves without sequelae
involves poor oral-pharyngeal coordination and decreased following a non-specific febrile illness in the majority of
pharyngeal contraction, but not upper oesophageal sphincter patients. About 1–5% of patients develop the paralytic form,

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 Peripheral nerve disorders

featuring motor symptoms involving respiratory, bulbar disease. Existing neurological deficits may worsen, and
and/or limb weakness, which are in some cases permanent. new weakness may affect previously uninvolved muscle
Sensory symptoms are absent. groups. This phenomenon, termed post-polio syndrome,
Largely eradicated in developed countries, affects swallowing in a high proportion of patients.
poliomyelitis remains relevant because some 25% of Vocal fold paresis and paralysis in these patients are
patients will experience a reactivation of neurological well documented.69–71 These appear to be amenable to
symptoms 20–30 years after their acute episode, probably standard techniques to maintain the airway and improve
due to age-related loss of anterior motor horn cells phonatory glottal closure.
from a population already depleted by the primary

Peripheral nerve disorders

latter reports suggest an explanation for the discrepancy.
Idiopathic vagal or recurrent The delay in diagnosis, typically 4 weeks or more, probably
­laryngeal nerve neuropathy dooms anti-inflammatory treatment, as used for Bell’s palsy
or sudden sensorineural hearing loss, to ineffectiveness.
Most cases of VFP or paresis of unknown cause are Recovery generally takes place between 1 and 9 months
peripheral neuropathies that do not form part of a systemic after onset, with rare cases returning after 1 year. Postma and
neurological illness. Based on serologies, cases of unknown Shockley85 pointed out even more short-lived paralyses,
cause have been attributed to neurotropic infections caused and it is likely that some cases resolve before the patient
by Lyme borreliosis72, herpes zoster73–76, herpes simplex77,78, seeks medical attention. Treatment consisting of surgical
Epstein-Barr virus79,West Nile virus80 and cytomegalovirus measures to restore glottic closure is covered elsewhere in
in the immunocompromised patient.81 Although these this volume.
clinical relationships are convincing, the majority of cases
of idiopathic VFP present with normal serologies and no Guillain–Barré syndrome
antecedent history of viral disease.
Most series suggest that some 20–40% of patients with Guillain–Barré syndrome, also known as acute inflammatory
idiopathic VFP recover full mobility (Table  5.2) and an polyneuropathy, is an idiopathic demyelinating disorder that
additional percentage regain acceptable voice. Occasionally, causes rapidly progressive weakness. In about half of cases it
both figures are much higher.82–84 No features of these follows an infectious illness, sometimes as trivial as an upper

Table 5.2  Idiopathic vocal fold paralysis (Adapted from Sulica L,

Blitzer A [2006] [eds.] Vocal Fold Paralysis. Springer, Heidelberg.)
Recovery of Recovery of voice
Study Number motion (%) without motion (%)
Lacourreye et al.111 40 35
Loughran et al.112 9 44
Leon et al.83 50 14 72
Havas et al.82 36 75 14
Benninger et al.113 50 24
Ramadan et al.114 16 19 6
Verhulst et al.115 67 39 15
Willat & Stell116 28 22 25
Fex & Elmqvist[A]117 16 31
Blau & Kapidia118 21 48
Williams84 29 83
Work119 8 25
[A] = combined unilateral and bilateral cases.

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 Neurological and neuromuscular disorders of the larynx

respiratory infection.The motor deficits evolve over hours to the important exception of patients with HMSN type 2C.
days and usually resolve completely, although this may take This is attributed to aspiration and respiratory complications
months. Treatment in the meantime is supportive, and may from laryngeal abnormalities.90,91
include mechanical ventilation. Steroids are not helpful, but
plasmapheresis may be effective in reducing the duration of Clinical findings
the disorder if used early.
Bilateral VFP may develop rapidly in patients with Characteristic clinical features include distal muscle weakness
Guillain–Barré syndrome and occasionally may be the and atrophy of the legs, with bone changes over the long term.
initial sign.86–88 Because the deficit is likely to be temporary, ‘Stork leg’ or ‘inverted champagne bottle thigh’ describes the
no destructive airway widening procedure should be appearance of the lower extremity with distally atrophied
contemplated until neurological recovery is complete. muscles. Upper extremity findings are similar and patients
Tracheostomy, on the other hand, may be necessary for may have claw hand. Sensory loss is often subtle, and most
safety and to permit ventilation. often affects vibration. Peripheral nerves are palpably enlarged
in about half of patients with HMSN types  1  and  3.91
An  affected greater auricular nerve is particularly helpful
Hereditary motor and sensory to the examining otolaryngologist. The  disorder is slowly
progressive, and treatment is supportive.
­neuropathy It was once held as axiomatic that HMSN nearly always
spares the CNs. Numerous reports have made it plain that
Aetiology/pathogenesis this observation does not hold true, and the pathological
Hereditary motor and sensory neuropathy (HMSN), also process can affect the laryngeal nerves to produce vocal
known as Charcot–Marie–Tooth neuropathy or peroneal fold paresis.92 It is not clear how many HMSN patients
muscular atrophy, is a genetic disorder that has weakness have laryngeal involvement, and it is possible that many
and sensory loss in the distal limbs as its most prominent cases go unnoticed. Paresis is usually bilateral, although the
features. It accounts for 80–90% of all genetic neuropathies, degree of vocal fold hypomobility is typically asymmetric
which in turn make up about 20% of all neuropathies. In (Figures 5.3a, b). Because of the slow progression of the
the United States, this amounts to an incidence of 42 per disease, patients can sometimes tolerate surprising degrees
100,000, or more than 250,000 cases.89 It is more prevalent of glottic restriction; many are stridulous at presentation, but
than myasthenia gravis. Most forms are inherited in an accept this as a matter of course, having been so for months
autosomal dominant manner.Typically, the disease begins to or years. Despite this, the treating physician should have no
manifest in the first or second decade and progresses slowly. hesitation in intervening when clinical criteria indicate that
In general, life expectancy is not markedly diminished, with the potential for airway difficulties is high.

a   b
Figures 5.3a, b The range of motion of the vocal folds of a 44-year old man with HMSN is markedly restricted, producing inspiratory noise
during conversation and dyspnoea on exertion. Maximum abduction is shown on the left. Laryngeal EMG confirmed bilateral vocal fold
paresis, more dense on the left than the right. One year after this examination, vocal fold abduction deteriorated further and a surgical
procedure was required.

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 Disorders of muscle

Disorders of the neuromuscular junction

Myasthenia gravis Botulism
Aetiology/pathogenesis Classic botulism results from ingestion of a clostridial
neurotoxin that blocks acetylcholine release from the nerve
Myasthenia gravis is an autoimmune disorder of fluctuating
terminal. Clinically, the disease manifests as rapidly evolving
weakness and fatigue of cranial, limb and trunk musculature
weakness and autonomic dysfunction, marked by diplopia,
caused by antibodies to post-junctional acetylcholine
dysphagia, dysphonia, dry mouth and postural hypotension.
receptors. Although remissions and relapses are typical, the
Death results from respiratory failure. Recent outbreaks
disease is overall slowly progressive.
have been associated with improperly canned fish products
Clinical findings/diagnosis and honey, although the disease was initially observed after
Diagnosis is suggested by fatigability of muscle with repetitive sausage ingestion (botulus [Latin] = sausage).
or sustained contraction (typically, the development of ptosis Because BTX is used therapeutically in otolaryngology,
or diplopia with sustained upward gaze). Three tests are used one is more likely to see local effects from intramuscular
to confirm clinical suspicion: administration of intravenous overdose than systemic toxicity from ingestion. Symptoms
edrophonium should correct signs of muscle weakness depend on the muscle treated. Adductor muscle overdose
attributed to myasthenia; anti-acetylcholine receptor antibodies will result in incomplete glottic closure, breathy dysphonia
are found in the serum; and repetitive stimulation of peripheral and, in the worst case, dysphagia to liquids. Frank aspiration
nerves should yield a decreased number of muscle twitches. is extremely rare. Abductor muscle overdose will result in
It is not necessary for all tests to be positive for diagnosis. an immobile vocal fold; if bilateral, airway narrowing may
be significant and even dangerous.The effect of the toxin is
Management temporary, so treatment is aimed at avoiding complications
Steroids and other immune-modulating drugs, and until function returns; the duration of effect of BTX is
plasmapheresis for severe cases, are the mainstays of treatment. approximately 90 days.
Some 10% of myasthenia patients have thymomas, but all are
thought to benefit from a thymectomy. Anticholinesterase
drugs, which potentiate the acetylcholine effect by inhibiting its
Organophosphate toxicity
breakdown, are used for additional symptomatic relief, but are Organophosphates found in chemical warfare agents (‘nerve
no longer regarded as first-line agents since the autoimmune gas’ [e.g. tabun, sarin]) and commercially available pesticides
nature of the disease has become fully appreciated. inhibit acetylcholinesterase, causing massive parasympathetic
Vocal fold paresis, typically bilateral, may occur in discharge and muscle weakness in acute toxicity. Low or
myasthenia gravis, contributing to respiratory difficulties; intermediate dose exposure may produce a more subtle
occasionally, it may be the presenting symptom.93–97 Despite muscle weakness and bilateral VFP, which contributes to the
the availability of medical treatment, most reported patients distress caused by dysfunction of respiratory muscles.98–100
ultimately underwent tracheostomy, as vocal fold paresis was VFP tends to be reversible, although intubation is occasionally
not identified until dangerously symptomatic. Conceivably, necessary to secure the airway. Atropine, which is given to
anticipation and early identification of laryngeal involvement counteract parasympathetic effects, is generally not helpful in
might make non-surgical management possible. reversing paralysis; pralidoxime, a cholinesterase activator, is
used for this purpose.

Disorders of muscle
Other cranial muscle and limb muscle weaknesses may
Oculopharyngeal muscular also occur, but are extremely variable. Clusters of disease,
­dystrophy a reflection of immigration of affected individuals – so
called ‘founder effect’ – exist in Quebec and among
Oculopharyngeal dystrophy is a late-onset autosomal Bukhara Jews in Israel; in Quebec, the couple who
dominant, slowly progressive myopathy whose most brought the disease from Europe in 1648 have actually
prominent findings are eyelid ptosis and dysphagia. been identified.101

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 Neurological and neuromuscular disorders of the larynx

Treatment is supportive and features surgical correction Alzheimer’s brain, including amyloid-beta, phosphorylated
of ptosis as well as cricopharyngeal myotomy for dysphagia. tau protein and 20 other proteins.105 In addition, there is
Both interventions have been shown to effect meaningful a pronounced inflammatory infiltrate. Diagnosis depends
improvement in daily function and quality of life.102,103 on these and other characteristic histological findings on
muscle biopsy.
Inclusion body myositis IBM causes weakness of both proximal and distal muscles,
and usually progresses slowly to severe disability, as well as
Inclusion body myositis (IBM) is the most common morbidity from falls. There is no specific treatment that has
progressive muscle disease in people over 50.104 It is an been shown to be effective.
inflammatory myopathy of uncertain cause and distinct Up to 80% of IBM patients develop dysphagia from
from immune disorders such as dermatomyositis and involvement of pharyngeal musculature106, almost always
polymyositis. Most forms are sporadic, although a including the cricopharyngeus muscle. Treatment of this
hereditary form has been described. The ‘inclusion body’ muscle – whether by dilatation, BTX chemodenervation or
of the name refers to accumulations of proteinaceous myotomy – has been very effective in improving swallowing
material within muscle fibres that are similar to those in the and avoiding aspiration.107–110

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24 Silber MH, Levine S (2000) Stridor and death in reinnervation: a new surgical treatment for adductor
multiple system atrophy. Move Disord 15:699–704. spasmodic dysphonia. Ann Otol Rhinol Laryngol
25 Wenning GK,Tison F, Schlomo B et al. (1997) Multiple 108:227–231.
system atrophy: a review of 203 pathologically proven 39 Elble RJ (2000) Diagnostic criteria for essential tremor
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26 Umeno H, Ueda Y, Mori K et al. (2000) Management 40 Louis ED (2005) Essential tremor. Lancet Neurol
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21:344–348. tremor? The genetic epidemiology of essential tremor.
27 Smith RL, Brown DH (2000) Shy–Drager syndrome: Neurology 46:1200–1205.
an otolaryngology perspective. J Otolaryngol 29: 42 Louis ED, Ford B, Barnes LF (2000) Clinical subtypes
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28 Blumin JH, Berke GS (2002) Bilateral vocal fold 43 Jankovic J (2000) Essential tremor: clinical
paresis and multiple system atrophy. Arch Otolaryngol characteristics. Neurology 54(Suppl 4):S21–S25.
Head Neck Surg 128:1404–1407. 44 Koller WC, Busenbark K, Miner K (1994) The
29 Isozaki E, Naito A, Horiguchi S et al. (1996) Early relationship of essential tremor to other movement
diagnosis and stage classification of vocal cord abductor disorders: report on 678 patients. Ann Neurol 35:​
paralysis in patients with multiple system atrophy. 717–723.
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30 Bannister R, Gibson W, Michaels L et al. (1981) tremor. Adv Neurol 49:239–253.
Laryngeal abductor paralysis in multiple system 46 Tomoda H, Shibasaki H, Kuroda Y et al. (1987) Voice
atrophy: a report on three necropsied cases, with tremor: dysregulation of voluntary expiratory muscles.
observation on the laryngeal muscles and the nuclei Neurology 37:117–122.
ambuguii. Brain 104:351–368. 47 Koda J, Ludlow CL (1992) An evaluation of laryngeal
31 Bawa R, Ramadan HH, Wetmore SJ (1993) Bilateral muscle activation in patients with voice tremor.
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Head Neck Surg 109:911–914. 48 Finnegan EM, Luschei ES, Barkmeier JM et al. (2003)
32 Shiba K, Isono S (2006) Tracheostomy abolishes Synchrony of laryngeal muscle activity in persons
paradoxical activation of the vocal cord adductor with vocal tremor. Arch Otolaryngol Head Neck Surg
in multiple system atrophy. Auris Nasus Larynx 33: 129:313–318.
295–298. 49 Mendoza E, Carballo G (1999) Vocal tremor and
34 Ghorayeb I, Bioulac B, Tison F (2005) Sleep disorders psychological stress. J Voice 13:105–112.
in multiple system atrophy. J Neural Transm 112: 50 Gamboa J, Jimenez-Jimenez FJ, Nieto A et al. (1998)
1669–1675. Acoustic voice analysis in patients with essential
35 Blitzer A, Brin MF, Stewart CF (1998) Botulinum tremor. J Voice 12:444–452.
toxin management of spasmodic dysphonia (laryngeal 51 Koller WC, Hristova A, Brin M (2000) Pharmacologic
dystonia): a 12-year experience in more than 900 treatment of essential tremor. Neurology 54(Suppl 4):​
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52 Hartman DE, Vishwanat B (1984) Spastic dysphonia 68 Polkey MI, Lyall RA, Green M et al. (1998) Expiratory
and essential (voice) tremor treated with primidone. muscle function in amyotrophic lateral sclerosis. Am J
Arch Otolaryngol 110:394–397. Respir Crit Care Med 158:734–741.
53 Koller WC, Graner D, Micoch A (1985) Essential 69 Abaza MM, Sataloff RT, Hawkshaw MJ et al. (2001)
voice tremor: treatment with propranolol. Neurology Laryngeal manifestations of postpoliomyelitis
35:106–108. syndrome. J Voice 14:291–294.
54 Muenter MD, Daube JR, Caviness JN et al. (1991) 70 Driscoll BP, Gracco C, Coelho C et al. (1995)
Treatment of essential tremor with methazolamide. Laryngeal function in postpolio patients. Laryngoscope
Mayo Clin Proc 66:991–997. 105:35–41.
55 Busenbark K, Ramig L, Dromey C et al. (1996) 71 Robinson LR, Hillel AD, Waugh PF (1998) New
Methazolamide for essential voice tremor. Neurology laryngeal muscle weakness in post–polio syndrome.
47:1331–1332. Laryngoscope 108:732–734.
56 Padilla F, Berthier ML, Campos-Arillo VM (2000) 72 Schroeter V, Belz GG, Blenk H (1988) Paralysis of
Temblor essencial de la voz y tratamiento con recurrent laryngeal nerve in Lyme disease. Lancet
gabapentina. Rev Neurol 31:798. 2(8622):1245.
57 Hertegard S, Granqvist S, Lindestad PA (2000) 73 Wu CL, Linne OC, Chiang CW (2004) Herpes zoster
Botulinum toxin injections for essential voice tremor. laryngis with prelaryngeal skin erythema. Ann Otol
Ann Otol Rhinol Laryngol 109:204–209. Rhinol Laryngol 113(2):113–114.
58 Warrick P, Dromey C, Irish J et al. (2000) The treatment 74 Nishizaki K, Onoda K, Akagi H et al. (1997) Laryngeal
of essential voice tremor with botulinum  toxin A: zoster with unilateral laryngeal paralysis. ORL J
a longitudinal case report. J Voice 14:410–412. Otorhinolaryngol Relat Spec 59(4):235–237.
59 Warrick P, Dromey C, Irish JC et al. (2000) Botulinum 75 Randel RC, Kearns DB, Nespeca MP et al. (1996)
toxin for essential tremor of the voice with multiple Vocal cord paralysis as a presentation of intrauterine
anatomical sites of tremor: a crossover design study infection with varicella-zoster virus. Pediatrics
of unilateral versus bilateral injection. Laryngoscope 97(1):127–128.
110:1366–1374. 76 Rothschild MA, Drake W 3rd, Scherl M (1994)
60 Adler CH, Bansberg SF, Hentz JG et al. (2004) Cephalic zoster with laryngeal paralysis. Ear Nose
Botulinum toxin type A for treating voice tremor. Throat J 73(11):850–852.
Arch Neurol 61:1416–1420. 77 Bachor E, Bonkowsky V, Hacki T (1996) Herpes
61 Scott BL. Jankovic J, Donovan DT (1996) Botulinum simplex virus type I reactivation as a cause of a
toxin injection into the vocal cord in the treatment unilateral temporary paralysis of the vagus nerve. Eur
of malignant coprolalia associated with Tourette’s Arch Otorhinolaryngol 253(4–5):297–300.
syndrome. Mov Disord 11:431–433. 78 Pou A, Carrau RL (1995) Bilateral abductor vocal cord
62 Trimble MR, Whurr R, Brookes G et al. (1998) Vocal paralysis in association with herpes simplex infection:
tics in Gilles de la Tourette syndrome treated with a case report. Am J Otolaryngol 16(3):216–219.
botulinum toxin injections. Mov Disord 13:617–619. 79 Parano E, Pavone L, Musumeci S et al. (1996) Acute
63 Kwak CH, Hanna PA, Jankovic J (2000) Botulinum palsy of the recurrent laryngeal nerve complicating
toxin in the treatment of tics. Arch Neurol 57:1190–1193. Epstein–Barr virus infection. Neuropediatrics 27(3):​
64 Porta M, Maggioni G, Ottaviani F et al. (2003) 164–166.
Treatment of phonic tics in patients with Tourette’s 80 Steele NP,Myssiorek D (2006)West Nile virus induced
syndrome using botulinum toxin type A. Neurol Sci vocal fold paralysis. Laryngoscope 116:494–496.
24:420–423. 81 Small PM, McPhaul LW, Sooy CD et al. (1989)
65 Neville H, Ringel SP (1999) Neuromuscular Cytomegalovirus infection of the laryngeal nerve
diseases. In: Neurology for the Non-Neurologist. (eds. WJ presenting as hoarseness in patients with acquired
Weiner, CG Goetz) Lippincott, Williams & Wilkins, immunodeficiency syndrome. Am J Med 86(1):​
Philadelphia, pp. 273–298. 108–110.
66 Higo R, Tayama N, Nito T (2004) Longitudinal 82 Havas T, Lowinger D, Priestly J (1999) Unilateral vocal
analysis of dysphagia in amyotrophic lateral sclerosis. fold paralysis: causes, options and outcomes. Aust N Z
Auris Nasus Larynx 31:247–254. J Surg 69:509–513.
67 Chen A, Garrett CG (2005) Otolaryngologic 83 León X,Venegas MP, Orús C et al. (2001) Inmovilidad
presentations of amyotrophic lateral sclerosis. glótica: estudio retrospectivo de 229 casos. Acta
Otolaryngol Head Neck Surg 132:500–504. Otorrinolaringol Esp 52:486–492.

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84 Williams RG (1959) Idiopathic recurrent laryngeal 100 Indudharan R, Win MN, Noor AR (1998) Laryngeal
nerve paralysis. J Laryngol Otol 73:161–166. paralysis in organophosphorous poisoning. J Laryngol
85 Postma GN, Shockley WW (1998) Transient vocal Otol 112(1):81–82.
fold immobility. Ann Otol Rhinol Laryngol 107: 101 Bouchard JP (1997) Andre Barbeau and the

236–240. oculopharyngeal muscular dystrophy in French
86 Yoskovitch A, Enepekides DJ, Hier MP et al. (2000) Canada and North America. Neuromuscul Disord
Guillain–Barre syndrome presenting as bilateral vocal 7(Suppl 1):S5–S11.
cord paralysis. Otolaryngol Head Neck Surg 122(2):​ 102 Gervais M, Dorion D (2003) Quality of life following
269–270. surgical treatment of oculopharyngeal syndrome.
87 Panosian MS, Quatela VC (1993) Guillain–Barre J Otolaryngol 32:1–5.
syndrome presenting as acute bilateral vocal cord 103 Perie S, Eymard B, Laccoureye L et al. (1997)

paralysis. Otolaryngol Head Neck Surg 108(2):171–173. Dysphagia in oculopharyngeal muscular dystrophy:
88 Rodrigues JF,York EL, Nair CP (1984) Upper airway a  series of 22 French cases. Neuromuscul Disord
obstruction in Guillain–Barre syndrome. Chest 86(1):​ 7(Suppl 1):S96–99.
147–148. 104 Engel WK, Askanas V (2006) Incusion body myositis:
89 Lovelace RE (1999) Charcot–Marie–Tooth disorders clinical, diagnostic and pathologic aspects. Neurology
and other hereditary neuropathies. In: Motor Disorders. 66(Suppl 1):S20–S29.
(ed. DS Younger) Lippincott, Williams & Wilkins, 105 Askanas V, Dalakas MC, Engel WK (2006) Inclusion
Philadelphia, pp. 203–211. body myositis: clinical and pathologic aspects, and basic
90 Dyck PJ, LitchyWJ, Minnerath S et al. (1994) Hereditary research potentially relevant to treatment. Neurology
motor and sensory neuropathy with diaphragm and 66(Suppl 1):S1.
vocal cord paresis. Ann Neurol 35:608–615. 106 Houser SM, Calbrese LH, Strome M (1998) Dysphagia
91 Mendell JR (1998) Charcot–Marie–Tooth in patients with inclusion body myositis. Laryngoscope
neuropathies and related disorders. Semin Neurol 18(1):​ 108:1001–1005.
41–47. 107 Darrow DH, Hoffman HT, Barnes GJ et al. (1992)
92 Sulica L, Blitzer A, Lovelace RE et al. (2001) Vocal fold Management of dysphagia in inclusion body myositis.
paresis of Charcot–Marie–Tooth disease. Ann Otol Arch Otolaryngol Head Neck Surg 118:313–317.
Rhinol Laryngol 110:1072–1076. 108 Liu LW.Tarnopolsky M,Armstrong D (2004) Injection
93 Osei–Lah V, O’Reilly BJ, Capildeo R (1999) Bilateral of botulinum toxin A to the upper esophageal
abductor vocal cord paralysis due to myasthenia gravis. sphincter for oropharyngeal dysphagia in two patients
J Laryngol Otol 113:678–679. with inclusion body myositis. Can J Gastroeneterol 18:​
94 Fairley JW, Hughes M (1992) Acute stridor due to 397–399.
bilateral vocal fold paralysis as a presenting sign of 109 Danon MJ, Friedman M (1989) Inclusion body

myasthenia gravis. J Laryngol Otol 106:737–738. myositis associated with progressive dysphagia:
95 Job A, Raman R, Gnanamuthu C (1992) Laryngeal treatment with cricopharyngeal myotomy. Can J
stridor in myasthenia gravis. J Laryngol Otol 106: Neurol Sci 16(4):436–438.
633–634. 110 Wintzen AR, Botz GT, deBakker HM et al. (1988)
96 Teramoto K, Kuwabara M, Matsubara Y (2002) Dysphagia in inclusion body myositis. J Neurol
Respiratory failure due to vocal cord paresis in Neurosurg Psychiatry 51(12):1542–5.
myasthenia gravis. Respiration 69:280–282. 111 Laccourreye O, Papon JF, Kania R et al. (2003) Paralysies
97 Todisco T, Baglioni S, Eslami A et al. (2000) Myasthenic laryngeés unlatérales: données épidemiologiques et
inspiratory vocal cord dysfunction: efficacy of nasal évolution thérapeutique. Presse Med 32:781–786.
continuous positive airway pressure treatment. 112 Loughran S, Alves C, MacGregor FB (2002) Current
Respiration 67:94–97. aetiology of unilateral vocal fold paralysis in a teaching
98 DaSilva HJ, Sanmuganathan PS, Senanayake N (1994) hospital in the West of Scotland. J Laryngol Otol 116:​
Isolated bilateral recurrent laryngeal nerve paralysis: a 907–910.
delayed complication of organophosphorus poisoning. 113 Benninger MS, Gillen JB, Altman JS (1998) Changing
Hum Exp Toxicol 13:171–173. etiology of vocal fold immobility. Laryngoscope 108:​
99 Thompson JW, Stocks RM (1997) Brief bilateral 1346–1350.
vocal cord paralysis after insecticide poisoning. A new 114 Ramadan HH, Wax MK, Avery S (1998) Outcome
variant of toxicity syndrome. Arch Otolaryngol Head and changing cause of unilateral vocal cord paralysis.
Neck Surg 123(1):93–96. Otolaryngol Head Neck Surg 118:199–202.

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115 Verhulst J, Lecoq M, Marraco M et al. (1997) Paralysie 118 Blau JN, Kapadia R (1972) Idiopathic palsy of

recurrentielle idiopathique: analyse retrospective de the recurrent laryngeal nerve: a transient cranial
67 cas. Rev Laryngol Otol Rhinol 118:263–265. mononeuropathy. Br Med J 4:259–261.
116 Willatt DJ, Stell PM (1989) The prognosis and
119 Work WP (1941) Paralysis and paresis of the vocal cords:
management of idiopathic vocal cord paralysis. a statistical review. Arch Otolaryngol 34:267–280.
Clin Otolaryngol 14:247–250.
117 Fex S, Elmqvist D (1973) Endemic recurrent laryngeal
nerve paresis. Acta Otolaryngol 75:368–369.

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 CHAPTER 6

Vocal fold paralysis

Matthew S. Broadhurst

Introduction
Vocal fold paralysis (VFP) is fortunately not common, be a dense paralysis. As such, the immobile cord can lie
comprising 0.2–0.4% of patients presenting to the author’s laterally creating severe dysphonia from a large glottal gap
ENT clinics. However,VFP can create significant morbidity and inadequate airway protection. The flow-on effect can
for patients through disabling dysphonia or aspiration have a major impact on a worker’s productivity or social
with or without pneumonia. Regardless of whether such involvement, leading to absence from work, loss of income,
a nerve injury is temporary or permanent, there can still loss of job opportunities or even social withdrawal.

Aetiology
The cause for the paralysis can be considered by following Iatrogenic nerve damage
the paired nerves involved: vagus, superior laryngeal
The main regions where surgery is undertaken and potential
nerve (SLN) and the recurrent laryngeal nerve (RLN).
nerve injury exists are neck surgery, thoracic surgery and
The technical description of a VFP requires a proven
skull base surgery.
electromyography (EMG) pattern. Despite this, the majority
of cases of an immobile vocal fold are paralysis rather than
cricoarytenoid joint (CAJ) fixation, although diagnostic
Neck surgery
EMG is not routinely used. Regardless of the aetiology Thyroid surgery remains the single most common
of the nerve injury, the fundamental process is disruption surgical procedure complicated by unilateral VFP (UVFP),
to axonal transport and demyelination preventing neural comprising 14–67% of all surgical regions.3,4 The incidence
transmission. This arises from nerve transection during of temporary or permanent VFP from thyroid surgery alone
surgery (inadvertent or deliberate) in a difficult tumour is 1–7.7%. The temporary paralysis rate is 1–5.1% and the
removal or from nerve manipulation/traction where permanent paralysis rate is 1–8.6%. Anterior cervical spine
there is a reasonable chance for recovery. Compression of surgery and carotid surgery represent 1–19% and 0–27%,
the nerve can occur at any course along its length from a respectively, of the iatrogenic VFP group.5
tumour arising around or within it. Finally, disruption to the
vasculature of the nerves can arise from radiation causing Thoracic surgery
ischaemia and subsequent cell death. Surgery involving the aortic arch, coronary artery bypass
Multiple studies have reviewed the aetiology and grafting, hilum of the lung, mediastinum or oesophagus
approximately 40% of VFP cases remain idiopathic can be complicated by VFP with up to 41% of such surgery
(11–53%).1,2 Other major causes of paralysis include surgery reporting this injury.6–8 In this setting, patients may be
(thyroid surgery being the highest specific contrib­utor), blunt intubated for a variable postoperative period so such injury
or penetrating neck trauma, tumour compression/invasion or may only be noted on extubation. A high index of suspicion
intubation trauma (Table 6.1). with early assessment and intervention is critical to reduce
the morbidity of VFP in this situation.
Table 6.1  Aetiology of unilateral vocal fold paralysis
Idiopathic
Skull base surgery
Iatrogenic: surgery, intubation Skull base surgery may involve the vagus, causing a VFP,
Malignancy
and it is important to realise in this setting that multiple
lower cranial nerves (CNs) may be involved. As such,
Neurological
patients tend to have limited capacity for compensation
Other medical (including viral) with multiple nerve deficits, particularly in the elderly.

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 Vocal fold paralysis

VFP was reported in 100% of patients in one study CAJ dislocation is extremely rare, particularly when the
involving paraganglioma surgery even where complete intubation is not technically difficult. The forces involved
nerve preservation was achieved.9 in such a dislocation are severe and highly unlikely during
controlled intubation in the elective surgery.11
Other causes Radiation fibrosis in the cervical region along the
The incidence of VPF following intubation is very difficult course of the vagus or RLN does occur, with vascular
to determine as only a fraction of post-intubation patients compromise leading to ischaemia and subsequent loss of
with hoarseness are formally assessed with laryngoscopy. It is neural transmission. As a latent complication, this may be
estimated to be under 0.05%.10 Mechanisms thought to be seen many years following radiation treatment.
involved include pressure neuropraxis from the endotracheal Non-surgical causes of VFP account for approximately
tube cuff or direct trauma from the tube tip to the anterior 60% of cases with 29–50% of those being from malignancy.12
branch of the RLN as it becomes relatively superficial to Malignancy includes skull base nerve compression, cervical
the mucosa inferior to the cricothyroid joint. As with most nerve compression/invasion or thoracic nerve compression/
neuopraxias, spontaneous recovery is the expected outcome. invasion or traction injury.

Clinical assessment
The presentation of a UVFP arises from glottal Medical history
incompetency. Failure of complete glottal closure causes
A history is sought including preceding surgery or
air leakage through the glottis presenting as breathy
trauma. Common surgical causes are listed in Table 6.2
dysphonia, reduced volume/projection, reduced vocal
with the mechanisms of nerve injury listed in Table 6.3.
stamina, diplophonia and aspiration. This creates mild vocal
Trauma can be external blunt cervical trauma causing a
fatigue with prolonged voice use, from moderate dysphonia
vagal neuropraxia or a CAJ injury. It may also result from
to totally disabling aphonia. Aspiration with/without
endotracheal tube placement. If a stroke is suspected, signs
pneumonia can result from both glottal incompetency
of dysphagia, velopharyngeal insufficiency, dysarthria
and a significant sensory deficit. The presence of a weak
or general signs of ataxia and limb weakness must be
or ineffective cough must be noted. In a high vagal lesion,
elicited. A history of chemotherapy may be relevant as
dysphagia for solids may also be reported.
vinblastine, vincristine and cisplatin are reported to be
Patients develop varying degrees of compensation from
neurotoxic.
UVFP but this usually involves significant muscle tension.
History of an upper respiratory tract infection of a
Supraglottic constriction in an attempt to improve glottal
cervical or thoracic malignancy must be sought.
closure is common but usually counterproductive. In fact,
if a simple case of severe muscle tension dysphonia is seen,
the clinician should look carefully to make sure an obscured
UVFP is not overlooked. The voice for UVFP is usually Table 6.2  Surgical causes of vocal fold paralysis
monotone, rough or strained and in females is typically
significantly elevated in pitch and weak. Cervical surgery: thyroid/parathyroid
The surgeon must gain knowledge of the patient’s vocal Cervical spine procedures
requirements, both at work and socially, and the impact Carotid endarterectomy
the paralysis has on these. How critical voice use is to the Neck dissection
patient will usually determine whether or not they opt for
Thoracic surgery: lung resection
a temporary augmentation procedure.
It is important to realise that a patient can present with Aortic arch surgery
apparent ‘shortness of breath’ from a UVFP. This subjective Aortic valve surgery
report results from the inability to control air escape Coronary artery bypass grafting
through the incompetent glottis rather than being a true Oesophageal resection
airway narrowing. This highlights how critical the Valsalva
Mediastinoscopy
manoeuvre is in the normal individual in bending down,
putting on shoes and socks, lifting, running up a flight of Other surgery/procedures: endotracheal intubation, skull base
stairs and so on. surgery

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 Clinical assessment

Table 6.3  Mechanism of nerve injury from surgery (From Sulica L, Blitzer A [2006] [eds.] Vocal Fold
Paralysis. Springer, Berlin, Heidelberg, p. 56.)
Surgery/procedure Mechanism of nerve injury/relevant anatomy
Anterior cervical fusion Retraction; stretch injury of RLN (right more common)
Oesophagectomy RLN injury in tracheo-oesophageal groove
Carotid endarterectomy Vagal injury during dissection
Mediastinoscopy RLN injury (usually left)
Coronary artery bypass grafting Retraction/direct injury to vagus/RLN during internal
mammary artery harvest for grafting. Hypothermic nerve injury
from ice cardioplegia
Pulmonary resection Usually left upper lobe/RLN injury
Endotracheal intubation Possible pressure neuropraxia from compression of anterior
rami of RLN due to a high-riding endotracheal cuff in
the subglottis

Table 6.4  Videostroboscopic assessment

parameters
Vocal fold/arytenoid mobility
Vocal fold edges
Vocal cord closure
Mucosal wave
Supraglottic compression
Other findings

flexible endoscope allows good visibility. An adequate

period of endoscopic observation of the glottis at rest
is critical, particularly if a significant degree of muscle
tension is present. Phonating with a ‘sigh’ or ‘hmmmm’
Figure 6.1 A left vocal fold paralysis showing a lateral lying cord can reduce the muscle tension and improve the glottal
approximately 5 mm from the midline. assessment.13 Similarly, hyperfunction can be minimised to
allow better glottal closure visualisation with inspiratory
phonation.
Examination Strobolaryngoscopy assessment should include the
A thorough examination of the head and neck is expected arytenoid height, location and mobility along with the
including the thyroid gland, cervical lymph nodes, laryngeal degree of glottal incompetence. The mucosal wave is
framework and lower CNs.The voice is assessed for quality, noted, as impairment of this may limit the outcome
roughness, breathiness, fundamental frequency, pitch of voice restoration surgery. Rapid alternating ‘ee….
range and maximum phonation time (MPT). An MPT sniff ’ assesses abduction and adduction at the glottis.
under 5 seconds in a permanent paralysis suggests a lateral It is important to recall the bilateral innervation of the
cord indicating an arytenoid procedure may be required inter-arytenoid muscle where its contraction may give a
(Figure 6.1). false sense of movement in the setting of UVFP. Useful
Close proximity video strobolaryngoscopy is required information recorded on videostroboscopy is listed in
to assess the structure and function of the vocal folds. Table 6.4.
Although the author’s preference is 70-degree rigid A paralysed cord can lie at any point along the curve of the
laryngoscopy because of the superior clarity, a distal chip cricoid facet. To describe a vocal cord’s position, the author

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 Vocal fold paralysis

prefers estimation in millimetres of the distance between

midline and the medial surface of the paralysed arytenoid
(Figure 6.1).This also aids in assessing the posterior glottal
closure and the suitability for an arytenoid repositioning
procedure to maximise glottal closure. Classical terms
of lateral, median, paramedian and intermediate are not
specific for the site of lesions but are commonly used for
description.
The location of the paralysed cord is based on the degree
of reinnervation and synkinesis. It was initially thought to
relate to the anatomical level of the lesion, but this has been
shown to be incorrect.13–15 Be aware that an arytenoid and
corniculate cartilage can significantly prolapse anteriorly,
termed ‘hooding’, and may be mistaken for an arytenoid
dislocation (Figure 6.2).
The Jostle sign may be reported where brief lateral
movements of the immobile arytenoid result from the
unaffected arytenoid adducting and striking against it. This
causes brief minimal lateral excursion movements of the Figure 6.2 A left vocal fold paralysis showing hooding of the left
paralysed arytenoid. arytenoid/corniculate cartilage anteriorly.

Investigations
The extent for investigating a UVFP is strongly based Serology has a limited role and screening tests should
on history. If there is a clear surgical event leading to be avoided. Specific tests may be useful if the examination
a postoperative paralysis, then no work up is required to suggests a systemic cause. One study reported a 0% yield in
elicit the aetiology. However, in the setting of an idiopathic 84 cases of UVFP.17
UVFP, specific investigations are recommended. The role of EMG remains somewhat controversial.
A CT scan covering the course of the vagus and RLN is Laryngology centres vary from using it as routine
required. There is no significant added benefit to an MRI assessment to total absence of its use. EMG can be helpful
scan when an adequate CT scan has been performed and in differentiating between CAJ fixation and UVFP.
reported by an experienced head and neck radiologist. For It  may also provide information in a dense paralysis
consideration of a skull base lesion, an MRI brain scan as to whether the nerve is transected or intact, thus
may identify a high vagal lesion. In one study16, 100% of providing prognostic information for potential recovery.
chest lesions responsible for a UVFP were identified on An extensive review of the role of EMG in VFP is beyond
chest radiography alone, suggesting that more extensive the scope of this chapter, but the reader is referred to
imaging is unnecessary. A modified barium swallow a comprehensive review in the textbook Vocal Fold
may assess the extent and level of pharyngeal muscular Paralysis.18
involvement and the degree of aspiration.

Treatment
The treatment of UVFP can be formulated in many involves speech therapy and may utilise temporary injection
different ways depending on the nature of the classification. laryngoplasty. Long-term management mostly involves
These include temporary and permanent nerve injury, acute permanent reconstructive intervention and is therefore usually
and chronic, conservative and surgical or short term and implemented at least 6 months following the onset of UVFP.
long term.The latter classification is used in this chapter. Dysphonia can be severely disabling when considering
Short-term management begins at the first realisation of occupational voice requirements, loss of income and social/
nerve injury whether it be intraoperatively or in the post- family interaction.The author commonly sees tertiary referral
surgery recovery period before discharge. It can also be defined UVFP patients and is amazed how often a recommendation
as the first 6 months following onset of paralysis. Intervention of just accepting the voice deficit and considering a trial of

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 Treatment

speech  therapy is given. Rarely is a temporising injection The assessment tools utilised for speech therapy are
offered based on lack of ‘significant’ voice requirements. In classified as perceptual and patient-rated tools. The
contrast, it is the author’s belief that no matter the place a important consequences of the paralysis are assessed: effects
patient is in life’s journey, striving for maximal voice restoration on phonation, respiration, resonance and swallowing.
is the goal and a patient’s end point should not be limited based Perceptual assessment includes analysis of volume, pitch
simply on age or social setting. Elderly patients sometimes and voice quality by reading a set passage and assessing
require more effort as their environment frequently involves conversational speech. Pitch range, fundamental frequency,
partners or friends with significant hearing impairment, so S/Z ratio, loudness and MPT are measured. Use of the
they rely heavily on vocal projection, stamina and clarity. GRBAS21 perceptual scale is common, with the most
beneficial perceptual symptoms being breathiness, reduced
Short-term management volume, roughness, diplophonia and reduced cough.22,23
These symptoms result directly from incomplete glottal
Patient management for UVFP commences at the first
closure and differential pliability between the paralysed
recognition of nerve injury. When this occurs in the
vocal fold and the contralateral normal vocal fold. The
intraoperative setting, the immediate postoperative
phonetogram can also provide valuable data on vocal range
management is critical. Speech therapy review is required the
and loudness for statistical analysis.
day after surgery and the patient is maintained nil by mouth
Self-rated tools used include the Voice Handicap Index
overnight until review. Therapy is aimed at minimising
(VHI), a shortened version VHI-1024, and voice-related
aspiration and maximising glottic closure. A  modified
quality of life.25 These are valuable in assessing the patient’s
barium swallow or bedside functional endoscopic
perceived response to therapy or surgical intervention.
evaluation of swallowing may be beneficial in assessing for
Voice therapy also aims to reverse compensatory behaviour,
aspiration. Oral intake is slowly reintroduced under strict
with most studies suggesting 4–6 weeks as a minimum
observation of speech therapy. Should aspiration be a risk
requirement.26,27 Unfortunately, despite the best efforts of
despite swallowing exercises and protective techniques, then
a highly competent speech therapist, there are patients who
other feeding options may be implemented (nasogastric
simply cannot make appropriate improvements in their
feeding tube, percutaneous endoscopic gastrostomy tube).
voice over time and regular review with ENT can enable
In the operative setting of multiple lower CN resection,
consideration for a temporary awake injection laryngoplasty.
severe dysphagia can result. Fortunately, in the majority of
cases normal per oral intake is resumed quickly as the more Immediate injection laryngoplasty
common nerve deficit is isolated to the vagal nerve or RLN.
Aside from the potentially serious dysphagia with UVFP, In the immediate setting following onset of a UVFP, a simple
dysphonia from such an injury can also have a dramatic temporary augmentation procedure can be invaluable.
impact. Losing complete glottal closure can cause a range In  2005 the author began using hyaluronic acid (HA)
of voice outcomes from mild dysphonia (partial glottal injection laryngoplasty in the awake, clinic setting with the
competence), where the voice approaches the pre-injury patient unsedated for immediate post-paralysis management.
voice but lacks volume and stamina, to the paralysed This 10-minute technique has become very popular because
vocal cord lying lateral with the arytenoid anteriorly and of its simplicity, low cost and convenience for both patient and
inferiorly displaced. With a significant true cord height and surgeon, and for providing immediate glottal closure.
length mismatch, the large glottal gap on phonation causes The key points to consider for this injection are
severe dysphonia if not aphonia. the route of delivery (Figure 6.3) and the duration of

Speech therapy
Behavioural voice therapy as standalone therapy or in
conjunction with surgical intervention can be highly
valuable in the setting of mild to moderate dysphonia from
UVFP. It is preferable in the setting of a larger glottal gap
and breathy voice to combine therapy with early injection
laryngoplasty rather than rely on months of therapy alone
to slowly improve voice quality. Such combined early
intervention provides far quicker return to optimal voice
function and rapid return to work or social activities along Figure 6.3 A transoral laryngeal injection device with a disposable
with reduced respiratory morbidity.19,20 25-gauge needle. Medtronic orotracheal injector.

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 Vocal fold paralysis

desired augmentation. Critical to both these points is the is of temporary effect and low tissue reactivity, but it lacks
composition of the substance used. The ideal substance has the enzymatic ability to dissolve a suboptimal injection.
low viscosity for minimal resistance through the injection Temporary injection will allow the patient to complete
device, inert or extremely low tissue reactivity, predictable at least a 6 month ‘wait and see’ period while having an
duration of effect, can be easily removed in a suboptimal optimal voice and minimising aspiration by maximising
placement injection and has a reasonable cost. Extreme glottal competency. Should longer than 6 months be desired,
care must be taken for any permanent substance injected, a repeat injection can by employed. If there is complete
as the author not infrequently removes permanent silicone nerve recovery, the HA or carboxymethylcellulose gel will
paste injected in tertiary referral patients. In these cases, the completely dissolve and an entirely normal paraglottic
injection was perceived as ‘straightforward’ but resulted in soft tissue contour will return. Should there be inadequate
poor voice outcome as there was gross overfilling on the recovery of nerve function, then the patient can proceed
subcordal space. to a formal reconstruction after allowing sufficient time for
Paraffin was the first recorded substance used 28 and the temporary gel to have dissolved entirely and allowing
highlighted many shortcomings of the ideal component. the contour of the paraglottic soft tissue region to stabilise.
Paraffin was difficult to inject due to increased resistance, Other substances that have been described for use in the
required a large gauge needle and required general temporary setting include, but are not limited to, Gelfoam,
anaesthetic with a significant paraglottic soft tissue reconstituted dermis and collagen. Such products can
reaction resulting in granuloma formation. Teflon was the be technically time-consuming to prepare, require pre-
next widely used substance29, with similar issues, the most injection allergy testing, have substantial cost or lack suitable
significant being uncontrollable granuloma formation viscosity for simple injection in the awake, unsedated clinic
replacing the entire paraglottic soft tissue region with patient, so are discouraged.
a non-pliable and undulating mass. The removal of The injection is performed as an awake, unsedated
both these substance was extremely difficult. The use of clinic procedure with either a transoral or a transcervical
silicone is currently creating similar problems (multiple approach. Both routes require a simple set-up present in
communications with collaborating laryngologists). most ENT clinics and can be performed without an assistant
The substance most suited to temporary injection is HA (an assistant does simplify the procedure). The route for
gel. It is essentially inert, has low viscosity and a predictable delivery of the gel varies with patient and surgeon. Limited
duration of effect. Should the gel be placed in a suboptimal gagging and adequate oropharyngeal space suit a transoral
location, the enzyme hyaluronidase may be injected to injection while a competent assistant, relatively thin neck
dissolve the HA as a subsequent awake clinic procedure. and adequate nasal space may suit a flexible nasendoscopy
The author prefers HA for the above listed reasons. Using with transcutaneous approach.
a high-cross linked form of HA can increase the duration
of effect, but the corresponding high viscosity increases Transoral injection laryngoplasty
resistance during transoral injection.The expected duration This is the author’s preference due to clarity and resolution
of effect for various commercially available HA gels are of the image from a rigid 70-degree telescope coupled to a
listed in Table 6.5. Another product that has gained high definition camera and monitor. In addition, with the
popularity is a carboxymethylcellulose gel. Like HA, this gel patient providing traction of their own tongue, there is no

Table 6.5  Properties of various substances used for paraglottic injection

laryngoplasty
Substance Base material Duration of effect Ease of use
Restylane Hyaluronic acid 3 months Easy
Perlane Hyaluronic acid 4–6 months Easy
Juvaderm Hyaluronic acid 4–6 months Easy
SubQ Hyaluronic acid 12–18 months Moderate
Radiesse Voice Carboxymethylcellulose 3 months Easy
Vox Silicone Permanent Moderate
Bioplastique Silicone Permanent Moderate
Cymetra Collagen 3 months Moderate

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 Treatment

Figure 6.4 The technique of performing a transoral injection

laryngoplasty with the patient stabilising his tongue and the
surgeon using the non-dominant hand for the 70-degree rigid
telescope and the dominant hand for the orotracheal injector.

need for an assistant as the surgeon has the rigid telescope in

one hand and the orolaryngeal injection device in the other
while observing the monitor (Figure 6.4). Figure 6.5 The needle must be precisely placed in the paraglottic
The key to a successful injection with this route is patient space with at least 3 mm of shaft on view. If the hub is flush down on
education and adequate topical anaesthesia.After a thorough the superior vocal fold surface, then the needle tip is too far caudal
explanation of the procedure, anaesthesia is applied as and results in an overfilled subglottis and inadequate glottal closure.
a topical spray of 10% lidocaine to the anterior tongue,
tongue base, pharyngeal wall, tonsil region and soft palate. After minor overinjection, the patient is asked to cough
Subsequently, 1–2 ml of 4% lidocaine is atomised over the numerous times and to phonate. This redistributes the gel
tongue base, vallecula, epiglottis and glottis. Finally 1–2 ml to some degree and immediate stroboscopy is used to assess
of 4% lidocaine is dripped directly onto the phonating for adequate glottal competency. Further gel is placed if
glottis through the orolaryngeal injection cannula. Five necessary and then the patient is maintained nil by mouth
minutes are allowed to pass for full anaesthesia. The patient for 2 hours.
provides tongue stabilisation/traction with a 10 × 10 cm
gauze. The telescope is introduced over the lateral tongue Transcervical injection laryngoplasty
base with care being taken to minimise depression of the This approach uses either the cricothyroid space, thyroid
tongue with any instruments. The orolaryngeal injection notch or lateral thyroid lamina to place the needle for
cannula is placed transorally under direct vision until the paraglottic injection. Use of the cricothyroid space is
needle tip becomes visible on the monitor. The surgeon ideally performed similar to botulinum toxin injections,
uses the monitor for the remainder of the procedure. with the needle maintained submucosal for the entire
The first point of injection is immediately lateral and procedure (Figure 6.6a). This obviates the need for
anterior to the affected arytenoid, with enough injection extensive topical mucosal anaesthesia, aside from that
to cause adequate medialisation. It is not expected that the required to view the larynx. In using the lateral thyroid
arytenoid cartilage will fully medialise.The second injection lamina approach, the needle is also maintained submucosal,
point is lateral to the mid-musculomembranous vocal fold. being advanced through the lateral thyroid lamina at the
The needle tip must not be too caudal, as this overfills the level of the paraglottic space. The needle is moved so the
subcordal region and compromises the augmentation. tip briefly displaces the paralysed cord medially, enabling
Knowing the length of the exposed needle shaft enables the the surgeon to verify the exact location for the injection.
surgeon to accurately estimate the depth of the needle tip This ensures that the vertical level of the injection is ideal
for optimal placement of the gel (Figure 6.5). Gagging has for medialisation.This is usually not suitable in patients over
not been a significant issue with patients with this approach. 40 years of age due to increasing calcification of the lower
A chart review of 76 consecutive patients undergoing portion of the thyroid lamina making passage of the needle
injection laryngoplasty by the author at the Queensland impossible.
Centre for Otolaryngology & Voice showed failure to The thyroid notch approach requires extensive mucosal
complete the injection due to gagging was 2.6% (2 patients). anaesthesia similar to the transoral approach, as the needle

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 Vocal fold paralysis

a   b
Figures 6.6a, b (a) Cricothyroid injection showing the needle entering the cricothyroid space and angling approximately 30 degrees
superior and lateral. Maintaining the needle submucosal for this approach limits patient reactivity from local mucosal irritation and can
minimise the need for topical laryngeal anaesthesia. (b) Thyrohyoid injection with the needle entering the skin at the thyroid notch. It then
angles sharply inferiorly to achieve a suitable angle for the injection.

Permanent reconstructive procedures fall into three main

categories: medialisation laryngoplasty (paraglottic soft
tissue is medialised by an implant placed through the thyroid
lamina from an external approach); injection laryngoplasty
(where paraglottic space augmentation is undertaken by
injection); and arytenoid procedures (arytenoid adduction
Figure 6.7 A needle with two bends each at 45 degrees optimises [AA] or adduction arytenopexy [ADA]). Choosing the
access to the paraglottic space.
technique for reconstruction depends on patient and
passes over the thyroid notch and then enters the lumen surgeon factors.
through the petiole of the epiglottis (Figure 6.6b). It is
then directly visualised as it enters the same injection points Medialisation laryngoplasty (Isshiki thyroplasty
of the paraglottic space as listed for the transoral approach. type 1)
To enhance the ease of a thyroid notch injection, two bends All forms of implant essentially achieve the same goal of
are placed in the needle (Figure 6.7).30 soft tissue medialisation through an external approach. The
With either technique the patient is made aware that ideal setting for this is a mostly medial arytenoid position,
it requires approximately 1–2 weeks for the gel to fully accessible thyroid cartilage for window placement, adequate
redistribute and the voice to settle. At that point speech cessation from anticoagulants, reasonable neck extension,
therapy can commence.The author prefers monthly patient patient tolerance to local anaesthetic with sedation and
review to assess for symptom resolution and signs of nerve surgeon competency. Depending on the surgeon’s training,
recovery. various implant materials will have been encountered
including Gore-Tex, silastic, Montgomery® Thyroplasty,
Long-term management titanium and VoCoM. Each substance has perceived, or real,
Long-term management of UVFP in surgical terms is pros and cons, so individual training and experience tends
synonymous with formal reconstruction. As such, it is not to dictate choice. The author’s preference is Gore-Tex, as
necessarily delayed 6–12 months before intervention, but it is easy and rapid to insert and mould to provide optimal
rather at the time point where no nerve recovery is expected medialisation. The window is not millimetre critical as
but full denervation has occurred. This may be 12 months the Gore-Tex is directed by a small probe to the optimal
for an idiopathic paralysis or as early as 2 months following location within the paraglottic space. It can be removed or
a known nerve transection. At least 2 months is required for revised with minimal effort and is free from tissue reactivity.
the denervated paraglottic muscles to lose tone and bulk Silastic implants require repeated intraoperative
and become a stable soft tissue mass. Speech therapy in this placement and removal from the thyroid window while the
setting is similar to the short-term management for UVFP. block is carved down to suitable proportions, which can be

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 Treatment

time-consuming. The repeated trauma to the paraglottic lesion can cause severe dysphonia and therefore necessitate
soft tissues creates oedema, which can artificially improve microlaryngoscopy and removal. Hydroxylapatite is a safe
the glottal closure during the surgery. Once the oedema and easily injected substance but again may require surgical
resolves postoperatively, the glottal closure may be removal if its placement overfills the subcordal region.31
incomplete. The Montgomery® Thyroplasty kit is basic Teflon requires nothing other than a historical mention as
and entirely preformed so is unable to be easily modified it is well and truly out of use. It typically created cement-
should there be anatomical constraints. In addition, the type highly uneven granulomas, often worsening the voice,
window is required to be critically placed  as this is the and patients still present today at times to an ENT clinic
sole determinant of where the implant will sit. There are requiring removal. The author utilises the Netterville
anatomical variants not suited to this kit but this would lateral thyroid lamina flap for this removal, performing a
only be realised intraoperatively after the window was microscopic submucosal resection followed by delayed
placed. The author has revised a tertiary referral case Gore-Tex augmentation.32
recently of such an implant that was carefully measured
and placed yet was entirely located in the false cord. Arytenoid repositioning
Titanium implants are relatively new and seem to be Consideration of the immobile arytenoid is critical
well tolerated. Some bending of the implant is required is providing optimal voice restoration. Along with a
to achieve suitable augmentation. The VoCoM system is medialisation laryngoplasty, combining an arytenoid
similar to a Montgomery® implant but lacks the anterior- repositioning procedure may be necessary. For example,
posterior expanse of the latter and is a more vertically consider a patient with a self-rated voice being normal at
placed implant. As such, achieving a uniform medialisation 10/10 pre-paralysis that was reduced to 2/10 from a lateral
along the length of the true cord is not ideal. In essence, lying UVFP. With a simple medialisation, the voice may
the ideal implant is easily adjusted once placed while achieve a 6 or 7/10 and both patient and surgeon can feel
having the patient regularly phonate intraoperatively. This there has been reasonable voice restoration. However, by
allows the most precision in medialisation laryngoplasty. relocating the arytenoid to the posterior-medial position
From a technical aspect, for all implants the patient on the cricoid facet, there is optimal posterior glottal
should receive pre-operative steroids and antibiotics and be competency and the voice can be substantially improved
initially sedated for skin preparation, draping and placement to an 8 or 9/10. In light of this example, surgeons should
of local anaesthetic. Following this, flexible nasendoscopy be aiming for far higher than a 6/10 for their patients and
is performed to confirm the side of the paralysis. When the arytenoid repositioning can provide this. Multiple studies
surgeon is ready to place the implant, the sedation should be have confirmed that an arytenoid repositioning procedure
reversed so the patient is entirely coherent and cooperative. gives a significantly improved voice outcome over simple
This will allow various vocal tasks to direct the surgeon’s medialisation laryngoplasty.33–35 When the immobile
precise placement of the implant for optimal medialisation. arytenoid lies more than 2  mm from the midline with
inadequate overclosure from the contralateral side, it is
Permanent injection laryngoplasty the author’s opinion that an arytenoid procedure should
As with medialisation laryngoplasty, the concept of be planned. The final decision requires careful patient
permanent injection laryngoplasty is similar in that the assessment to ensure the contralateral arytenoid has
goal is uniform medialisation of the paralysed unilateral adequate abduction. When the immobile arytenoid is
vocal fold. The substance used can vary with surgeon medialised, the glottis can be too narrowed and result
preference. Commonly used substances are autologous fat, in increased respiratory effort if the mobile arytenoid
silicone paste, calcium hydroxylapatite and the historical does not adequately abduct with inspiration. In addition,
Teflon paste. All have undesirable properties, which make significant dysphagia may suggest an arytenoid procedure
injection laryngoplasty less precise in achieving an ideal and is not suitable, as swallowing difficulties may worsen with
reliable medialisation. Autologous fat requires significant the dissection to access the CAJ. Having performed over
preparation time for the graft, has a variable absorption rate, 50 ADA procedures, the author has not observed any
requires general anaesthetic and a large bore needle and can deterioration in swallowing post procedure.
have lipomatous calcification formation. There is also an Which arytenoid procedure is ideal? The landmark paper
intense initial inflammatory reaction creating oedema and of Isshiki in 197836 described the first arytenoid repositioning
a very strained voice for approximately 1 month following procedure. In the AA procedure, a suture was placed through
the injection. Silicone paste is permanent and causes a giant the muscular process to simulate the lateral cricoarytenoid
cell foreign body reaction.A suboptimal injection overfilling muscle pull, thereby rotating the vocal process medially and
the subcordal region or a delayed silicone granulomatous somewhat posteriorly. This gave significant improvement to

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 Vocal fold paralysis

posterior glottal closure for paralysis presenting with a lateral The less than widespread adoption of the ADA procedure
arytenoid. In 1999 Zeitels37 described a unique procedure, since its inception  is most likely because of its perceived
the ADA (Figures 6.8a, b). There was an anatomical and difficulty. Having discussed this notion with many leading
physiological improvement from Isshiki’s procedure where laryngologists who prefer the AA technique, the universal
the arytenoid was relocated medially and posteriorly on the feeling is that ADA is technically more difficult. This,
cricoid facet, not simply rotated in its paralysed location. together with the limited laryngology fellowships where
The arytenoid relocation places it in the normal anatomical ADA is taught, will continue to limit its wider acceptance
position for phonation. It also re-establishes the physiological as a viable alternative to the AA procedure. It has been
location for optimal length and tension in the true cord the author’s experience that the AA procedure is actually
during connected speech while in addition, normalising the technically more challenging than the ADA. Given the
arytenoid height. In the lateral immobile arytenoid, the height limited descriptions of the ADA, a short summary will follow.
is significantly lower than the neurologically intact side and For a successful ADA the inferior constrictor is detached
correcting this with the ADA is also a key reason for maximal from the thyroid lamina, the cricothyroid joint disarticulated,
voice restoration. Similarly to AA procedure papers, ADA the superior thyroid ligament divided and the posterior
papers show improvements in phonation when compared ‘free’ edge of the thyroid lamina retracted anteriorly. The
with simple medialisation procedures alone. However, pyriform mucosa is identified and swept cephalad. Inferior
an important addition to the ADA is the cricothyroid to this, the posterior cricoarytenoid muscle (PCA) is
subluxation suture. This is placed from the inferior thyroid identified and followed cephalad to its insertion into the
cornu to the anterior cricoid region to simulate the pull of arytenoid. Palpation with the tip of tenotomy scissors over
the cricothyroid muscle.After appropriate tension is achieved the PCA muscle near the CAJ can identify the joint line.
intraoperatively, voice outcomes can be near normal for The PCA is then divided at the CAJ and the joint entered
patients by adding this suture placement to the ADA. sharply. After division of the posterior joint capsule fibres,
The author has performed both AA and ADA procedures the body of the arytenoid is then sutured posteromedial
and has a strong preference for ADA. It seems more onto the cricoid facet. Its location can be confirmed as
logical to relocate a displaced and immobile arytenoid ideal when there is substantial lateral cricoid facet exposed,
into its most anatomical position for phonation (ADA) indicating that the arytenoid is lying in the most medial
than rotate it medially from its paralysed position (AA). position.

a   b
Figures 6.8a, b Adduction arytenopexy. (a) After precise postero-medial placement with the adduction arytenopexy, there should be
a large lateral aspect of the cricoid facet exposed. This ensures adequate medial placement of the arytenoid body. (b) The placement of
the suture in an adduction arytenopexy is critical in fixing the arytenoid in its most anatomical position for phonation. The height and
length mismatch is corrected with this arytenoid mobilisation procedure.

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 Treatment

Bilateral vocal fold paralysis in a caudal direction, entering the superior aspect of the
vocal process and then exiting through the inferior aspect
Bilateral medialisation laryngoplasty of the vocal process into  the lumen. Once this is placed,
On rare occasions the ENT surgeon will encounter the needle is removed leaving the non-absorbable suture
bilateral VFP. When there is glottal incompetency, a in situ. Following this, the two free ends of the suture are
bilateral medialisation procedure can be undertaken with fed through two 18 guage needle tips that have been passed
care. This can be either as an injection laryngoplasty or transcutaneously through the thyroid cartialge to enter
as external medialisation laryngoplasty. In either setting the glottis immediately above and below the vocal process
the procedure should never be performed under general (Figures 6.9a, b). The suture is passed externally through
anaesthesia, minimising any risk of overcorrection and the needles and tied over the thyroid lamina with the aid
compromising the glottic airway. The author prefers Gore- of a  cutaneous stab incision, approximately 3–4 mm in
Tex for this procedure for its ease of placement and precision length, superficial  to the thyroid lamina.  By viewing the
in gaining adequate posterior placement adjacent to the glottis under microscopy, appropriate tension is generated
arytenoid. There is a shorter operative time than sculpting on  the suture and adequate improvement in the glottal
bilateral silastic implants and less paraglottic trauma than airway is achieved with gentle lateralisation of the arytenoid
placement of bilateral Montgomery® Thyroplasty implants. (Figure  6.9c).  At any point in the postoperative period,
Perioperative steroids and close airway observation in the should there be nerve recovery, the suture can be removed
postoperative setting are critical. under local anaesthetic and voice can normalise.
Airway interventions in bilateral vocal fold paralysis
In the setting of bilateral VFP, where the arytenoids are Reinnervation
closely approximated and there is airway compromise, A detailed discussion of reinnervation is beyond the
intervention is usually necessary. If nerve recovery is scope of this chapter so a brief summary is provided. Very
possible, then irreversible or destructive procedures should few centres around the world undertake reinnervation
be avoided. A simple tracheostomy can be suitable but is procedures, so these techniques are not essential to the
associated with the difficulties of managing a tracheostomy practising laryngologist or ENT surgeon but an awareness
while waiting for potential nerve recovery, and may be is useful. Techniques include ansa cervicalis or hypoglossal
undesirable for many patients due to its morbidity. Laser nerve to RLN anastomosis for a UVFP, which can be
cordotomy is frequently implemented but is moderately performed with a temporary medialisation procedure to
destructive to the delicate layered microstructure of the reduce the glottal incompetency while the reinnervation
vocal fold, causing permanent scar and hoarseness, so should establishes activity. An advancement on these techniques
be discouraged. A suitable short-term option to widen is the phrenic nerve root technique described by
the glottal narrowing can be a lateralisation suture placed Marie et al.39 This is a very thoughtful concept where the
similarly to the description by Kirchner.38 The author’s C5 nerve root is joined to the PCA muscles bilaterally
modification of this involves passing a 3/0 Prolene suture with an interposition free graft to establish selective
on a small needle endoscopically. The suture is passed abduction. The perceived benefits of reinnervation

a   b   c
Figures 6.9a–c Suture lateralisation to improve airway in bilateral VPF. A suture is passed through the vocal process (a) and then the
sutures at the entry and exit points are passed directly into the needles’ lumens (b) and directed laterally through the thyroid lamina
and secured over its lateral surface. (c) With careful increase in tension the arytenoid body moves laterally, opening the glottic airway
to a suitable size, and then the suture is tied securely. The arrow indicates the site of maximal lateralisation; note that the suture lies
submucosal so is not visible.

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 Vocal fold paralysis

procedures are the restoration of muscle tone and bulk to limited training and requirement for identification of
the paraglottic muscles, but purposeful movement is not the fine motor branches of the RLN. Further research
the rule unless utilising selective reinnervation techniques. in this area, including reinnervation of abductor muscles
Reinnervation potentially restores the viscoelastic and the cricothyroid muscles, is critical for successful
symmetry of the glottis, which is not restored with static laryngeal transplantation. A future option will be pacing
medialisation procedures. The downsides of reinnervation of the paralysed muscles by a signal from the contralateral
include the cost, the delay before benefit may be realised, neurologically intact intrinsic laryngeal muscles.

Summary
VFP causes glottal incompetence with varying degrees commonly being performed providing immediate glottal
of dysphonia and dysphagia/aspiration. Minimising the competency and dramatic symptom resolution. In long-
impact of a paralysis on the patient by providing temporary term management for these patients, simple medialisation
or permanent glottal closure significantly improves quality may inadequately close the posterior glottis in many,
of life and productivity. There is certainly a paradigm so  arytenoid medialising procedures can provide optimal
shift with a range of simple clinic injection techniques glottal competency.

References
1 Isshiki N, Tanabe M (1978) Arytenoid adduction 11 Paulsen FP, Jungman K, Tillmann BN (2000) The
for unilateral vocal cord paralysis. Arch Otolaryngol cricoarytenoid joint capsule and its relevance to
104:555–558. endotracheal intubation. Anesth Analg 90:180–185.
2 Zeitels SM (1999) Adduction arytenopexy with 12 Netterville JL, Stone RE, Luken ES et al. (1993)
medialization laryngoplasty and cricothyroid Silastic medialization and arytenoid adduction: the
subluxation: a new approach to paralytic dysphonia. Vanderbilt experience. A review of 116 phonosurgical
Oper Tech Otolaryngol Head Neck Surg 10:9–16. procedures. Ann Otol Rhinol Laryngol 102(6):413–424.
3 Zeitels SM, Hillman RE (1999) Cricothyroid 13 Koufman JA, Postma GN, Cummins NM (2000)
subluxation for enhancing laryngoplastic phonosurgery. Vocal  fold paresis. Otolaryngol Head Neck Surg 122:
Ann Otol Rhinol Laryngol 108:1126–1131. 537–541.
4 Cunning DS (1955) Unilateral vocal fold paralysis. 14 Woodson GE (1993) Configuration of the glottis in
Ann Otol Rhinol Laryngol 64:47–494. laryngeal paralysis. Clinical study. Laryngoscope 103:
5 Terris DJ, Arnstein DP, Nguyen HH (1992) 1227–1234.
Contemporary evaluation of unilateral vocal fold 15 Koufman JA, Walker FO, Joharji GM (1995) The
paralysis. Otolaryngol Head Neck Surg 107:84–90. cricothyroid muscle does not influence vocal fold
6 Ramadan HH, Wax MK, Avery S (1998) Outcome position in laryngeal paralysis. Laryngoscope 105: 369–372.
and changing cores of unilateral vocal fold paralysis. 16 Benninger MS, Crumley RL, Ford CN (1994)
Otolaryngol Head Neck Surg 118:199–202. Evaluation and treatment of the unilateral paralysed
7 Loughran S, Alves C, McGregor FB (2002) Current vocal fold. Otolarngol Head Neck Surg 111:497–508.
aetiology of unilateral vocal fold paralysis in a teaching 17 Terris DJ, Arnstein DP, Nguyen HH (1992)
hospital in the West of Scotland. J Laryngol Otol Contemporary evaluation of unilateral vocal cord
116:97–910. paralysis. Otolaryngol Head Neck Surg 107(1):84–90.
8 Havas T, Lowinger D, Priestley J (1999) Unilateral 18 Sulica L, Blitzer A (2006) (eds.) Vocal Fold Paralysis.
vocal fold paralysis – causes, options and outcomes. Springer, Berlin, Heidelberg.
Aust N Z J Surg 69:509–513. 19 Friedman AD, Burns JA, Heaton JT et al. (2010) Early
9 Netterville JL, Civantos FJ (1993) Rehabilitation of versus late injection medialization for unilateral vocal
cranial nerve deficits after neurotologic skull base surgery. cord paralysis. Laryngoscope 120(10):2042–2046.
Laryngoscope 103(11 Pt 2 Suppl 60): 45–54. 20 Arviso LC, Johns MM 3rd, Mathison CC et al. (2010)
10 Sariego J (2010) Vocal fold hypomobility secondary to Long-term outcomes of injection laryngoplasty in
elective endotracheal intubation: a general surgeon’s patients with potentially recoverable vocal fold paralysis.
perspective. J Voice 24(1):110–112. Laryngoscope 120(11):2237–2240.

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 References

21 Hirano M (1981) Clinical Examination of Voice. Springer, injection of calcium hydroxylapatite. Laryngoscope
Berlin, Heidelberg, New York. 118(12):2260–2263.
22 Boone DR, MacFarlane S (1988) The Voice and Voice 32 Netterville JL, Coleman JR. Jnr, Chang S et al.
Therapy. Prentiss-Hall, Englewood Cliffs. (1998) Lateral laryngotomy for the removal of Teflon
23 Schneider B, Schickinger-Fischer B, Zumbotel M et al. granuloma. Ann Otol Rhinol Laryngol 107(9 Pt 1):
(2003) Concept for diagnosis and therapy of unilateral, 735–744.
recurrent laryngeal nerve paralysis following thoracic 33 Woo P, Pearl AW, Hsiung MW et al. (2001)
surgery. Thorac Cardiovasc Surg 51:327–331. Failed medialization laryngoplasty: management
24 Rosen CA, Lee AS, Osborne J et al. (2004) by revision  surgery. Otolaryngol Head Neck Surg
Development and validation of the voice handicap 124(6):615–621.
index-10. Laryngoscope 114(9):1549–1556. 34 Green DC, Berke GS, Ward PH (1991) Vocal fold
25 Hogikyan ND, Sethuraman G (1999) Validation of an medialization by surgical augmentation versus
instrument to measure voice-related quality of life. arytenoid adduction in the in-vivo canine model. Ann
J Voice 13:557–569. Otol Rhinol Laryngol 100(4 Pt 1):280–287.
26 Roy N, Gray SD, Simon M et al. (2001) An evaluation 35 Noordzij JP, Perrault DF, Woo P (1998) Biomechanics
of the effects of two treatment approaches for teachers of combined arytenoid adduction and medialization
with voice disorders: a prospective randomised clinic laryngoplasty in an ex-vivo canine model. Otolaryngol
trial. J Speech Lang Hear Res 44: 286–296. Head Neck Surg 119(6):634–642.
27 Sabol JW, Lee L, Stemple JC (1995) The value of vocal 36 Isshiki N, Tanabe M, Sawada M (1978) Arytenoid
function exercises in the practice regimen of singers. adduction for unilateral vocal cord paralysis.
J Voice 9:27–36. Arch Otolaryngol 104(10):555–558.
28 Brunings W (1911) Uber eine meue bahndlungs – 37 Zeitels SM, Hochman I, Hillman RE (1998) Adduction
Methode der Rekurrens Lihmung. Vehr dtsch Laryngol arytenopexy: a new procedure for paralytic dysphonia
18:93–151. with implications for implant medialization. Ann Otol
29 Lewy RB (1963) Glottic reformation with voice Rhinol Laryngol 173(Suppl):2–24.
rehabilitation in vocal cord paralysis. The injection of 38 Kirchner FR (1979) Endoscopic lateralization of
Teflon and Tantalum. Laryngoscope 73:547–555. the vocal cord in abductor paralysis of the larynx.
30 Achkar J, Song P, Andrus J et al. (2012) Double-bend Laryngoscope 89(11):1779–1783.
needle modification for transthyrohyoid vocal fold 39 Marina MB, Marie JP, Birchall MA (2011) Laryngeal
injection. Laryngoscope 122(4):865–867. reinnervation for bilateral vocal fold paralysis. Curr
31 Chheda NN, Rosen CA, Belafsky PC et al. (2008) Opin Otolaryngol Head Neck Surg 19(6):434–438.
Revision laryngeal surgery for the suboptimal

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 CHAPTER 7

Principles of speech and language therapy

Christella Antoni

Introduction
This chapter will describe the practical aspects of working in voice difficulties will be described, including vocal fold
the field of voice as a specialist speech and language therapist nodules, safe loud voicing and restoration of singing voice.
(SLT). It will outline voice work as a clinical SLT specialism There is no set therapy exercise(s) that will work for every
and the scope of practice. Referral to speech and language patient.The majority of clinicians have gathered, adapted or
therapy and the SLT’s scope of practice will be addressed. developed an eclectic mix of exercises in their therapeutic
Methods of voice assessment, analysis and evaluation will repertoire, which they select from on a case by case basis.
not be discussed as there are dedicated chapters on these Several valuable therapy texts and chapters list a plethora
aspects within this text. Reference to organic and non- of exercises for the treatment or development of voice.They
organic voice disorders will be included with particular are usually organised in sections that relate to the basic
reference to muscle tension dysphonia and psychogenic voice parameters such as breath, posture, onset of the note,
dysphonia and aphonia. Aspects of one-to-one voice resonance, pitch, volume and articulation. The skill of the
therapy versus group therapy are outlined in Appendix 7.1 clinician, however, lies in gaining the trust of the patient
at the end of this chapter. and in selecting appropriate exercises and techniques that
More specifically, aims of therapy and stages of the will treat the presenting difficulty as successfully as possible,
therapeutic process will be discussed. Vocal hygiene and according to the ability of each individual patient.
the advantages of individual and group therapy sessions are Modelling exercises to patients and providing feedback
listed as separate Appendices at the end of the chapter. The and assistance following their own efforts aids secure
main focus of this chapter will be selected therapy practice experiential learning for the patient. Further, establishing
and techniques that take place in a one-to-one therapy a sustained rapport and actively engaging patients in the
setting. Therapy approaches that are applicable to a variety treatment and carryover of the therapy into habitual
of voice disorders will be included. Particular exercises voicing is vital to achieve successful long-term treatment
that target remediation of specific laryngeal pathology and outcomes.

Referral to speech and language therapy

Dysphonic patients require an ENT assessment prior to are not always apparent on first view.This is illustrated in the
referral to speech and language therapy. Referring doctors two laryngoscopic images shown (Figures 7.1a, b).
vary in the amount of information they provide on the
referral form. Diagrams of the vocal folds indicating the site Clinical voice specialism
of any lesions or pathology are useful for clinicians, as well A wide range of SLTs may offer voice therapy to clients
as information regarding any asymmetry of the vocal folds who have some type of voice difficulty. This can include
and any impairment to function or structure observable SLTs who work with the hearing impaired, learning
with laryngeal endoscopy. The author’s clinical practice disabled, individuals with progressive neurological
experience is that specialist voice clinics tend to provide more disorders or children with cleft palate. In the latter client
detailed and more accurate findings than those  following groups, a laryngeal examination and formal diagnosis of
nasendoscopic examinations, which take place in a busy a voice disorder has usually not taken place and the voice
general ENT clinic. This is most likely due to the greater impairment is part of a much wider condition.
use of rigid endoscopy in voice clinics and the longer time SLTs who specialise in clinical voice work generally have
allocation to see patients. Similar findings were reported by at least 2 years post-qualification experience before working
Phillips et al.1 Pathology such as subtle vocal fold swellings in the field of voice. While a voice component is part of all

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 Principles of speech and language therapy

a b
Figures 7.1a, b An apparently ‘normal’ view of the vocal folds (a). A closer view with subtle small nodules evident (b). (From Thomas JP
(2012) Why is There A Frog in My Throat? A Guide to Hoarseness. James P. Thomas, Portland, with permission.)

formal undergraduate and postgraduate SLT training, there Voice disordered patients emanate from a wide and varied
is no specific training for SLTs to become voice specialists. cross-section of society including non-professional voice
The clinical skill of each SLT is obtained over time, generally users. However, professional voice users such as teachers,
by working alongside more experienced colleagues and by actors, broadcasters and singers can form a significant
attending postgraduate voice courses and workshops. SLTs part of the clinician’s caseload. The extent to which the
who work in a hospital or clinical setting where there is a therapist works with the acting or singing voice, beyond
dedicated voice unit will benefit from close collaborative initial remedial work, depends on the clinician’s confidence,
working with ENT and have better access to visualisations expertise and work setting. Private practice allows more
of the larynx. scope for this for suitably experienced clinicians. With
Although there are very few courses that offer publicly funded services, resource constraints tend to limit
experiential voice work, clinicians who take the time to the clinician in offering extended voice development work
work on their own voice and to experience the ways the and caseloads need to be prioritised according to provision
vocal mechanism can be adapted to facilitate voice change of services. In many cases, once no laryngeal pathology
will most likely be the more skilled clinicians when it comes or significant psychogenic overlay or muscle tension
to applying theoretical knowledge. dysphonia is present, a referral to a voice teacher/vocal
It is common for SLTs to work in posts that combine coach is indicated.
voice and head and neck cancer, although specialist Voice teachers work with the spoken voice of many
dedicated voice posts also exist. It is also not unusual for professional voice users to help develop power and improve
voice specialist SLTs to have a background or strong interest quality and vocal confidence. Their work with actors
in singing, acting or performance work and/or psychology includes interpretation of text and presence on stage.
and counselling therapies. There is no other field in speech As there is currently no professional or regulating body for
and language therapy that allows for such a merger of voice teachers, most voice specialist SLTs tend to gather a
science, art and emotion. list of names of experienced vocal coaches and singing
teachers to suggest to patients if they feel further work will
Scope of practice be of benefit to the patient. The British Laryngological
The clinical experience gained by the clinician, in Association (BLA) contains contact information for Voice
addition to their clinical background and work settings, teacher organisations in its resource section.The British Voice
tends to determine the range of clients seen. The bulk of Association and the  American Voice and Speech Trainers
voice disordered patients tend to be those with laryngeal Association also provide a list of voice teachers.
pathology and muscle tension dysphonias. As voice is Increasingly, voice conferences encourage delegates
closely linked to personality and emotions, clinicians from a wide voice field, in particular ENT surgeons,
develop skills in treating psychogenic voice and voice voice scientists and all voice practitioner groups (SLTs,
difficulty where anxiety and emotional aspects are strong vocal coaches and singing teachers). Other delegates may
influencing factors. include laryngeal osteopaths and professional and amateur

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 Referral to speech and language therapy

voice users. Opportunities to network and collaborate are psycho-emotional  aetiology. The alternative term of
plentiful. While there is scope for shared working between ‘muscle misuse voice disorders’ has been proposed.3
SLTs and vocal coaches with much voice development Muscle tension dysphonias describe a varied group of
work (where no laryngeal pathology is present), some client clinical profiles. Persistent voicing with abnormal laryngeal
groups fall more specifically under the medical model posture leads to a disturbance of vocal function that may
of treatment. In these cases, treatment is offered within a lead to organic changes. Further, these can be compounded
clinical setting such as the treatment of transgender voice. by psychogenic factors. An organic trigger such as an upper
Although it is a growing field, only a small proportion respiratory tract infection can also lead to, or influence,
of voice specialist SLTs work with transgender voice. These a muscle tension dysphonia.
therapists may form a part of the multidisciplinary team of Broadly speaking, muscle tension dysphonia is a term
the few Gender Identity Clinics that exist nationally. There often given to describe non-organic dysphonias where there
is huge geographical variation of SLT treatment availability are no structural abnormalities. Under this classification,
both nationally and internationally. Clinicians working in vocal behaviour or technique leads to vocal impairment.
this field require advanced voice therapy and interpersonal More specifically, it can relate to competing muscles
skills as well as a firm understanding of the psychiatric, and posterior phonatory gap. The lateral cricoarytenoid
surgical, endocrinological and psychological management muscle brings the vocal cords together, but if the posterior
of these individuals. cricoarytenoid muscle is tightened (typically it will appear
thicker), the vocal cords will be slightly pulled apart. Air will
Classification of voice disorders escape through the gap, reducing the vocal fold vibrations
Several extensive classifications of voice disorders necessary for a clear note, and a husky voice quality is
exist.2,3 They are broadly divided into organic versus heard instead. Usually this will become more apparent if
non-organic or structural versus behavioural disorders. the patient is asked to voice with less volume. A posterior
Structural dysphonias include those relating to congenital, phonatory gap will vary according to the effort the patient
neurological, inflammatory and endocrine conditions as employs, therefore the voice disturbance tends to be variable
well as trauma and tumours. (Figures 7.2a, b).4
Voice disorders that are unrelated to identifiable
organic disease are generally referred to as muscle tension Psychogenic dysphonia
dysphonia or ‘functional dysphonia’. However, the “The voice collects and translates your bad physical health,
‘functional dysphonia’ classification can be particularly your emotional worries, your personal troubles”. (Placido
problematic, particularly as the term psychogenic has at Domingo).
times been used interchangeably with the term ‘functional’. An overlap of presenting phonatory and laryngeal signs
‘Psychogenic’ diagnoses should be reserved for those and symptoms exists between muscle tension dysphonias
muscle misuse voice disorders that clearly have a primary and psychogenic dysphonias. However, there are often

a b
Figures 7.2a, b Contrasting appearance of relaxed posterior cricoarytenoid muscle and closed vocal folds (a) versus contracted posterior
cricoarytenoid muscle (and increased thickness of right posterior cricoarytenoid muscle) causing a posterior phonatory gap (b). (From
Thomas JP (2012) Why is There A Frog in My Throat? A Guide to Hoarseness. James P. Thomas, Portland, with permission.)

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 Principles of speech and language therapy

specific features pertaining to psychogenic dysphonia that Complete resolution of a long-standing psychogenic
help diagnosis.These may include: voice disorder generally requires the exploration and
addressing of psycho-emotional or psychosocial issues.
●● A significantly abnormal voice despite absence of
(A  comprehensive understanding and treatment approach
laryngeal pathology.
can be found in the text by Butcher, Elias & Cavalli.5)
●● Inconsistent voice – periods of normal voice and highly
dysphonic voice during the course of one session, which The voice clinic
may be context-specific.
Voice disordered patients may present initially in a joint
●● Laughing and crying may be normal in spite of
voice clinic (JVC), where both the surgeon and the SLT
dysphonia.
are present. The practice of joint decision making and
In pyschogenic dysphonia, normal vegetative functions treatment planning is common in the majority of specialist
are usually present. Although a normal cough can usually voice centres. Some clinics ask patients to complete a case
be elicited, typically patients only whisper or mouth their history form or voice questionnaire prior to their first clinic
words, although small squeaks of voice can sometimes be appointment. Gathering information in this way can save
heard. The loss of voice may be of sudden onset and there time, but the main drawback is that voice clinics tend to be
may be a history of frequent aphonic episodes. busy with only a limited time allocation per patient, which
In psychogenic dysphonia, the physical presentation of can make reviewing the material within clinic challenging.
the larynx can be varied. It can range from normal larynx In any event, questionnaires and self-evaluation forms are
to laryngeal pathology such as vocal nodules. Laryngeal not to be solely relied on in the clinic or in the therapy
constriction may be present as well as incomplete vocal process.
fold adduction or hyperadduction. With such varied The ability to review patients jointly is one of the most
presentations, perceptually, the voice can be rough, breathy, useful functions of the JVC. Clients who do not progress
strained or weak, or a combination of qualities. Some in therapy can be referred back for further assessment.
psychogenic voice patients can get locked into a falsetto In addition, at the early stages of therapy, the SLT may be
type voice and, not surprisingly, complain of excessive aware that the client’s voice difficulty does not correlate
dryness of the larynx due to the increase of breath coming perceptually with the original ENT diagnosis. In cases
through the vocal cords. where there is suspected laryngeal pathology in spite of a
The treatment of psychogenic dysphonia or aphonia NAD (nil abnormal detected) finding, further review in the
is generally less linear than the phases outlined above. voice clinic is indicated prior to continued therapy.
However, it can lead to some of voice therapy’s most “The role the speech therapist plays in the voice clinic
dramatic and privileged moments. Connecting a depends on experience, confidence and the working
person back to their voice in one session when perhaps relationship between the individual therapist and the voice
they have been voicing abnormally or not voicing for clinic surgeon. It would seem that the most effective clinics
a sustained period, sometimes extending to years, can are those where the therapist and surgeon have an equal
lead to a strong emotional awareness on the part of relationship”.6 As well as taking a case history and direct
the patient. The connection may come quickly and observation of the larynx, the presence of the SLT allows
through physical exercises alone – a general approach for more indirect aspects of the client’s presentation to
would be to work from a cough and to develop normal be noted: aspects such as breathing patterns, non-verbal
onset vowels. Once the vocal folds have come to vibrate communication, movement difficulties, signs of facial
normally, the new behaviour is often swiftly adopted by muscle weakness, tremor or rigidity, comprehension or
the patient. expressive language deficits, physical tension, emotional
However, when secondary gain on the part of the affect and tone of voice.
client is an issue, treatment generally takes longer. Many SLTs carry out flexible nasendoscopy in parallel
The term ‘Belle Indifference’ has also been ascribed to voice clinics and some therapists carry out laryngeal
psychogenic dysphonia. Patients in these cases tend to be endoscopy during voice therapy sessions to assess the
seemingly unconcerned regarding their voice difficulty, effects of therapy exercises. Demonstrating the nature of
in spite of the impact on their life. They may present as the problem to the patient and techniques that improve the
being somewhat disinterested in resolving their voice laryngeal posture can provide very useful visual feedback
difficulty. Patients may also profess extreme discomfort to patients. Moreover, the playback of acoustic voice
in the larynx yet be extremely talkative in spite of this recordings is vital in ensuring increased awareness levels in
and/or show varying degrees of resistance to carrying out patients who, more often than not, are surprised at what is
voice exercises. played back to them.

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 Aims of voice therapy

Aims of voice therapy

The general goal of voice therapy is to restore the best always individualised. However, certain aspects of therapy
voice possible, ‘a voice that will be functional for purposes tend to be universal to the majority of patients, particularly
of employment and general communication’.7 During the the initial goals, which generally include some or all of the
assessment process, the therapist will be selecting the aims following:
of therapy and the therapeutic approach to help the patient
improve their voice. Harris et  al.6 point out that voice ●● Vocal hygiene/voice care advice including possible
therapy will aim to affect some or all of the following: vocal dietary and lifestyle advice if indicated (see Mid-term
quality, comfort, stamina, pitch and volume. goals and mid-stage therapy).
Diagnosis will affect the treatment selected and the ●● Basic explanation of voice production.
length of treatment. It is useful to organise the therapy aims ●● Information regarding nature of voice difficulty or ENT
as short-term, mid-term and long-term goals and to discuss diagnosis.
these goals with the patient. As the duration of treatment is ●● Identification of possible vocal misuse and abuse factors.
variable, the length of these phases is also variable. However, ●● Postural awareness advice/exercises if indicated.
the stages of therapy correlate with the hierarchical nature ●● Breathing exercises to improve voice production.
of voice therapy exercises, which often start with indirect ●● Laryngeal postures to assist breath flow and reduce
therapy tasks such as improving client awareness of voice laryngeal tension.
production and non-voiced therapy tasks such as breathing ●● Reduction of extrinsic laryngeal musculature tension by
exercises. Direct exercises then follow, often beginning with laryngeal massage or manipulation.
single sounds or short utterances and progressively become ●● Referral or recommendations to additional or alternative
longer and more complex to assist carryover into habitual support services regarding patient’s physical health if
speech. This hierarchical progression is an important factor indicated. An example would be to suggest the patient
in the client gaining control and skill in the use of their seeks the services of an osteopath or physiotherapist for
voice. Without learning basic steps, no skill can become chronic back or neck pain.
effortless and automatic. Adherence to the steps involved ●● Referral or recommendation for the patient to seek
in voice rehabilitation or development work is one of the support regarding their emotional health if indicated,
guiding principles of successful voice therapy. such as psychological support service(s) for a severely
Patients are often impatient to ‘push’ their voice further depressed patient.
than may be advisable at certain points of the therapy process.
An example of this would be a female singer with unresolved The author’s approach is generally to cover the assessment,
vocal nodules who has noted a mild improvement in her outline the goals with the patient and begin treatment in the
singing range and wants to try and reach her highest note initial session.Working through at least one or two exercises
after two sessions of therapy. It is useful for therapists to make with the patient and then providing those exercises as a
clients aware of the stepwise progression of voice therapy and homework task often successfully engages the client into
to inform them that once the voice is rehabilitated, such that the therapy process and gives them a sense of something
there is no dysphonia, more extensive voice development practical being done. Of course, not all assessments go to
can be focussed on other factors such as projection skills and plan. With patients with a highly complex emotional
restoration of singing voice. presentation, it may only be possible to obtain a case history
There is also no set amount of therapy sessions for in the initial consultation.
patients.Therapy intervention can range from one to twenty The overall voice goal in the initial stages of therapy
sessions; as an example, an average course in the UK tends is for the patient to gain improved voice quality and
to be around six sessions. Full remediation of vocal fold laryngeal comfort in short-structured exercises. When ‘on
nodules may take approximately twelve sessions. Ensuring task’, guided by the SLT, patients can often produce an
that the therapy exercises have generalised consistently into improved voice, which instils in them a sense of confidence
the patient’s habitual voice will eliminate the need for them and achievement. It is very helpful and reassuring to
to return to therapy. patients to let them know that the goal at this stage is not
to improve spontaneous speech, since this requires some
time to effect. Individuals initially tend to revert back to
Short-term goals and initial stages of therapy their previous vocal habits in habitual speech or are unable
Every voice is unique and no two patients present in the to sustain improved voice due to the level of impairment.
same way.Therefore, treatment goals, to a certain extent, are It is logical that early stage exercises that involve word

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 Principles of speech and language therapy

or phrase level or short sentences are easier to produce. It is very useful to make voice recordings in the middle
Similarly, short structured reading tasks are also generally phase of therapy. Patients frequently struggle to hear voice
easier for patients to perform more successfully, as they do improvements or are convinced they have not made any
not have to create speech and voice at the same time. progress. When the mid-treatment recordings are played
back to patients, more often than not they express pleasure
Voice care advice and relief that their voice is improving. Lack of progress can
also be discussed at this point and a joint decision taken
The most usual starting point for treatment begins with
about the next step.
vocal hygiene or voice care information. This is often a
list of what not to do to prevent voice problems. However, Long-term goals and later stages of therapy
a list of what to do to keep your voice healthy generally
comes over as being more positive. There are many myths This phase of treatment aims to consolidate the improved
that surround voice difficulty and patients often come with voice so that the habitual speaking voice is maintained
their own impressions of what hinders their voice, such as without deterioration. The use of longer and more
changes in temperature, and what helps their voice, such challenging reading passages can facilitate this as well as
as wearing a scarf or drinking lemon and honey. In spite practising longer conversation tasks with the patient. From
of their own measures, however, their voice is disordered shorter length responses, the patient can then be asked to
and more direct advice and therapy is indicated. Certain describe events or topics such as ‘describe your day today’ or
things are known to affect and help the voice, although ‘tell me what you did at the weekend’. The patient can also
the advice given by SLTs is variable. The advice usually be encouraged to bring in their own practice material such
includes at least some of the points listed in Appendix 7.2 as a work presentation they may have to give or a wedding
at the end of this chapter. speech.
During the latter phases of therapy, volume work can
feature plus exercises and advice for return to singing.
Mid-term goals and mid-stage therapy Preparation for discharge also needs to be addressed, as some
Whichever therapy technique or combination of patients struggle with the termination of therapy. Repeating
techniques has been selected (for example, a breathing the initial baseline voice measures is strongly recommended
based programme such as the Accent Method or a forward followed by evaluating the outcomes with the patient, such
resonance approach), the main focus during the middle as by comparison of Voice Handicap Index scores and voice
phase of therapy is the increased use of longer structured recordings.
exercises to develop the patient’s skill, awareness and voice
control. Sentences that increase in length are very useful Voice rehabilitation
for developing these abilities and their repetitive nature Specific exercises tend to work well for specific voice
enhances skill acquisition. For example, a patient may be disorders. Just as there is basic good voice care advice for all
able to produce the sentences: ‘I like tea’ and ‘I like tea with patients, there are also certain universal principles of good
milk’, but their voice quality or comfort may deteriorate by voice production that can be covered with the patient in
the end of the longer sentence: ‘I like tea with milk and no the early stages of treatment.These include:
sugar’.
●● Establishment of an appropriately ‘supported’ voice by
Once longer structured sentences can be produced
employing a balanced diaphragmatic breathing pattern.
with improved voice, more variable sentences and texts
●● Retraction of the false vocal folds for voicing.
can be introduced. Since the majority of voice patients
●● A balanced use of the vocal tract in habitual speech,
treated are not cognitively impaired, the material used can
which includes the use of forward focus resonance and
become more interesting at this point, which also helps to
oral placing of voice rather than a voice is ‘placed’ in the
engage  the client. Medium to longer poems, quotations,
throat.
short speeches or extracts from novels are all acceptable
●● Appropriate vocal fold closure for phonation.
texts to use.
●● Reduction of head, neck and shoulder tension.
More spontaneous speech can be practised with the
patient, in a semi-structured way, to elicit short length Since breathing, jaw and upper body tension release
responses rather than a detailed account. For example, the exercises are covered extensively in voice therapy texts3,6,8
clinician could ask the patient to tell them three things they and are generally established skills in SLTs, they will not be
did that morning. When the conversation is less structured described in this chapter. In addition, no direct description
in this phase, the patient’s voice tends to deteriorate until of digital manipulation of the larynx or laryngeal
the improved voicing technique is fully established. osteopathy will feature. It is recommended that SLTs attend

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 Aims of voice therapy

specific training in the latter two therapeutic techniques. In these cases, the concept of a ‘supported voice’ has
Principles and techniques of manual therapy are provided gone too far and a focus away from the abdominal muscles
by Lieberman in The Voice Clinic Handbook.6 can therefore be helpful. Focussing instead on opening
Two frequently favoured direct therapy approaches, the laryngeal mechanism, breath is able to enter and exit
which have applications to many different types of voice the body freely. This may be referred to as an ‘open larynx
disorder, will be described.These wide-reaching techniques posture’, but it is also referred to as ‘open throat’ posture.
are false vocal fold retraction (based on Estill’s ‘Compulsory Constriction at the level of the larynx will interrupt breath
Figures for Voice Control’ or open larynx technique) and flow and voice production. In clinical work, retraction of
the use of resonant voice therapy (forward focus resonance). the vestibular folds is often the starting point of treatment,
An exercise example will be included for each. In addition, since correcting the narrowing of the voice channel at this
two specific Estill Compulsory Figure voice qualities will crucial area can quickly resolve laryngeal discomfort, voice
be outlined, sob and twang, which can be used to target distortion, poor breath intake and inadequate release of
vocal fold swellings and poor voice projection problems, breath when voicing.
respectively. Estill studied various voice qualities, such as speech, sob,
twang, falsetto and belting, using instrumentation such as
False vocal fold retraction for release of EMG, electroglottography and laryngeal endoscopy. Her
observations led her to put together a series of ‘compulsory
laryngeal constriction
figures’ or vocal postures that allow singers to develop
The strong basis for release of laryngeal constriction differentiated control of the various parts of the vocal tract
is very largely due to the body of work known as Estill’s and the different muscle groups of the voice. This control,
Compulsory Figures. Jo Estill was a singer who became when applied by singers, can provide greater range and
interested in researching the voice. She produced highly flexibility of style, without experiencing laryngeal strain or
beneficial exercises, applicable to both the singing and damage.
the speaking voice, which aimed to reduce glottal and Estill believed in the concept of the ‘necessary effort’
ventricular constriction. A laryngeal posture that was found that is involved in singing and speaking.6 This concept of
to release hyperadduction was laughing.9 Silent laughing (or necessary effort or ‘specific exertion’ of certain muscles was
giggle posture) is first taught and individuals can then learn later researched by the SLT Alison Bagnall10 with regards to
to maintain this posture internally for voicing. If sustained twang voice quality, which suitably trained therapists can
successfully, constriction is eliminated from voicing and the teach patients as a secure safe voice projection technique.
true vocal folds can vibrate freely. Bagnall also taught systematic courses in ‘voicecraft’ (which
The applications for this technique include: emanated directly from Estill’s Compulsory Figures).
●● Establishment of easy breath flow. This extended the work further to SLTs who work with
●● Reduction of noisy breathing. disordered voices, whether the cause be behavioural or
●● Facilitating a ‘free’ and clear voice both in speaking and structural. The vocal tract posture for sob voice quality, for
singing. example, and the simultaneous onset of the note is highly
●● Reducing glottal and ventricular constriction. beneficial for the remediation of vocal fold swellings such
●● Reducing rough voice quality. as nodules.The training offered via Estill Voice International
●● Reducing strained voice quality. courses allows therapists to train their own voices, gaining
●● Supporting pitch range extension. invaluable experiential vocal control.
●● An important aspect of safe loud voicing both in speech Thus not all relaxation is beneficial for good voicing.
and singing. Voices need to be energised and normal voice muscles need
to be used efficiently rather than overly rested. A link can
While the focus in breath work tends to be on the use be made here with Lee Silverman Voice Training (LSVT).
of a diaphragmatic breathing pattern, it may be the case LSVT has proven efficacy for the treatment of dysphonia
(particularly for drama or singing students) that the relating to Parkinson’s dsease, and is based on a ‘be loud’
technique can be overestablished such that the patient active approach to prevent voice deterioration rather than a
tends to overbreathe or strongly employ the abdominal voice conservation/rest approach.11,12
muscles even for the production of individual vowels or Learning to control specific muscles and vocal tract
short utterances. This hyperfunction distorts the natural parameters as for Estill’s Compulsory Figures leads to the
rhythmic breathing pattern and adds excess strain to ability to produce several voice qualities. Retraction of
the larynx and upper chest rather than supporting voice the false vocal folds is crucial to achieve this safely, both
production. in speaking and singing. A suggested method of teaching

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 Principles of speech and language therapy

retraction of false vocal folds, in which the therapist first spasms, the more difficult speaking becomes.We are literally
demonstrates each action and then asks the patient to repeat strangling ourselves, albeit not consciously.”15
it, follows: Forward placement of the voice generally improves
and can eliminate dysphonia. While the clinician can hear
●● Smile and open your mouth and part your teeth.
improvement instantly, for the patient it is often easier
●● Keep the cheeks lifted and the teeth at least one finger
(and important) for them to feel the reduction of laryngeal
width apart.
tension.
●● Take a breath in through your mouth (the breath tends
Of the structured resonant voice therapy systems that
to feel cool as it makes contact with the back of your
exist, probably the best known is the Lessac–Madsen
mouth). Release the breath through the mouth.
Resonant Voice Therapy (LMRVT) developed by Verdolini
●● The aim is for the inspiratory breath to be quiet, since
in the early 2000s, named in honour of two mentors,
this denotes that there is no laryngeal constriction
Dr  Arthur Lessac and Dr Mark Madsen.16 It is an all-
(impedance to the breath due to laryngeal narrowing as
inclusive therapy programme that can be applied to voice
it flows through the vocal cords). If breathing remains
disorders related to both hypo- and hyperadducted vocal
noisy, ask the patient to exaggerate the smile to a
folds. It addresses voice hygiene, voice modification and
laughing posture and to place the palm of their hand in
post-therapy self-care.
front of their mouth to feel the breath as it is released.
The exercises aim to guide vocal behaviour towards
The more open the larynx is, the more the patient
barely-abducted or barely-adducted laryngeal posturing
will be able to feel warm air on their palm. Negative
using perceptual measures to achieve the target
practice can aid the client considerably to feel and
behaviour, which is resonant voice. Resonant voice is
to hear the difference. Contrasting how much air is
characterised by vibratory sensations along the anterior
released when the breathing is very noisy and passing
alveolar ridge and a feeling of phonatory ‘ease’. If a
through a constricted larynx, compared with when the
patient can feel the forward vibrations and production
breathing is flowing through an open larynx, is often the
feels easy, the patient is producing a resonant voice
turning point in securing the patient’s skill acquisition in
quality. Verdolini advocates that sensory awareness is
adopting this technique.
more effective than verbal instruction. Resonant voice
●● Once quiet inspiratory and expiratory breathing has
quality corresponds to the barely abducted/barely
been established, ask the patient to voice vowels sounds
adducted vocal fold posturing. A study led by Berry17
such as /a/ /e/ /i/ /oh/ /oo/ on the out breath.
indicates that a barely ab/aducted glottal width of
●● If the onset of the note is clear, extend the task to vowel
0.6 mm produces maximum intraglottal pressure while
onset words and phrases and eventually into spontaneous
minimising impact stress to the vocal folds.
speech, with the patient maintaining retracted vocal
The therapy exercises are initiated by having patients
folds.
hum on the nasal sounds /m/ /n/ and /ng/ and to prolong
Resonant voice therapy voiced fricatives /z/ /v/. Verdolini advocates that the use
of resonant voice transfers readily to loud speech, so that
Resonant voice therapy is an approach widely used by many
by adhering to the therapy structure, patients do not have
SLTs. It can be useful for the treatment of hypoadducted
to compromise the strength of their daily performance in
vocal folds, hyperadducted vocal folds, muscle tension
either.
dysphonia, phonotraumatic lesions such as nodules or cysts,
LMRVT’s roots are deeply based in the principles of
post-surgical voice, spasmodic dysphonia (SD) and male to
biomechanics, cognitive learning, science and compliance.
female transgender voice.
A study led by Verdolini, which compared LMRVT with
More generally, it can be referred to as refocusing
the technique of ‘confidential voice therapy’, strongly
laryngeal tone.13,14 Focus refers to resonance of the voice
indicated that patient compliance was a better indicator of
in the airways. Forward focus resonance allows the voice
therapy effectiveness than the type of therapy given.18 While
to fully resonate through the cavities above the larynx, into
therapists can familiarise themselves with the full LMRVT
the pharynx and the face. This creates a balanced voice
system, other briefer examples of resonant voice therapy or
placement rather than a voice that is focussed in the throat.
forward focus resonance will be mentioned below:
Tension in the laryngeal muscles tends to ‘hold’ the voice
in the larynx. SLT Connie Pike, who suffered from SD ●● Saying uh-hum to find natural pitch.13,19 Ask the
writes: “In the case of SD, the focus is usually in the throat, patient to say uh-hum as if responding favourably to
possibly as an attempt to control the uncomfortable spasms. a question, keeping the lips together and using an up
The more we tense the throat to try to push through the rising intonation.

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●● Once a comfortable uh-hum has been established, ask to make contact with the paralysed vocal fold during
the patient to match that pitch with /m/ from the lips. phonation.The difficulty with this approach was that it also
Asking them to sustain /m/ while placing two fingers encouraged the vestibular folds to close and supraglottic
by the side of their nose helps them feel the vibration hyperfunction, therefore causing excessive tension.
move higher into the face.The patient can then progress Improving glottal closure for phonation can be
to adding vowels (ma, me, my, moh, moo, etc.) and then encouraged using hard glottal attack exercises.20,21 However,
to say words, phrases and sentences that begin with /m/ hard attack can encourage roughness due to asymmetry of
while aiming to keep the face and nose vibration. the vocal folds and glottal ‘popping’ or laryngeal valving
●● Uh-hum can be placed in front of automatic sequences exercises can be more successful and generally less traumatic
and longer sentences until the technique is established. for the vocal folds.
●● For clear, energised voice to be produced, it must A general approach would be to ask the patient to make
come to the front of the face, where it will ultimately a cough that is prolonged to a hum. Voice is produced
leave the body. If its journey to the resonating cavities as the cough adducts the vocal folds. The patient is
of the pharynx and face is not impeded by laryngeal then encouraged to progressively lighten the contact,
constriction, optimal voice can be produced. It is logical perhaps by going from cough to a throat clear that can
that fatigued, depressed or tense voices are less likely to be prolonged to a hum. (This technique is also a useful
do this. approach for patients with conversion aphonia.) A grunt
sound such as ‘ugh’ and then initially firm onset vowels
Treatment of vocal cord paralysis/paresis can also facilitate this. Vowel onset words can follow,
followed by vowel onset phrases and sentences loaded with
and reduction of breathy voice vowel initiated words.
due to vocal fold gap
Efficient vocal fold vibration is a standard goal in most
Sob voice therapy exercises for reduction of
therapy approaches. Insufficient vocal fold closure due benign vocal fold swellings: nodules, cysts
to vocal cord paralysis or paresis, hypofunctional voice and polyps
disorders or presbylaryngis leads to air escape and therefore Vocal fold cysts and polyps can respond well to speech
a breathy voice (Figure 7.3). therapy, but typically these swellings may require surgical
Traditionally, forced adduction exercises or pushing excision by an ENT surgeon (Figures 7.4a, b). The
exercises, such as pushing down on the arms of a chair or common practice now, however, is not to remove vocal
against a wall, were used to facilitate vocal fold closure. fold nodules surgically but to try and remediate them with
For patients with a paralysed vocal fold, the aim was to voice therapy. (In  some long-standing cases of nodules,
encourage the unaffected fold to cross over the midline which have become hardened, surgical excision may still be
offered in conjunction with voice therapy.)
Patients who present with nodules have been termed
‘vocal overdoers’.4 It is certainly true that thorough
remediation of these types of vocal fold swellings requires
both vocal behavioural modification and an exploration of
influencing lifestyle factors. Typically, patients with nodules
will be either in a vocally demanding job or be of a very
talkative nature. Further, they will tend to have a busy social
life and be fairly driven personality types. Upon therapeutic
exploration, they may admit to finding it difficult to rest
and relax.Very often, they favour ‘fast’ activity even in their
recreation time, such as running or cycling. Encouragement
by the therapist to explore the nature of consistent
overdoing leads to some significant moments of personal
discovery for many patients.
Both resonant voice therapy and retraction of false
vocal folds in voicing can be very beneficial approaches
Figure 7.3 Laryngeal image illustrating left vocal fold paralysis and for patients with any form of benign vocal fold swelling.
demonstrating vocal fold shortening and muscle loss. However, for suitably trained therapists, sob voice therapy

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 Principles of speech and language therapy

a b
Figures 7.4a, b Images of an intracordal cyst (a) and a vocal fold polyp (b).

(based on the vocal quality sob described by Estill) can be a shaping of the vocal tract.The bright tone produced carries
particularly efficient treatment for nodules.This quality is so over space and above noise very successfully and the levels
named because the vocal tone sounds sad and lamentful.The of twang can be adjusted according to the environment
vocal folds are thinned, the larynx is lowered, the thyroid or the needs of the speaker/singer. It is an excellent voice
cartilage is tilted and the false vocal folds are retracted. The quality for teachers and for any individual who needs to use
release of breath and the onset of the note is simultaneous a projected voice regularly. It can also be used successfully
and gentle, which reduces vocal fold trauma. Patients can for the treatment of vocal fold nodules.
be taught to make a quiet, mid-high pitch soft whimpering Twang quality is a component part of operatic voice, but
sound (like a small dog whining), on the nasal sound /ng/, it is heard in higher concentrations in musical theatre and
while exaggerating a mournful facial posture (to keep the popular singing where brightness is a necessary part of the
false vocal fold retracted) and sound. Vowels and vowel singing style. It is an essential component to ‘belting’ voice
onset words can follow the /ng/ onset to extend thin fold, quality and helps to keep the projected voice free from
simultaneous onset of the note such as /nga/; /ngany/; vocal injury.
/ngany day/; /ngany day now/etc. The nasal sound /ng/ Many voices and accents feature twang voice quality
is particularly beneficial to singers, not only for sob voice including London cockney, Bronx New Yorker and various
therapy, but also to produce a siren to develop or extend Australian dialects. This can be a useful starting point for
vocal range. teaching this quality, but the easiest place to begin is usually
with nasal twang, firstly demonstrated by an uninhibited
Twang voice therapy therapist! A suggested method of teaching this quality follows:
Supraglottic adjustments, specifically a narrowing and ●● Maintain giggle posture with cheeks lifted.
shortening of the vocal tract (a raised larynx and a raised ●● Raise the back of the tongue as for the vowel /ee/.
tensioned tongue) produces a brighter vocal tone, particularly ●● Make a cat like nasal ‘meyow’ sound slowly. Repeat.
in higher pitches. Narrowing in the pharynx and aryepiglottic ●● Make a cat like nasal ngyiaow slowly also. Repeat.
region in singers is a strong aspect of the ‘ring’ heard in the ●● Try the school children taunt sound of ngya-ngya,
voice, which relates to the higher formant frequencies keeping the vowel nasalised.
(resonating frequencies of vowels).9 The quality works best ●● Extend to nasalised vowels with this onset /ngy/: /ngya/;
with thin vocal folds and a closed velar port (Figures 7.5a, b). ngyee; ngyI; ngyoh; ngyoo.
As true twang voice quality does not involve constriction
at the level of the larynx, the voice is not at risk of vocal strain, There is an important distinction between nasal twang and
discomfort or irregularity. Rather, the sound production oral twang, which is sometimes overlooked.The goal (unless
feels effortless and voice amplification is not produced increased nasality is the target) is not to produce an overly
solely by breath support but also by the supraglottic and oral nasalised voice, since nasality tends to dampen  the  tone.

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a b
Figures 7.5a, b (a) Relaxed pharynx around the larynx. (b) Narrowed pharynx, which amplifies or improves resonance of high-pitched
sounds. (From Thomas JP (2012) Why is There A Frog in My Throat? A Guide to Hoarseness. James P. Thomas, Portland, with permission.)

The aim is for a pure oral twang to be produced on the singer is placed in the double vulnerable position of a loss
vowel sounds. Preceding vowels with a firm /y/ instead of of function with a likely temporary loss of employment/
a nasal sound can help to facilitate this such as Ya-Ya; Yee- earning potential. Even amateur singers can feel extreme
Yee. Extending to call out phrases such ‘hi’; ‘bye’; ‘dinner’s upset at the loss or deterioration of their singing voice.
ready’; ‘see you later’ etc. develops the skill further, such that For many, it limits pleasurable social activity such as
eventually the patient can remain in this vocal quality easily participation in choirs or singing in church. Voice therapy
and can use this voice quality as a tool, in varying degrees, to can be effective in restoring and in some cases improving
help him/her project in situations or in singing as required. the singing voice without the need for surgical assistance
or in conjunction with surgical intervention.
Restoration of singing voice The starting point with all voice patients, including
singers, can be their spoken voice. A singer experiencing
“Nothing can affect my voice, it’s so bad.” voice difficulty usually presents with at least mild dysphonia
(Bob Dylan) in their spoken voice also. Working to eliminate this often
has general carryover into the patient’s singing voice.
Voice quality in singing is subjective. In pop and However, specifically practising forward focus resonance
modern singing, voices do not need to be clear or even and false vocal fold retraction on different sung notes, pitch
pathology-free to be desirable, characteristic and the basis glides and sirens develops the exercise further. The latter
of a successful singing career. For other modern singers, and exercises, particularly sirening through the pitch range,
for classical and opera singers, healthy vocal folds are vital serve very well as a vocal warm up.
for vocal versatility and agility and contribute to the beauty, Semi-occluded vocal tract exercises, such as the blowing
appeal and technical ability of the voice. For these singers, exercises advocated by Titze, are also very useful for singers.22
loss of vocal function can be devastating: Typically, these exercises involve the patient blowing through
straws on the sound /oo/,  which increases subglottic
“I’ve been singing properly every day since I was
pressure and increases the efficiency and regularity of vocal
fifteen or sixteen, and I have never had any prob-
lems with my voice, ever…..but that day it just went
fold vibrations. The posture of light lip rounding also helps
while I was on stage in Paris during a radio show. to focus the tone forward into the face and encourages
It  was literally like someone had pulled a curtain steady release of breath. Pitch glides and sirens on /oo/ can
over it”. (Adele) be practised in this way. Increasing the resistance can further
extend this ability and can be achieved by asking the patient
A sensitive approach is required when working with to voice /oo/ and /oo/ sequences through the straw while
singers. At times of voice difficulty, the professional blowing into a small amount of water.

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 Principles of speech and language therapy

Post-surgical voice ●● Follow a soft diet during the 3-day voice rest period.
Sip drinks slowly.
Follow up by a SLT after laryngeal surgery is indicated.
●● Avoid coughing and throat clearing.
In many cases, the patient will have been known to the
●● Following the 3-day voice rest period, begin to use your
therapist and will have received a post-voice surgery advice
voice normally but avoid the following for a further
sheet in advance of the procedure. Most departments have
2-week period: shouting, voicing over loud background
their own in-house advice sheets, which contain some or all
noise, singing and whispering.
of the information listed below:
●● Avoid smoking.
●● Ensure that you have booked off the recommended time ●● Limit alcohol and caffeine.
from work suggested by your ENT surgeon. ●● Keep hydrated by drinking at least six glasses of water
●● Rest your voice (no speaking or singing) for 3 days daily as soon as it is safe for you to do so.
following your surgery. Keep a pen and note pad with ●● Do attend your post-surgery ENT and/or SLT
you during this time. appointment.

Summary and conclusions

SLT clinicians who practise in the field of voice work in The variations of the human vocal tract are extensive.Voices
a unique speech and language therapy discipline where are unique. They reflect a person’s identity or the identity
scientific, artistic and emotional elements can interact in they wish to present. Vocal injury can impact any individual
equal measures. The clinician’s scope of practice may be far negatively, restricting social interaction, reducing levels of
reaching and perceptual assessment skills are of paramount confidence and in some cases resulting in loss of employment.
importance, supported by objective analysis methods and A healthy, efficiently used vocal mechanism will serve
patient subjective evaluation. a person well throughout their life. Guidance from an
The aims of therapy are individualised, according to SLT can help restore a disordered voice whether this has
each patient, but the goals are always hierarchically ordered occurred due to structural or behavioural factors. Further,
ensuring secure acquisition of voice skills to facilitate weak or quiet voices can be strengthened and singing
effective vocal rehabilitation or development. Clinicians ability can be restored. As long as sounds and messages are
tend to have a wide repertoire of therapy approaches and conveyed by the human voice, the need for clinicians who
exercises. These, together with strong interpersonal skills treat voice will continue.
and effective liaison with ENT colleagues and other voice “Words mean more than what is set down on paper. It
practitioners, lead to successful therapy outcomes for the takes the human voice to infuse them with the shades of
majority of patients requiring vocal assistance. deeper meaning.” (Maya Angelou).23

Appendix 7.1:  Individual treatment sessions versus group therapy sessions

The scope of the SLT in some settings extends to offering ●● The therapist is able to try a variety of exercises tailored
group therapy as well as individual sessions.While individual to the patient’s needs and abilities and to adapt them
sessions are favoured by the majority of SLTs, there are more directly.
advantages and disadvantages to both methods of offering ●● Increased 1:1 time allows for responding to gaps in the
treatment. patient’s understanding or awareness.

Advantages of individual therapy sessions: Advantages of group therapy sessions:

●● The confidential nature of 1:1 sessions allows for a ●● Efficient use of therapy time.
strong level of rapport and trust to develop between the ●● General explanations of vocal hygiene, production of
therapist and the patient. normal voice and development of vocal pathology can
●● A strong working relationship can provide quick therapy be imparted to a larger number of patients.
outcomes. ●● General exercises beneficial to many voice patients, such
●● Influencing emotional and personality factors may be as breathing, relaxation and postural work, easily lend
more easily revealed and managed. themselves to group work.

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 References

●● Structured vocal programmes/techniques can work ●● Many voice patients require individual attention to learn
very well in group settings: these include Accent techniques and to practise exercises. Some patients feel
Method, Lessac–Madsen Resonant Voice Therapy and very inhibited and need time and encouragement from
Lee Silverman Voice Training. the therapist to be able to fully engage with the voice
●● Many patients benefit from the supportive nature of work.
group work and feel less isolated regarding their voice ●● Patients who have emotional difficulties may also
difficulty, which can increase motivation. not be appropriate for group work, particularly in the
●● May facilitate more practice on the part of the patient. early stages of treatment, as the emotional factors may
dominate and potentially sabotage the progress of the
Disadvantages of group work: group.
●● Group voice programmes do initially require a heavy ●● Patients who struggle with the voice exercises in a group
time allocation at the planning and organising stages. setting or who drop out of the group after one or two
●● It is generally easier for two therapists to be present in the sessions may fare better in individual sessions.
group and to share the record keeping and note taking.

Appendix 7.2:  Vocal hygeine/voice care advice

●● Do drink good amounts of water daily. (Between 1.5 ●● Do see your GP if you are aware of acid reflux or
and 2 litres is recommended or 6–8 glasses.) frequently awake with a metallic taste in your mouth or
●● Do avoid smoking and smoky environments. experience persistent coughing during the night.
●● Do avoid dusty environments. ●● Do rinse your mouth and gargle and spit following the
●● Do reduce alcohol and caffeinated drinks, as these use of oral spray asthma medications.
dehydrate the body and cause dryness to your larynx. ●● Do carry out steam inhalations twice a day for
●● Do avoid speaking for sustained periods over background 5 minutes if you are suffering from a sore or persistent
noise, as this may strain your voice. dry throat.
●● Do ensure you get adequate sleep and rest, as a tired ●● Do use a room humidifier in a centrally heated bedroom
body often makes for a tired voice. if you experience laryngeal dryness.
●● Do carry out exercises that aim to keep your body ●● Do seek a referral to an ENT doctor from your GP if
flexible, especially your neck, shoulders and back. you experience persistent hoarseness or voice loss for
●● Do seek the help of a voice practitioner to develop more than 2 weeks.
safe loud voicing techniques if you frequently need to ●● Do seek the help of a suitable voice practitioner/
project your voice. singing teacher if you wish to improve your singing
●● Do reduce spicy foods and eating late at night, as this technique, extend your vocal range or change your
may contribute to acid reflux (stomach acid travelling style of singing.
up the oesophagus and irritating the back of the larynx).

References
1 Phillips PS, Carlson E, Chevretton EB (2005) Does a 6 Harris T, Harris S, Rubin JS et al. (1998) The Voice
specialist voice clinic change ENT clinic diagnosis? Clinic Handbook. Whurr Publishers, London.
Logop Phoniatr Vocol 30:90–93. 7 Colton RH, Casper K (1996) Understanding Voice
2 Greene M, Mathieson L (2001)The Voice and its Problems. Lippincott Williams & Wilkins. Maryland.
Disorders, 6th edn. Whurr Publishers, London. 8 Shewell, C (2009) Voice Work: Art and Science in
3 Morrison M, Rammage L (1994) The Management of Changing Voices. Wiley-Blackwell, Oxford.
Voice Disorders. Chapman & Hall Medical, London. 9 Citardi M,Yanagisawa E,Estill J (1996)Videoendoscopic
4 Thomas JP (2012) Why is There A Frog in My Throat? analysis of laryngeal function during laughter. Ann
A Guide to Hoarseness. James P. Thomas, Portland. Otol Rhinol Laryngol 105(7):545–549.
5 Butcher P, Elias A, Cavalli L (2007) Understanding and 10 Bagnall AD, McCullock K (2005) The impact of
Treating Psychogenic Voice Disorder: a CBT Framework. specific exertion on the efficiency and ease of the
John Wiley, Chichester. voice: a pilot study. J Voice 3:384–390.

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 Principles of speech and language therapy

11 Baumgartner CA, Sapir S, Ramig LO (2001) Voice 17 Berry DA, Verdolini K, Montequin DW et al. (2001)
quality changes following phonatory-respiratory A quantitative output-cost ratio in voice production.
effort treatment (LSVT) versus respiratory effort J Speech Lang Hear Res 44(1): 29–37.
treatment for individuals with Parkinson disease. 18 Verdolini-Marston K, Burke MK, Lessac A et al. (1995)
J Voice 15(1):105–114. Preliminary study of two methods of treatment for
12 Ramig LO, Sapir S, Countryman S et al. (2001) laryngeal nodules. J Voice 9(1):74–85.
Intensive voice treatment (LSVT) for patients with 19 Cooper M (1984). Change Your Voice, Change Your Life.
Parkinson’s disease: a 2-year follow up. J Neurol Macmillan, New York.
Neurosurg Psychiatry 71:493–498. 20 Heuer RJ, Sataloff RT, Emerick K et al. (1997)
13 Boone D (1991) Is Your Voice Telling On You? Singular Unilateral recurrent llaryngeal nerve paralysis: the
Publishing, San Diego. importance of preoperative voice therapy. J Voice
14 Lee L (2000) Refocussing laryngeal tone. In: Voice 11(1):88–94.
Therapy: Clinical Studies. Delmar Learning, New York, 21 Stemple JC, Lee L, D’Amico B et al. (1994) Efficiency
pp. 145–154. of vocal function exercises as a method of improving
15 Pike C M (2005) Free to Speak: Overcoming Spasmodic voice production. J Voice 8:271–278.
Dysphonia: a Non-Drug Holistic Rehabilitation Model. 22 Titze IR (2006) Voice training and therapy with a
BookSurge Publishing, Charleston. semi-occluded vocal tract: rationale and scientific
16 Verdolini K (2002) Lessac-Madsen Resonant Voice underpinnings. J Speech Lang Hear Res 49:448–459.
Therapy: Sensory Processing – Broad Practice. University 23 Angelou M (1984) I Know Why The Caged Bird Sings.
of Pittsburgh. Virago Press, London.

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 CHAPTER 8

Swallowing disorders
Jacqui Allen & Peter C. Belafsky

Introduction
Dysphagia is a symptom. It may be caused by multiple mortality in rest home residents and people in long-term
different disorders or insults and has far-reaching residential care.1
consequences. The prevalence of dysphagia is increasing The degree of dysphagia expression is hugely variable;
rapidly worldwide and will continue to rise as society ages. it may be subtle or profound, short-lived or permanent,
In the United States, more than 15 million people were specific to certain textures or pervasive. Likewise, the impact
estimated to be affected by dysphagia in 2010.1 Hospital of dysphagia may vary from undetectable, requiring no
stays for dysphagic patients are twice as long as non- change in lifestyle, to severely disabling resulting in non-oral
dysphagic patients and are estimated to cost $547 billion diet or even mortality secondary to aspiration or pulmonary
annually.2 Data from the United States demonstrates that a complications.2,6 Patients with dysphagia commonly
diagnosis of oropharyngeal dysphagia (OPD) is associated present to otolaryngologists and a thorough assessment
with an adjusted mortality rate of 13.7.2 Epidemiological and thoughtful management can greatly improve quality
studies suggest that dysphagia impacts 22% of adults 50 years of life and avoid serious and life-threatening consequences.
or older, 50% adults 65 years and older and most individuals A multidisciplinary approach provides the best care and
by 80 years of age.3–5 Dysphagia is the most common support for dysphagic patients, regardless of the aetiology.
symptom following stroke and is associated with increased

Anatomy
Swallowing is a complex motor function that is centrally the NA with contributions from the hypoglossal nucleus
coordinated, predominantly involuntary but also modulated of CN XII (tongue fibres). Excitation of proximal (rostral)
by cortical voluntary override. The primary pathways run motor neurons results in inhibition of more distally-
via the glossopharyngeal (cranial nerve [CN] IX) and innervating motor neurons, thereby maintaining sequential
vagus (CN X) nerves to and from the brainstem, through activation of muscles from proximal to distal (i.e. larynx
interneurons to and from the cortex, with integration in before pharynx before oesophagus). The CPG contains
a central pattern generator (CPG) for swallowing in the several pools of interneurons and premotor neurons that
medulla.The nucleus tractus solitarius (NTS) in the medulla are interlinked with CN nuclei and centres controlling
houses the cell bodies of afferent neurons and the nucleus airway protective reflexes. The dorsal swallowing group
ambiguus (NA) the cell bodies of efferent neurons. Sensory receives and integrates afferent information from the
information converges on the NTS from trigeminal, periphery and from the cortex. Projections then pass to the
glossopharyngeal and vagal fibres (primarily via the ventral swallowing group, which drives the motor output
pharyngeal plexus).This information may modify the motor and coordinates the rostral to caudal muscle sequence that
swallowing output adjusting for bolus type, consistency propels bolus in an orad direction. There are significant
and size. However, the sequence of coordination of muscle connections to respiratory centres, the oesophagus and the
contraction is invariant. Motor outflow is primarily from gut, and to the tongue, facial muscles and facial nerves.7–9

Aetiology of dysphagia
Otolaryngologists will most commonly see patients pathology will be seen in ENT clinics. It is important
with OPD, but more and more frequently, oesophageal to recognise that 57% of people with a bolus impacted
problems manifesting with pharyngeal and laryngeal at the gastro-oesophageal junction will localise

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 Swallowing disorders

symptoms to the sternal notch or above.10 This means is much they can offer by way of advice and management
that a proportion of patients with globus sensation, in this setting.
solid food dysphagia, chronic cough and food anxiety Dysphagia may also be due to oral cavity pathology
will have normal pharyngeal examination findings and including poor dentition, abnormal oral control of bolus
investigations but abnormalities in the oesophageal (particularly in neurological disease), xerostomia or post-
phase of swallowing. It is important not to dismiss these surgical defects. Remedies may need to be applied directly
patients without considering distal disease giving rise to these areas where appropriate (e.g. dentures, prostheses,
to oropharyngeal complaints. Otolaryngologists are not feeding strategies, oromotor therapy, saliva substitutes or
gastroenterologists or gastrointestinal surgeons, but there reconstruction).

Oropharyngeal dysphagia
OPD is the most common form of dysphagia and carries Peripheral deficits may cause more focal pathology that may
the greatest risk of pulmonary sequelae. Disordered be amenable to targeted strategies.
swallowing at the level of the oropharynx leads to an airway
threat. OPD may arise from head and neck cancer; after Assessment
treatment for head and neck cancer (even years later, when Ideally assessment is based on a multidisciplinary (MDT)
radiotherapy has been the primary treatment modality); team approach. In-patient and out-patient assessment
after nearly all neurological insults (cerebrovascular may differ slightly in that a speech and language therapist
accident, brain tumours, traumatic brain injury, progressive (SLT) or nurse may initially assess patients admitted acutely,
neurological disease [e.g. Parkinson’s disease, multiple whereas in an out-patient setting this may not be the case.
sclerosis], congenital neurological conditions [e.g. Assessment must include a thorough history with specific
cerebral palsy, syringobulbia]); following surgery in attention to diet tolerance for food types and textures, food
the neck region (carotid endarterectomy, spinal fusion, avoidance, weight loss, medications, associated voice or
thyroidectomy); secondary to reflux (hypopharyngeal breathing problems and pain. The onset (gradual or acute)
diverticuli, cricopharyngeal [CP] bar); from degenerative of dysphagia is often helpful in understanding the aetiology.
disease (vertebral osteophytes, ageing); or from inherited Many patients may minimise dysphagic symptoms as they
or congenital diseases (muscular dystrophies, polymyositis, have often adjusted their diet to cope. It is worth asking
inclusion body myositis, polysaccharidoses, storage diseases) specifically about dysphagia to food, fluid or pills and
(Table 8.1). questioning food avoidance. Subtle changes can herald
The aetiology of OPD influences manifestations and onset of neurological disease and early detection may
determines the success of treatment strategies. Central prevent rapid dysfunction or complications. Medication
nervous system or systemic disease may result in broad can cause dysphagia directly (pill oesophagitis) or by
impairment of the pharynx, larynx and coordination. systemic effects (e.g. reducing saliva, reducing motility).

Table 8.1  Aetiology of oropharyngeal dysphagia

Neurological Cerebrovascular accident, Parkinson’s disease, cranial nerve injury (e.g. post-schwannoma resection), amyotrophic
lateral sclerosis, multiple sclerosis, Shy–Drager syndrome (multisystem atrophy), pseudobulbar palsy, traumatic
brain injury
Autoimmune Guillain Barré disease, Sjögren’s syndrome, scleroderma
Neuromuscular Myasthenia gravis, ageing, cerebral palsy, polio and post-polio syndrome
Muscular Muscular dystrophies (Duchenne, myotonic, oculopharyngeal), myopathies, cricopharyngeal bar/Zenker diverticulum
Metabolic Lysosomal storage disorders (e.g. Hunter/Hurler’s syndrome), xerostomia (Sjögren’s syndrome, radiotherapy,
medications)
Neoplastic Oropharyngeal cancer/head and neck cancer, post-radiation therapy
Infectious Tonsillitis and pharyngitis, viral (cytomegalovirus, herpes simplex), candidiasis
Inflammatory Gastro-oesophageal reflux, caustic ingestion
Traumatic Post-surgical defect (e.g. tumour resection), osteophytes
Iatrogenic Medications (multiple), surgery (cervical spine surgery, carotid endarterectomy, thyroidectomy)

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 Oropharyngeal dysphagia

An  appreciation  of  co-morbidities is valuable and often material passes inferior to the vocal folds, and therefore
might suggest loss of physiological reserve or help determine will not be detected by this type of screen. However, these
the prognosis of symptoms. Previous interventions, both are the most important patients to identify as they carry
medical and surgical, must be elucidated and the level of the greatest risk of pulmonary soiling. To assess aspiration
cognition and manual dexterity should be appreciated in and dysphagia more accurately and reliably, instrumental
the context of self-feeding ability. examinations are required.

Patient-reported assessment tools Objective assessment

The viewpoint of the patient regarding their symptom When an otorhinolaryngology surgeon assesses the patient,
of dysphagia is critical to understanding its impact and a history and examination will be performed and should
strategies for management. It is also surprising how many be followed by an endoscopic examination of the larynx
patients do not admit to particular difficulties unless and pharynx. Laryngeal motor and sensory function is
questioned directly. As a method of understanding further assessed, particularly vocal fold mobility and glottal closure.
a patient’s degree of dysphagia impairment and of gauging Where possible, videostroboscopy should be used if vocal
the effect of treatment over time, patient-reported tools abnormalities are identified and a functional endoscopic
may be helpful.The Eating Assessment Tool-10 (EAT-10) is evaluation of swallowing (FEES) should be performed (by
a validated 10-item questionnaire encompassing aspects of the otorhinolaryngology surgeon or a trained SLT). FEES
deglutition such as what food types can be managed as well is a dynamic real-time assessment of the swallow from
as the social effect of swallow problems (see Appendix 8.1).11 a luminal perspective. The mucosa may be assessed along
It may be completed in 5 minutes by rating each item from with the mobility and health of the vocal folds. Safety of
0 (no problem) to 4 (severe problem) and then calculating deglutition, particularly penetration, aspiration and residue,
the sum total. Validation studies demonstrate that scores may be evaluated. FEES is performed at the bedside or
>3 indicate a swallowing problem. Alternative assessment in the clinic, and requires only a nasopharyngoscope and
tools include the MD Anderson Dysphagia Inventory food to administer. Advantages include: lack of exposure
(MDADI; specific for head and neck cancer patients) to ionising radiation; ability to assess patients who are
(see Appendix 8.2), the Sydney Swallowing Questionnaire unfit for transport to other departments at bedside; direct
(SSQ) (see Appendix 8.3), and the Swallowing Quality of visualisation of glottic function; ability to test strategies or
Life (SWAL-QOL) (see Appendix 8.4). The MDADI is compensatory manoeuvres; and speed of the study. FEES
a 20-item survey with three domains and a single global guides dietary recommendations and may be repeated
question. It is designed to assess swallow in the patient with frequently as the patient’s condition changes. The main
head and neck cancer.12 The SSQ contains 17 items and disadvantage of FEES is the period of obscuration of view,
patients score on a visual analogue scale, and the SWAL- termed the ‘whiteout’, that occurs with constriction of the
QOL contains 10 domains with multiple questions and luminal space as swallowing occurs. For a brief moment
is correlated with symptom frequency.13–16 Although the  endoscope tip is enveloped in mucosa and no view
not diagnostic, rating scales do help define the extent of of the bolus or glottis is possible. Airway violation occurring
symptoms and impact on the patient’s life. at this point cannot be seen.Technical proficiency in passing
the endoscope is required and difficult nasal anatomy may
Subjective assessment make this uncomfortable for the patient or impossible to
A team approach is vital in managing the dysphagic patient. achieve. There is also a need for appropriate sterilisation of
Assessment at admission is often initially performed by the endoscope and equipment used.
a nurse or junior doctor. This may identify swallowing Further assessment depends on availability of resource
problems and then be followed by a more in-depth and personal training. In-clinic transnasal oesophagoscopy
bedside assessment by a SLT. This includes history followed can be extremely valuable in assessment, identification
by examination of CN function, dentition, hydration, and treatment of dysphagia, and is becoming more widely
cognition and nutritional status. As laryngeal function is practiced.17,18 Transnasal oesophagoscopy is a safe, efficient
critical in normal deglutition, voice problems are noted and and effective method of examining the digestive tract
may require further investigation. The SLT may perform a from the mouth to the duodenum, with the ability to take
bedside water-swallow test, administering a small volume biopsies, perform therapeutic manoeuvres and obtain a
of water to the patient and then assessing response such video recording of the findings. In particular, the ability to
as cough or choking. Although this is helpful if a cough is examine the oesophagus can be illuminating when trying
elicited, this trial will not identify patients who are silently to discern the aetiology of dysphagia or non-specific
aspirating. By definition, these patients do not cough when pharyngeal symptoms.

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 Swallowing disorders

An alternative or complementary instrumental Protect the airway

assessment is the dynamic swallowing study (modified
Advanced Trauma Life Support education teaches us A, B,
barium swallow, videofluoroscopic swallowing study).19
C – airway, breathing, circulation. In humans, protecting
This contrast study evaluates the swallow, from the oral
the airway is the ultimate goal and primary function of
cavity, through the pharyngeal phase and oesophageal
the larynx. Deglutition that has gone awry may violate the
phases of swallowing. It has a proven track record having
tracheobronchial tree. If there is impairment of laryngeal
been the gold standard for dysphagia assessment for the past
function, re-mediation may assist airway protection,
40 years. Dynamic information is obtained and multiple
cough generation and swallow efficiency. Options that
textures, manoeuvres and strategies can be trialled to assess
are directed at improving airway protection include
and manage dysphagia. The airway is visible and airway
swallow therapy (teaching strategies for voluntarily
violation can be assessed. Valuable information from the
closing the airway and holding it closed or elevated for
upper oesophageal sphincter (UOS) and oesophagus may
the duration of the swallow), vocal fold medialisation and
also be obtained and should be evaluated for a complete
augmentation (in the clinic or operating room) with or
study. Disadvantages of this study are the exposure to
without arytenoid adduction (AA), laryngeal suspension,
ionising radiation (low dose), the need for specialised
tracheostomy, laryngotracheal separation and total
equipment (radiology suite), the fact that the images are
laryngectomy.
two-dimensional, with superimposition on lateral view,
and the vocal folds are not able to be assessed directly. Swallow therapy
SLTs may educate the patient regarding swallow mechanics
Management and safe airway closure prior to bolus being swallowed.
Information obtained via the subjective assessment, Several manoeuvres have been used to target aspects
objective endoscopic assessment and any instrumental of laryngeal closure. The supraglottic swallow teaches
examinations should be combined to obtain a clear voluntary and protracted closure of the glottis followed by
understanding of the aetiology of dysphagia and possible expiration to clear any penetrated material from the vocal
remedies. folds (Table 8.2). The super-supraglottic swallow enhances
Dysphagia treatment must address aspects of a patient’s this by also encouraging laryngeal aditus closure.20
diet, lifestyle, underlying co-morbid conditions and primary
aetiology of the dysphagia where possible. It may be that Surgical options
several strategies or multiple treatments are used to optimise If there is a paretic or immobile vocal fold resulting in glottal
deglutition, both for safety and functionality. In OPD, three incompetence, then laryngoplasty is appropriate to improve
broad approaches may be taken: protect the airway, improve safety and enhance cough strength. Injection augmentation
bolus transit and enhance pharyngo-oesophageal segment of the vocal fold may be performed in the clinic or under
opening. Failure of these avenues leads to the unpleasant general anaesthesia utilising either autogenous material or
options of non-oral feeding or airway separation. allograft implant (Figures 8.1–8.3). Many types of material

Table 8.2  Aetiology of oesophageal dysphagia

Neurological Hirschsprung’s disease
Autoimmune Scleroderma
Congenital Duplication, tracheo-oesophageal fistula/stenosis
Neuromuscular Ineffective oesophageal motility, nutcracker oesophagus, ageing
Muscular Diffuse oesophageal spasm
Metabolic Storage disorders
Neoplastic Oesophageal or gastro-oesophageal cancer, benign tumours, fibroepithelial polyps
Infectious Bacterial, fungal and viral oesophagitis
Inflammatory Reflux disease, myositis
Traumatic Perforation
Iatrogenic Post-surgical defect, strictures, perforation, pill oesophagitis
External Compression (e.g. dysphagia lusoria, hilar adenopathy)

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 Oropharyngeal dysphagia

Figure 8.1 Right vocal fold paralysis.

Figure 8.2 Right vocal fold paralysis during in-clinic injection

have been reportedly used during injection laryngoplasty
augmentation.
including autogenous fat, fascia lata, methylcellulose,
collagen, Teflon, hyaluronic acid gels, calcium hydroxylapatite,
polymethylmethacrylate spheres and Bioplastique/Vox
(silicone microspheres in carrier).21–36 Each substance
has advantages and disadvantages in terms of ease of use,
longevity  and tissue reaction.21-36 Medialisation may be
achieved using non-injectable elements, usually requiring
external access (e.g. Gore-tex thyroplasty or silicone pre-cut
or hand-carved prostheses).37,38 Laryngeal framework surgery
including AA may be necessary if the glottal gap is large, and
may be combined with injection  techniques.39 In some
cases, if there is known recurrent laryngeal nerve damage
that will not recover, neural anastomosis and reinnervation
may be useful. Synkinetic function will produce tone in
the laryngeal adductor muscles around 6–12 months after
surgical neurorrhaphy.40
Laryngeal suspension provides a dual benefit: airway
protection by repositioning the airway anteriorly beneath
the tongue base, and assisting transit of bolus by physically
enhancing the UOS opening (through anterosuperior
traction).This will be discussed further below.
Tracheostomy provides easy access to the airway
anteriorly, enabling suction of secretions, control of Figure 8.3 Right vocal fold paralysis following in-clinic injection
augmentation.
ventilation pressures (with cuffed tubes) and less dead space
during respiration. A tracheostomy may be a temporary
measure when recovery is expected, but if recovery Oral care has been shown to decrease the rate of aspiration
is not possible, a permanent stoma may be fashioned. pneumonia in dysphagic patients.41,42
Tracheostomy in the presence of an intact airway and When soiling of the airway from native secretions is
pharynx does not completely prevent aspiration, nor does causing pulmonary complications, aggressive surgical
a non-oral diet. In both cases patients may still aspirate treatment may be required. In this setting laryngotracheal
secretions into the lower respiratory tract and (particularly separation (isolating the deglutitive pathway from the
when oral hygiene is poor) this may lead to pneumonia. airway) or total laryngectomy (narrow field laryngectomy)

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 Swallowing disorders

can be performed if appropriate and no other intervention may focus on enhancing propulsion or reducing impedance
is feasible or safe. Laryngotracheal separation closes the to flow.
trachea at the level of the second or third ring, fashioning
a blind superior pouch and preventing material entering Swallow therapy
the airway, but requiring a tracheostoma for respiration. Swallow therapy can utilise manoeuvres to improve bolus
Normal phonation is no longer possible. A modification of transit and influence function of the UOS. The Masako
Biller’s laryngoplasty, termed the ‘steamboat laryngoplasty’, manoeuvre stabilises the tongue during a swallow and
has been described.43 The laryngeal aditus is closed by induces increased effort from the pharyngeal constrictor
bisecting the aryepiglottic folds along their length and muscles. It may also enhance UOS opening. Effortful
approximating the mucosa in the midline. A small posterior swallowing increases awareness and sustained muscle
communication is maintained to allow phonation, but the contraction of all pharyngeal musculature. Shaker exercises
rest of the airway is protected by the closure and swallowed strengthen the hyoid musculature in an effort to improve
material traverses the pharynx as normal. Glottal speech is the hyolaryngeal elevation that assists in UOS opening
still possible; however, gross aspiration is prevented.43 (Table 8.3).20
Narrow field laryngectomy removes the larynx
permanently, requiring a stoma for respiration and Surgical options
completely separating the pharynx from any airway Common surgical procedures in dysphagic patients have largely
communication. Phonation is lost as a consequence of focused on the UOS and in particular the CP component of
preventing aspiration and this should only be considered the UOS. As an anatomical target, the CP may be treated by
when there is no hope of recovery. Laryngectomy represents dilation, botulinum toxin (BTX) injection, myotomy +/-
failure of all conservative management protocols. diverticulum management and laryngeal  suspension. Other
pharyngeal procedures include cervical osteo­ phytectomy
Improving bolus transit and enhancing (or plate removal) and hypopharyngeal pharyngoplasty. Palatal
pharyngo-oesophageal segment function procedures (palatal pharyngoplasty) are utilised to augment
Bolus must receive adequate propulsive impetus to traverse velopharyngeal closure, particularly when the velopharyngeal
the pharynx and encounter a coordinated and compliant seal is not reliable leading to nasal escape of material and
UOS to achieve access to the oesophagus. Improving transit reduced pressure gradients.44

Table 8.3 Swallow rehabilitation exercises

Exercise Method Target
Shaker exercises Lie supine without a pillow. Lift your chin off the bed, flexing your neck. Look at Hyoid musculature that
your toes and hold for 60 seconds. Rest head back to bed for 60 seconds. Repeat. stabilises the larynx and
OR: Lie supine without a pillow. Lift your chin off the bed to look at your toes elevates the
without raising your shoulders. Immediately relax the head back to the bed. hyolaryngeal complex
Perform 30 repetitions. Rest for 2 minutes during swallow
Masako Bite tongue between anterior teeth to stabilise. While holding perform swallow. Posterior pharyngeal
manoeuvre Repeat wall musculature
Supraglottic Hold bolus in oral cavity. Breathe in and hold breath. Swallow mouthful while Airway protection
swallow holding breath and then exhale with a cough immediately after swallow. Swallow
again
Mendelsohn Feel thyroid notch on anterior neck. During swallow, when larynx is maximally Hyolaryngeal elevation
manoeuvre elevated, hold the position for 10 seconds
Effortful swallow Swallow as hard as possible imagining that you are swallowing a whole grape. All swallow musculature,
Use moisture if necessary biofeedback
Tongue exercises Tongue vs roof of mouth for 10 seconds, tongue vs fingers in each cheek for Tongue thrust and
10 seconds, tongue vs spoon outside mouth for 10 seconds. Combine with range mobility
of motion exercises – tongue protrusion and side-to-side motion
Super-supraglottic Hold bolus in oral cavity. Breathe in and hold breath hard and bear down during Airway protection
swallow swallow. Swallow mouthful then exhale with a cough immediately after swallow

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 Oropharyngeal dysphagia

The cricopharyngeus muscle constitutes the inferior

fibres of the inferior pharyngeal constrictor and the most
obvious anatomical element of the UOS. These sling-like
fibres (lacking a median raphe) encircle the lumen of the
oesophageal inlet attaching to the posterior cricoid laminae
and arch. Primarily slow twitch fibres, they maintain tonic
contraction except when deglutition occurs, during which
time contraction ceases. No active relaxation occurs and
distraction of the UOS by hyolaryngeal elevation must
occur to open the inlet (effectively by pulling the laryngeal
skeleton away from the vertebrae and dragging open the
UOS). If the cricopharyngeus muscle fibres hypertrophy,
become poorly compliant or develop increased tonic
pressures, then UOS opening duration and extent will be
reduced. Bolus flow may be impaired, leading to pharyngeal
residue and incomplete bolus transit. Balloon dilation
Figure 8.5 Endoscopic image of a cricopharyngeal bar following
of a fibrotic sphincter or scar bands, with or without the
stapler myotomy.
addition of BTX injection to the CP fibres, can improve
UOS opening.45 When marked muscle bulk is present,
formal myotomy may be more effective in improving of the diverticulum depends on approach. In cases of open
transit and reducing pharyngeal residue.45,46 CP myotomy myotomy the pouch may be resected, inverted or closed.47,48
may be performed endoscopically or as an open procedure. During endoscopic myotomy the pouch is generally left
Advantages of endoscopic treatment are speed of the surgery in situ, as myotomy provides drainage into the oesophagus
and reduction in complications, but this is balanced by a and removes the obstructive effect, while excision of pouch
higher rate of recurrent dysphagia (Figures 8.4, 8.5).47,48 mucosa may increase risk of perforation. Mortensen et al.52
Many tools have been used for division of the CP muscle reported resection of pouch mucosa in small diverticuli
endoscopically, including needle cautery, cold steel, CO2 (<3 cm) via an endoscopic approach, closing the defect with
laser, harmonic scalpel and stapling devices.46,49–51 When a sutures in six patients. Satisfactory resolution of dysphagia
diverticulum is associated with CP hypertrophy, management was achieved without significant leak.
Laryngeal suspension acts to assist opening of the
pharyngo-oesophageal segment by elevating the laryngeal
complex. This permanent fixation of the laryngeal skeleton
to the mandible (either at midline or laterally) results in
sustained distraction of the UOS in combination with
offering a degree of airway protection by positioning the
laryngeal aditus beneath the tongue base and deflecting
the epiglottis. Suspension may assist when disease has
curtailed normal hyolaryngeal elevation either functionally
or through resection (e.g. following head and neck cancer
resection or radiotherapy). Suspension is usually combined
with CP myotomy to maximise elevation and UOS
compliance and can be combined with airway protective
procedures such as augmentation or medialisation.53,54
Patients exhibiting prominent osteophytes arising from
the anterior surface of the cervical vertebrae or metalware
from previous spinal fusion surgery may experience
dysphagia through diversion of bolus flow. Mechanical
trauma and friction in tissue overlying the osteophyte or
plate can result in soft tissue inflammation and oedema and
restriction of epiglottic retroversion. Selected cases may
Figure 8.4 Endoscopic image of a cricopharyngeal bar with benefit from osteophytectomy or removal of metalware
a nasogastric tube sitting in the oesophageal lumen. (Figure 8.6).55–57

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 Swallowing disorders

closure of the piriform fossa) in combination with type 1

thyroplasty and AA to improve bolus transit through
the mobile pharynx and reduce residue. They reported
improvement in a small case series (eight patients).
Surgeons should consider, however, that reducing capacity
in an immobile pharynx may result in ‘funnelling’ of bolus
directly toward the airway and increase the risk of violation
rather than reducing the risk.58

Novel approaches
Given the diversity of aetiology in dysphagic patients,
the severity of consequences and the imperfect treatment
options that are available, researchers continue to develop
novel approaches for diagnosis and treatment. Selective use
of injectable fillers to augment airway closure following
partial laryngectomy extends the utility of currently
available products.59 Artificial pacing of the vocal folds to
Figure 8.6 Videofluoroscopic image of cervical spine metalware match respiration and reduce aspiration in neurologically
with an associated cricopharyngeal bar. impaired individuals has been reported and seeks to correct
the fundamental pathophysiological disorder.60 Manual
opening of the UOS, using a small implant (the Swallow
Although uncommon, a patulous piriform fossa  can Expansion Device™) surgically attached to the cricoid
retain bolus and be a source of airway threat. Mok et al.58 arch, has been trialled with success in animal models and is
reported a novel hypopharyngeal pharyngoplasty (unilateral now being tested in humans.1

Summary
Swallowing disorders are common in laryngology practice. Surgery may also bring improvement by augmenting
Although the aetiology is diverse, the fundamental problem airway closure, enhancing hyolaryngeal elevation, increasing
may be considered as one of poor airway protection, reduced UOS opening or permanently separating respiration from
bolus transit or abnormal UOS opening. More than one deglutition. A range of options should be considered and
aspect may be affected. Conservative measures, including tailored to each individual in order to achieve the best
dietary alteration, reformulation of medications, swallowing outcomes. An MDT team approach is advantageous in the
manoeuvres and swallow rehabilitation, can offer assistance. management of this complex range of disorders.

Appendices: Dysphagia indices

Appendix 8.1 6. Swallowing is painful.
7. The pleasure of eating is affected by my swallowing.
EAT-10 (Eating Assessment Tool-10)11
8. When I swallow food sticks in my throat.
Patient scores each statement “To what extent are these
9. I cough when I eat.
scenarios problematic for you?”
10. Swallowing is stressful.
0 = no problem; 4 = severe problem.

1. My swallowing problem has caused me to lose Appendix 8.2

weight. MDADI (MD Anderson Dysphagia Inventory)12
2. My swallowing problem interferes with my ability to The following statements have been made by people who
go out for meals. have problems with their swallowing. Some of the statement
3. Swallowing liquids takes extra effort. may apply to you. Please read each statement and circle the
4. Swallowing solids takes extra effort. response which best reflects your experience in the past
5. Swallowing pills takes extra effort. week.

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 Appendices: Dysphagia indices

(Response options are strongly agree, agree, no opinion, 5. How much difficulty do you have swallowing hard
disagree, or strongly disagree) foods (e.g. steak, raw fruit, raw vegetables)?
My swallowing ability limits my day-to-day activities. 6. How much difficulty do you have swallowing dry
foods (e.g. bread, biscuits, nuts)?
E2. I am embarrassed by my eating habits. 7. Do you have any difficulty swallowing your saliva?
F1. People have difficulty cooking for me. 8. Do you have any difficulty starting a swallow?
P2. Swallowing is more difficult at the end of (Never to occurs every time I swallow.)
the day. 9. Do you ever have a feeling of food getting stuck in
E7. I do not feel self-conscious when I eat. your throat when you swallow? (Never to occurs
E4. I am upset by my swallowing problem. every time I swallow.)
P6. Swallowing takes great effort. 10. Do you ever cough or choke when swallowing solid
E5. I do not go out because of my swallowing foods? (Never to occurs every time I swallow.)
problem. 11. Do you ever cough or choke when swallowing
F5. My swallowing difficulty has caused me to lose ­liquids? (Never to occurs every time I drink.)
income. 12. How long does it take you to eat an average meal?
P7. It takes me longer to eat because of my s­ wallowing (Less than 15 min/15–30 min/30–45 min/​45–60
problem. min/>60 min/unable to swallow.)
P3. People ask me “Why can’t you eat that?” 13. When you swallow does food or liquid go up behind
E3. Other people are irritated by my eating problem. your nose or come out of your nose? (Never to
P8. I cough when I try to drink liquids. occurs every time I swallow.)
F3. My swallowing problems limit my social and 14. Do you ever need to swallow more than once for
­personal life. your food to go down? (Never to occurs every
F2. I feel free to go out to eat with my friends, time.)
­neighbours, and relatives. 15. Do you ever cough up or spit out food or liquids
P5. I limit my food intake because of my swallowing during a meal? (Never to occurs every time.)
difficulty. 16. How do you rate the severity of your swallowing
P1. I cannot maintain my weight because of my problem today? (No problem to extremely severe
­swallowing problem. problem.)
E6. I have low self-esteem because of my swallowing 17. How much does your swallowing problem
problem. ­interfere with your enjoyment or quality of life?
P4. I feel that I am swallowing a huge amount of food. (No ­interference to extreme interference.)
F4. I feel excluded because of my eating habits.

First question scored alone. E = emotional; F = functional; Appendix 8.4

P = physical. Items added together for each domain then SWALQOL (Swallowing Quality of Life)14
mean score of each scale multiplied by 20 to give range 10 domains and symptom frequency (SP = swallowing
0–100 for each scale. (Higher score shows better quality problem)
of life.)
Domain
Burden
Appendix 8.3
Dealing with my SP is very difficult.
SSQ (Sydney Swallowing Questionnaire)13 SP is a major distraction in my life.
Patient scores each statement on a 100 mm VAS scale with
left end = no difficulty at all and right end = unable to Eating duration
swallow at all. It takes me longer to eat than other people.
It takes me forever to eat a meal.
1. How much difficulty do you have swallowing at
present? Eating desire
2. How much difficulty do you have swallowing thin Most days, I don’t care if I eat or not.
liquids (e.g. tea, soft drink, beer, coffee)? I don’t enjoy eating anymore.
3. How much difficulty do you have swallowing thick I’m rarely hungry anymore.
liquids (e.g. milkshakes, soups, custard)? Food selection
4. How much difficulty do you have swallowing soft Figuring out what I can eat is a problem for me.
foods (e.g. Mornays, scrambled egg, mashed potato)? It is difficult to find food I both like and can eat.

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 Swallowing disorders

Communication Fatigue
People have a hard time understanding me. Feel exhausted.
It’s been difficult for me to speak clearly. Feel weak.
Feel tired.
Fear
I fear I may start choking when I eat food. Sleep
I worry about getting pneumonia. Have trouble falling asleep.
I am afraid of choking when I drink liquids. Have trouble staying asleep.
I never know when I am going to choke. Symptom frequency
Mental health Coughing
My SP depresses me. Choking when you eat food.
I get impatient dealing with my SP. Choking when you take liquids.
Being so careful when I eat or drink annoys me. Having thick saliva or phlegm.
My SP frustrates me. Gagging
I’ve been discouraged by my SP. Having excess salvia or phlegm.
Social Drooling
I do not go out to eat because of my SP. Problems chewing.
My SP makes it hard to have a social life. Food sticking in your throat.
My usual activities have changed because of my SP. Food sticking in your mouth.
Social gatherings are not enjoyable because of my SP. Food/liquid dribbling out your mouth.
My role with family/friends has changed because of Food/liquid coming out your nose.
my SP. Coughing food/liquid out your mouth.

References
1 Belafsky PC (2010) Manual control of the upper 9 Broussard DL, Altschuler SM (2000) Central
esophageal sphincter. Laryngoscope 120:S1–S16.1. integration of swallow and airway-protective reflexes.
2 Altman KW,Yu GP, Schaefer SD (2010) Consequence Am J Med 108:62S–67S.
of dysphagia in the hospitalized patient. Impact on 10 Smith DF, Ott DJ, Gelfand DW et al. (1998)
prognosis and hospital resources. Arch Otolaryngol Lower esophageal mucosal ring: correlation of
Head Neck Surg 136:784–789. referred symptoms with radiologic findings using a
3 Howden CW (2004) Management of acid-related marshmallow bolus. Am J Roentgend 171:1361–1365.
disorders in patients with dysphagia. Am J Med 11 Belafsky PC, Mouadeb DA, Rees CJ et al. (2008)Validity
117(Suppl 5A):44S–48S. and reliability of the Eating Assessment Tool (EAT-10).
4 Meng NH, Wang TG, Lien IN (2000) Dysphagia in Ann Otol Rhinol Laryngol 117:919–924.
patients with brainstem stroke: incidence and outcome. 12 Chen AY, Frankowski R, Bishop-Leone J et al. (2001)
Am J Phys Med Rehabil 79:170–175. The development and validation of a dysphagia-
5 Robbins J, Langmore S, Hinds JA et al. (2001) Dysphagia specific quality-of-life questionnaire for patients with
research in the 21st century and beyond: proceedings head and neck cancer. Arch Otolaryngol Head Neck Surg
from Dysphagia Experts Meeting, August  21, 2001. 127:870–876.
J Rehabil Res Dev 39:543–548. 13 Wallace KL, Middleton S, Cook IJ (2000) Development
6 Ramsey DJC, Smithard DG, Kalra L (2003) Early and validation of a self-report symptom inventory
assessments of dysphagia and aspiration risk in acute to assess the severity of oral-pharyngeal dysphagia.
stroke patients. Stroke 34:1252–1257. Gastroenterol 118:678–687.
7 Leonard R, Kendall K (2008) Dysphagia Assessment and 14 McHorney CA, Robbins J, Lomax K et al. (2002)
Treatment Planning: a Team Approach. Plural Publishing, The SWAL-QOL and SWAL-CARE outcomes
San Diego, pp. 265–294. tool for oropharyngeal dysphagia in adults: III.
8 Mittal RK (2011) Motor function of the pharynx, Documentation of reliability and validity. Dysphagia
esophagus and its sphincters. In: Integrated Systems 17:97–114.
Physiology: From Molecule to Function to Disease. Morgan 15 McHorney CA, Bricker DE, Kramer AE et al. (2000)
& Claypool Life Sciences, San Rafael. The SWAL-QOL outcomes tool for oropharyngeal

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dysphagia in adults: I. Conceptual foundation and 31 Lim JY, Kim HS, Kim YH et al. (2008) PMMA
item development. Dysphagia 15:115-121. (polymethylmethacrylate) microspheres and stabilized
16 McHorney CA, Bricker DE, Robbins J et al. (2000) hyaluronic acid as an injection laryngoplasty material
The SWAL-QOL outcomes tool for oropharyngeal for the treatment of glottal insufficiency: in  vivo
dysphagia in adults: II. Item reduction and preliminary canine study. Eur Arch Otorhinolaryngol 265:321–326.
scaling. Dysphagia 15:122–133. 32 Perazzo PSL, Duprat A de C, Lancellotti CLP
17 Rees CJ (2007) In-office unsedated transnasal balloon (2007) Histological behaviour of the vocal fold after
dilation of the esophagus and trachea. Curr Opin hyaluronic acid injection. J Voice 23:95–98.
Otolaryngol Head Neck Surg 15:401–404. 33 Belafsky PC, Postma GN (2004) Vocal fold
18 Postma G, Cohen J, Belafsky P et al. (2005) Transnasal augmentation with calcium hydroxylapatite.
esophagoscopy: revisited (over 700 consecutive cases). Otolaryngol Head Neck Surg 131:351–354.
Laryngoscope 115:321-323. 34 Rosen CA, Gartner-Schmidt J, Casiano R et al. (2007)
19 Leonard R, Mackenzie S (2008) Dynamic swallow Vocal fold augmentation with calcium hydroxylapatite
studies: measurement techniques. In: Dysphagia (CaHA). Otolaryngol Head Neck Surg 136:198–204.
Assessment and Treatment Planning: a Team Approach. (eds. 35 Rees CJ, Mouadeb DA, Belafsky PC (2008)Thyrohyoid
R Leonard, K Kendall) Plural Publishing, San Diego, vocal fold augmentation with calcium hydroxyapatite.
pp. 265–294. Otolaryngol Head Neck Surg 138:743–746.
20 Logemann J (2007) Swallowing disorders. Best Pract 36 Tanna N, Zalkind D, Glade RS et al. (2006) Foreign
Res Clin Gastroenterol 21:563–573. body reaction to calcium hydroxylapatite vocal
21 Prodinger PM, Windisch G, Hammer GP et al. (2008) fold augmentation. Arch Otol Head Neck Surg 132:​
Lipoaugmentation of the vocal folds: a survey on 1379–1382.
alternative donor sites for graft harvesting. J Voice 37 Hendricker RM, deSilva BW, Forrest LA (2010)
23(5):625–630. Gore-Tex medialization laryngoplasty for treatment
22 Dursun G, Boynukalin S, Ozgursoy OB et al. (2008) of dysphagia. Otolaryngol Head Neck Surg 142:536–539
Long-term results of different treatment modalities for 38 Carrau RL, Pou A, Eibling DE et al. (1999) Laryngeal
glottic insufficiency. Am J Otolaryngol 29:7–12. framework surgery for the management of aspiration.
23 Remacle M, Lawson G, Jamart J et al. (2006) Treatment Head Neck 21:139–145.
of vocal fold immobility by injectable homologous 39 Woodson G (1997) Cricopharyngeal myotomy and
collagen: short-term results. Eur Arch Otorhinolaryngol arytenoid adduction in the management of combined
263:205–209. laryngeal and pharyngeal paralysis. Otolaryngol Head
24 Hsiung MW, Woo P, Minasian A et al. (2000) Fat Neck Surg 116:339–343.
augmentation for glottic insufficiency. Laryngoscope 40 Blumin JH, Merati AL (2008) Laryngeal reinnervation
110:1026–1033. with nerve-nerve anastomosis versus laryngeal
25 Reijonen P,Tervonen H, Harinen K et al. (2009) Long- framework surgery alone: a comparison of safety.
term results of autologous fascia in unilateral vocal fold Otolaryngol Head Neck Surg 138:217–220.
paralysis. Eur Arch Otorhinolaryngol 266(8):1273–1278. 41 Yoneyama T, Yoshida M, Ohrui T et al. (2002) Oral
26 Milstein CF, Akst LM, Hicks D et al. (2005) Long-term care reduces pneumonia in older patients in nursing
effects of micronized Alloderm injection for unilateral homes. J Am Geriatric Soc 50:430–433.
vocal fold paralysis. Laryngoscope 115:1691–1696. 42 Yoshino A, Ebihara T, Ebihara S et al. (2001) Daily oral
27 Randhawa PS, Ramsay AD, Rubin JS (2008) care and risk factors for pneumonia among elderly
Foreign body reaction to polymethylsiloxane gel nursing home patients. J Am Med Assoc 286:2233–2236.
(Bioplastique™) after vocal fold augmentation. 43 Ku PK, Abdullah VF, Vlantis AC et al. (2009) ‘Steam-
J Laryngol Otol 122:750–753. boat’ supraglottic laryngoplasty for treatment of
28 Baijens L, Speyer R, Linssen M et al. (2007) Rejection chronic refractory aspiration: a modification of Biller’s
of injectable silicone ‘Bioplastique’ used for vocal fold technique. J Laryngol Otol 123(12):1360–1363.
augmentation. Eur Arch Otorhinolaryngol 264:565–568. 44 de Almeida JR, Park RC, Villanueva NL et al. (2014)
29 King JM, Simpson CB (2007) Modern injection A  reconstructive algorithm and classification system
augmentation for glottic insufficiency. Curr Opin for transoral oropharyngeal defects. Head Neck
Otolaryngol Head Neck Surg 15:153–158. 36(7):934–941.
30 Lee SW, Son YI, Kim CH et al. (2007) Voice outcomes 45 Allen J, White CJ, Leonard RJ et al. (2010) Effect of
of polyacrylamide hydrogel injection laryngoplasty. cricopharyngeal muscle surgery on the pharynx.
Laryngoscope 117:1871–1875. Laryngoscope 120:1498–1503.

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46 Allen J,Belafsky PC (2010) Endoscopic cricopharyngeal suspension and cricopharyngeal myotomy. Laryngoscope
myotomy for Zenker diverticulum using the harmonic 117:1343–1348.
scalpel. Ear Nose Throat J 89:216–218. 54 Aviv JE, Mohr JP, Blizter A et al. (1997) Restoration
47 Safdar A, Curran A, Timon CV (2004) Endoscopic of laryngopharyngeal sensation by neural anastomosis.
stapling vs conventional methods of surgery for Arch Otolaryngol Head Neck Surg 123:154–160.
pharyngeal pouches: results, benefits and modifications. 55 Oppenlander ME, Orringer DA, La Marc F et al. (2009)
Ir Med J 97:75–76. Dysphagia due to anterior cervical hyperosteophytosis.
48 Van Eeden S, Lloyd RV, Tranter RM (1999) Surg Neurol 72:266–270.
Comparison of the endoscopic stapling technique with 56 Kos MP, van Royen BJ, David EF et al. (2009) Anterior
more established procedures for pharyngeal pouches: cervical osteophytes resulting in severe dysphagia
results and patient satisfaction survey. J Laryngol Otol and aspiration: two case reports and literature review.
113:237–240. J Laryngol Otol 123:1169–1173.
49 Kos MP, David EF, Klinkenberg-Knol EC et al. (2010) 57 Carlson ML, Archibald DJ, Graner DE et al. (2011)
Long-term results of external upper esophageal Surgical management of dysphagia and airway
sphincter myotomy for oropharyngeal dysphagia. obstruction in patients with prominent ventral cervical
Dysphagia 25:169–176. osteophytes. Dysphagia 26:34–40.
50 Ozgursoy OB, Salassa JR (2010) Manofluorographic 58 Mok P, Woo P, Schaefer-Mojica J (2003)
and functional outcomes after endoscopic laser Hypopharyngeal pharyngoplasty in the management
cricopharyngeal myotomy for cricopharyngeal bar. of pharyngeal paralysis: a new procedure. Ann Otol
Otolaryngol Head Neck Surg 142:735–740. Rhinol Laryngol 112:844–852.
51 Pitman M, Weissbrod P (2009) Endoscopic CO2 laser 59 Bergamini G, Alicandri-Ciufelli M, Molteni G
cricopharyngeal myotomy. Laryngoscope 119:45–53. et al. (2009) Rehabilitation of swallowing with
52 Mortensen M, Schaberg MR, Genden EM et al. polydimethylsiloxane injections in patients who
(2010) Transoral resection of short segment Zenker’s underwent partial laryngectomy. Head Neck 31:​
diverticulum and cricopharyngeal myotomy: an 1022–1030.
alternative minimally invasive approach. Laryngoscope 60 Broniatowski M, Moore NZ, Grundfest-Broniatowski
120:17–22. S et al. (2010) Paced glottic closure for controlling
53 Fujimoto Y, Hasegawa Y, Y  amada H et al. (2007) aspiration pneumonia in patients with neurologic
Swallowing function following extensive resection deficits of various causes. Ann Otol Rhinol Laryngol
of oral or oropharyngeal cancer with laryngeal 119:141–149.

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 CHAPTER 9

Laryngeal trauma
Guri Sandhu & S. A. Reza Nouraei

Introduction
The principal function of the larynx is to protect the external trauma. Laryngeal trauma can disrupt one or
airway and in humans it plays a part in voice production all of the functions of the larynx, and as the ‘gateway’
and the Valsalva manoeuvre. In common with other to the lungs, injury can be acutely life-threatening. 2–4
mammals, the larynx lies high in the neck at birth. In Laryngeal trauma often co-exists with cervical and
humans it starts to descend within the first few months intracranial injuries, and frequently forms part of a
of life to eventually lie at the level of the sixth cervical multiple trauma scenario.4 It is vital, therefore, that all
vertebra. Charles Darwin noted in On the Origins of patients with suspected laryngeal injury be managed
Species that homo sapiens is the only animal species by a multidisciplinary trauma team. The role of the
whose upper aerodigestive tract fails to adequately otolaryngologist is to detect and appropriately manage
serve its principal evolutionary functions of preventing the acute laryngeal injury and minimise long-term
aspiration and acting as the gateway to the lungs.1 This sequelae.4–6 Laryngeal trauma can be broadly divided
adult position of the larynx allows humans to meet the into external trauma, which can be blunt or penetrating,
requirements of complex speech through resonance and internal trauma, which can be caused by iatrogenic,
and articulation, but also leaves it more exposed to thermal, caustic or foreign body injuries.

External laryngeal trauma

Aetiology/pathogenesis Laryngeal injury can be confounded by the process of
laryngeal calcification, which begins during the third
External laryngeal trauma has a population incidence of
decade of life, is more pronounced in males, and can lead to
1 in 137,000 in adults4 and accounts for 0.5% of trauma
fracture (Figure 9.1) comminution.15
admissions in children.7 The larynx, which is superiorly,
Over the last 50 years, with improvements in public
inferiorly, posteriorly and laterally well protected by the
education, reductions in speed limits and improved
mandible, sternum, the cervical spine and strap muscles
vehicle design with increased use of airbags and seatbelts,
of the neck, is susceptible to crushing anterior cervical
the number of blunt laryngeal trauma cases has declined.
trauma. Rapid motor vehicle deceleration can thrust the
Penetrating laryngeal trauma, which is due predominantly
neck against the steering wheel or dashboard in a person
to interpersonal violence or war, is becoming the
not wearing a seatbelt. Another important mechanism of
predominant form of laryngeal trauma2,3,6,16–24 in the USA,
injury is clothes line injury, in which a rider encounters a
although in the UK blunt trauma still dominates.25
fixed horizontal object at neck level. Clothes line injuries
are often associated with major neck trauma, which may
not be initially apparent8,9, and frequently cricotracheal Clinical signs and symptoms
separation. Suicidal or homicidal strangulations can Clinical presentation of laryngeal trauma ranges from
also cause laryngeal trauma. Homicidal strangulation cardiopulmonary arrest due to airway obstruction to subtle
is more likely to cause cricotracheal separation and changes in voice quality. The commonest presenting feature
neurovascular trauma when compared with suicidal of laryngeal trauma is hoarseness (85%), followed by dysphagia
strangulation.10 All strangulation injuries can cause loss (52%), anterior cervical pain (42%), breathlessness (21%) and
of airway due to laryngeal oedema 12–24 hours after the haemoptysis (18%).5 Symptoms will vary depending on
event, despite minimal initial findings.11–13 Strangulation the nature and degree of injury and the time at which the
injuries may also be associated with thyroid and hyoid patient presents after the event. Frequently, symptoms may
fractures, rupture of the thyrohyoid membrane and torn not correlate with the extent of injury but the attending
strap muscles.14 physician must maintain a high index of suspicion.

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 Laryngeal trauma

a b

d
Figure 9.1 Larynx (a) exposed to external trauma (b). A cartilaginous larynx may develop a fracture (c) but rebound into its original
position, whereas a calcified larynx may suffer multiple fractures and remain compressed (d).

Initial management
Examination and initial management of laryngeal trauma
should follow Advanced Trauma Life Support guidelines
to ensure that concomitant injuries are not missed.4 The
overriding priority is to establish a safe airway with cervical
spine protection and this may necessitate performing
an emergency tracheostomy under local anaesthesia.
Endotracheal intubation is not favoured in this situation as
it can exacerbate a laryngeal injury26 and precipitate total
airway obstruction. If endotracheal intubation has been
performed, it is converted at the earliest opportunity to a
tracheostomy to prevent long-term laryngeal injury. No
manipulation of the neck is permissible until the stability of
the cervical spine has been confirmed.
The neck is inspected for evidence of injury such as skin
abrasions, bruising and entry and exit wounds in penetrating
trauma, and is palpated for crepitations, laryngeal tenderness
and any obvious changes in laryngeal anatomy such as loss
of the prominence. Open wounds should not be explored
at this stage as instrumentation may restart haemorrhage. Figure 9.2 Axial CT scan of a larynx demonstrating multiple
Flexible nasendoscopy is then performed, and the oropharynx thyroid cartilage fractures and surgical emphysema.
and hypopharynx are examined for injuries. The laryngeal
mucosa is examined for lacerations and haematomas, and High definition CT is performed in all patients
particular care is taken to assess the vibratory edge of the vocal presenting with ‘impending airway obstruction’ once
cords and the anterior commissure. Arytenoid adduction is the airway has been secured (Figure 9.2), and in those
examined during phonation; abduction is assessed by asking patients with a ‘stable airway’ who are found on flexible
the patient to say ‘eee’ followed by a sniff. Impairment of nasendoscopy to have endolaryngeal abnormalities.
arytenoid mobility may be secondary to structural damage or Imaging may reveal further laryngeal injuries and, most
due to recurrent laryngeal nerve injury. Note is taken of any importantly, confirm the stability of the cervical spine.
exposed or protruded cartilage or submucosal distortion of This is a particularly pertinent consideration as up to 13%
the framework. A sign of cartilaginous injury is failure of the of patients with laryngeal trauma can have an associated
vocal cords to meet in the same horizontal plane. cervical spine injury and the spinal injury may be masked

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 External laryngeal trauma

Table 9.1  Laryngotracheal injury classification by Schaefer–Fuhrman

Group I Minor endolaryngeal haematoma without detectable fracture
Group II Oedema, haematoma, minor mucosal disruption without exposed cartilage
Group III Massive oedema, mucosal tears, exposed cartilage, cord immobility
Group IV As group III, with more than two fracture lines or massive trauma to laryngeal mucosa
Group V Complete laryngotracheal separation

by the presence of a distracting laryngeal injury.4,27 CT

scanning can be deferred only in those patients where
the history makes a significant injury unlikely and where
there are minor physical findings. Laryngeal trauma
can be classified according the Schaefer–Fuhrman26,28
(Table 9.1) or the Lee–Eliashar systems.29

Management
The first priority in managing laryngeal trauma is to assess
and secure the airway while protecting the cervical spine.
A stepwise approach should be taken to securing the airway
based on information available at the different stages of
clinical assessment. A stridulous patient with respiratory
distress at presentation should immediately proceed to have a
tracheostomy under local anaesthesia. If the airway is judged
to be stable following initial history and examination, the
patient has a flexible nasendoscopy. In a small number of
cases, unexpected airway-encroaching injuries are identified
at this stage and the patient proceeds to have a tracheostomy. Figure 9.3 Glottic and subglottic stenosis due to failure to repair
More subtle endolaryngeal injuries are further assessed with laryngeal trauma early and prolonged endotracheal intubation.
CT and again, if airway-encroaching injuries are identified,
the patient proceeds to have a tracheostomy. a proton pump inhibitor and, if the laryngeal mucosa has
The decision on the most appropriate therapy for been breached, are also given prophylactic broad-spectrum
laryngeal trauma rests on assessing the stability of, and the antibiotics.
extent of injury to, the laryngeal framework, the extent of Patients with more significant injuries require surgical
mucosal injuries, the presence or otherwise of injury to the intervention. The optimal timing of repair is a subject of
vibratory apparatus and the integrity of the laryngotracheal debate and in multiple trauma the patient’s laryngeal surgery
junction. Jewett and colleagues4 demonstrated that 37% of may need to be coordinated with other surgeries. The
patients with laryngeal trauma could be managed with no authors aim to repair all laryngeal injuries within 24 hours
airway intervention and a further one-sixth of patients only of presentation, and are reluctant to accept delays beyond
required a tracheostomy. this. Delays in treatment can lead to granulation and scar
Patients with a normal endolarynx on nasendoscopy, formation, with the potential to progress to laryngeal stenosis
and patients with minimal endolaryngeal abnormalities (Figure 9.3), a more difficult surgical problem to correct.
and a stable laryngeal framework, whose airway patency All patients who are not managed conservatively should
has been confirmed by CT, can be conservatively managed. undergo a microlaryngoscopy and tracheoscopy, direct
Conservative management consists of a minimum of pharyngoscopy and direct oesphagoscopy. In a proportion
a 24-hour admission to a high-dependency unit, with of patients, definitive endolaryngeal treatment can be
regular observations, serial flexible nasendoscopy and use undertaken endoscopically. Haematomas can be drained,
of humidified oxygen. A mixture of oxygen and helium mucosal and selected vocal cord lacerations can be repaired
should be on standby in case respiratory embarrassment and dislocated cricoarytenoid joints (CAJs) can be reduced.
develops. The patient’s head is elevated to reduce further If there have been extensive injuries to opposing laryngeal
oedema and corticosteroids are administered if the patient mucosal surfaces, stents can also be deployed endoscopically
presents within 24 hours of injury.All patients are prescribed to prevent adhesions.30

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 Laryngeal trauma

The main indications for open repair are unstable The indications for stenting are controversial because
or comminuted laryngeal fractures, cricotracheal the need for endolaryngeal support needs to be considered
separation, detachment of the anterior commissure or against the potential for further mucosal injury.The authors’
extensive mucosal disruption. For open exploration, a primary indication for stenting is significant framework
transverse neck incision is placed over the cricoid and comminution. Stents can also be used to prevent anterior
the subplatysmal flaps are elevated. Strap muscles are commissure webbing  in cases of bilateral vocal fold
separated in the midline and retracted. In a proportion epithelial loss. The authors prefer to use soft silastic stents
of patients with unstable laryngeal fractures but with for this purpose in order to minimise further mucosal
minimal or endoscopically treatable endolaryngeal injury and foreign body reaction associated with the use
injuries, a thyrotomy can be avoided. Repair of the of stents fashioned from endotracheal tubes. Endolaryngeal
anterior commissure, or significant endolaryngeal injuries, stents are commercially available but can also be fashioned
is achieved through an anterior vertical laryngofissure. from the vertical limb of a Mongtomery T-tube, which is
However, a paramedian fracture close to the midline may oversewn at the top. The stent is held in place with a 2-0
also be used. Haematomas are evacuated and mucosa tears Prolene suture through the anterior stent and laryngeal
repaired with 5-0 or 6-0 absorbable sutures. Mucosal loss ventricles and knotted over the larynx following closure
can often be reconstructed with local mucosal flaps and in of the laryngofissure. With severe damage and stripping of
particular, posterior commissure injuries can and should the internal laryngeal mucosa, the authors prefer to stitch
be reconstructed with piriform fossa or supraglottic a superficial skin graft on to the laryngeal stent with the
mucosa to prevent laryngeal stenosis.The anterior margins epidermal surface against the stent (Figure 9.5). The stent
of the vocal folds are attached to the anterior limit of the is removed endoscopically 10–14 days later. The securing
thyroid cartilage or its outer perichondrium using a slow- suture can be cut flush with the endoluminal airway or
absorbing monofilament suture. It is very important to removed via a small neck incision.
re-establish the appropriate height of the vocal folds to Vocal cord mobility can usually be determined during
optimise voice outcomes. Thyroid cartilage fractures are preoperative flexible laryngoscopy. CAJ mobility can be
repaired using permanent or resorbable miniplates, with assessed preoperatively, but definitive assessment of joint
at least two points of fixation either side of the fracture mobility requires microlaryngoscopy and instrumentation.
line (Figure 9.4). Even in the older patient, the cricoid Vocal cord immobility due to CAJ dislocation can often
arch does not fully calcify and can be repaired using suture be managed with endoscopic manipulation and reduction.
material alone. Recurrent laryngeal nerves can be severed in penetrating
trauma or during cricotracheal separation, or crushed
during laryngeal trauma. Only if a complete palsy is
confirmed should exploration of the affected nerve be
considered. Anatomically intact nerves should be allowed
to regenerate. Where possible, severed nerves should be
repaired in a tension-free manner. If this is not possible,
then a cable graft using the greater auricular or sural nerve
should be considered. The other option is to consider
ansa cervicalis to recurrent laryngeal nerve repair. Nerve
repairs do not restore the intricate motor function of the
larynx, but may provide sufficient muscle tone to improve
vocalisation.
In cases of cricotracheal separation (Figures 9.6a, b),
following surgical exposure, a tracheostomy is fashioned
or moved to a healthy part of the lower trachea prior to
reanastomosis. During the surgery a small endotracheal
tube is placed through the tracheostomy for ventilation and
is replaced with a small tracheostomy tube at the end of the
procedure.The repair begins with the posterior anastomosis
using a combination of 3-0 absorbable sutures working
towards the anterior trachea. All knots are extraluminal and
Figure 9.4 Thyroid cartilage fracture repair with miniplates and the sutures run through the submucosal plane. Avascular
cricoid fracture repair with suture material. and damaged tissue is resected. If there is an associated crush

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 External laryngeal trauma

a   b
Figures 9.5a, b Piece of silastic T-tube sewn shut at one end to use as a laryngeal stent (a). In cases where there is significant loss of laryngeal
mucosa, a superficial skin graft (epidermis against stent) can be sewn over the stent (b).

a   b
Figures 9.6a, b CT scan demonstrating cricotracheal separation (a). Diagram to illustrate the injury (b).

injury to the trachea, a temporary soft silastic stent may is nursed in head-up position to minimise oedema and
need to be placed in the lumen prior to anastomosis. In standard tracheostomy care is provided. Early ambulation
cases of massive laryngeal injury with significant tissue loss, is encouraged. Stents are removed at 10–14 days and the
a partial or total laryngectomy may be indicated, although patient is decannulated. Regular endoscopic examinations
this is rarely required.23 are undertaken and granulation tissue is removed to prevent
Any repairs to the vocal folds should be followed by long-term scarring. In patients with cricotracheal separation,
strict voice rest for 48–72 hours. A nasogastric tube should the neck is kept in flexion for 7 days postoperatively to
be inserted at the time of surgery and should remain prevent traction on the anastomosis. A large monofilament
in situ until the safety of swallowing is confirmed.All patients suture from the submental skin to the anterior chest skin,
with mucosal tears should be placed on anti-reflux therapy placed at the time of surgery, may be necessary for the first
and prophylactic broad-spectrum antibiotics. The patient few postoperative days.The tracheostomy can be removed at

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 Laryngeal trauma

7 days and the airway stent can be removed endoscopically Furthermore, laryngeal mucosa is less firmly adherent to the
at 10–14 days. Management protocols for laryngotracheal cartilaginous framework in infants and children compared
trauma are summarised in Figure 9.7.31 with adults.This combination of factors means that while the
paediatric larynx is better shielded and is therefore less liable
Paediatric external laryngeal trauma to injury, if an injury does occur, it is more likely to result
The neonatal larynx lies at the level of C3 and descends in loss of airway due to mucosal oedema and haematoma
during the first 3 years of life to its adult position at the formation.7,23 Furthermore, it is usually not possible to
level of C6. The paediatric larynx is smaller in absolute perform tracheostomies under local anaesthetic in children.
and relative dimensions compared with the adult larynx. The child is therefore managed along the same lines as a

Suspicion of
laryngeal
trauma

History and examination

Impending
airway Airway stable
obstruction

Tracheostomy/
Airway Abnormal
convert ET tube CT scan FNE
encroachment endolarynx
to tracheostomy

CT scan
(if not already
done)

No airway
encroachment

MLT/DP/DO
Normal
endolarynx

Unstable/ Unstable fracture(s) Endolarynx intact

Cricotracheal comminuted fracture Significant mucosal Small haematoma
separation Massive mucosal injury/damaged and/or laceration
injury vibratory apparatus Stable framework

Débridement ORIF * ORIF Conservative

Primary anastomosis Thyrotomy and repair Thyrotomy/ management

Endolaryngeal stent endoscopic repair (with serial FNE)

* In rare cases, partial/total laryngectomy may be necessary.

MLT/DP/DO: Microlaryngoscopy and tracheoscopy/direct pharyngoscopy/direct oesophagoscopy.

ORIF: Open reduction and internal fixation. FNE: Flexible nasendoscopy CT: Computed tomography
Figure 9.7 Summary of laryngotracheal trauma management protocols.

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 Caustic/thermal laryngeal trauma

patient with acute epiglottitis. The surgeon is prepared for

an emergency tracheostomy but in most cases the airway
can be secured with an endotracheal tube or ventilating
bronchoscope, followed promptly by a tracheostomy under
general anaesthesia. CT may then be considered prior to
airway reconstruction. As with adult patients, selected, more
limited injuries can be managed endoscopically and without
tracheostomies.32,33

Sequelae of laryngeal trauma

Long-term morbidity may be due to laryngeal stenosis,
dysphonia or aspiration. These long-term injuries may
not become apparent for up to 12 months after the initial
injury. Vocal cord paralysis should be carefully observed
for recovery and in patients with a normal vibratory
apparatus structure and unilateral vocal cord paralysis,
definitive medialisation procedures should only be
attempted after 9–12 months. In the interim, the voice
can be improved with a temporary medialisation. In
cases of bilateral vocal cord palsy causing glottis airway
Figure 9.8 Scarring and granulation causing glottis airway
compromise, consideration should be given to retaining compromise.
the tracheostomy in preference to performing an early
laser arytenoidectomy, in anticipation of return of
vocal cord function. Laryngeal stenosis due to posterior
commissure or tracheal granulation tissue should be Outcome of external laryngeal trauma
promptly treated with intralesional steroid injections and This is dependent both on the nature and severity of the
reduction of granulation tissue. The granulation tissue original injury, and on whether the injury was promptly
should not be allowed to mature into a scar, as this is a recognised and adequately treated. Schaefer and, more
much more difficult problem to manage.34 In the authors’ recently, Luutilainen and colleagues found that the voice,
experience, the most difficult injuries to manage are but not the airway outcome, correlates with the severity of
laryngeal inlet obliteration followed by interarytenoid the initial injury as determined by Schaefer’s classification
scarring or webbing (Figure 9.8). The treatment of system (see Table 9.1)5,23, while Bent and colleagues17
glottic stenosis is almost always a compromise between found that intervention within 48 hours was associated
voice, airway and swallowing, and gains in one domain are with an improved outcome. Delays in intervention can lead
often at the expense of another. to complete laryngotracheal stenosis (LTS).

Caustic/thermal laryngeal trauma

Aetiology/pathogenesis Ingestion of alkali causes liquefaction necrosis of muscle,
collagen and lipids and creates an injury that becomes
Upper aerodigestive tract injury due to ingestion of caustic
more severe with time. By contrast, acids cause coagulation
substances occurs in 5,000 to 15,000 persons in the United
necrosis of the superficial tissues. Caustic substance ingestion
States annually and the majority of injuries are caused by
is virtually always accidental in children where small amounts
ingestion of alkaline substances.35 The larynx is involved in
of liquids are taken, but are almost always due to attempted
approximately 40% of cases.36 Thermal injury to the larynx
suicide in adults and is associated with ingestion of large
is a sequela of inhaling superheated air. Inhalation burns
volumes of liquid.36 The type of liquid taken varies widely
occur in 30% of all burn patients and 20% of patients with
with geography, with alkaline and acid ingestion being
inhalation injury have extensive laryngeal injury. A further
more common in the developed and developing countries,
7% of patients with inhalation injury have both laryngeal
respectively.35,38 Inhalation injury is typically a consequence
and tracheobronchial injuries.37

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 Laryngeal trauma

of fires in closed spaces and causes a six-fold increase in the

mortality rate associated with the burn.37
Management
All patients with caustic or thermal laryngeal injuries should
be admitted for a minimum of 24 hours for airway observation.
The first priority is establishment of a safe airway, followed
by cardiovascular resuscitation as per standard burns care
protocols.The presence of facial or body burns, soot in the oral
cavity and endoscopic finding of laryngeal oedema predict
the need for airway intervention.39 Endotracheal intubation
plays an even lesser role in managing these patients, compared
with external laryngeal trauma patients. Arevalo-Silva and
colleagues found a 100% association between endotracheal
intubation and subsequent tracheostomy for airway stenosis
in patients with laryngeal injury due to caustic ingestion.36
The situation with airway management in thermal injuries is
somewhat less clear, as there have been reports of increased
stenosis rates with tracheostomy, as opposed to intubation, in
patients with inhalation injury.40 However, unless there are
Figure 9.9 Scarring and stenosis of the glottis due to thermal
strong contraindications to performing a tracheostomy, such
damage from inhalation of hot gases during a house fire.
as extensive cervical burns, the authors maintain the view
that as glottic stenosis has a far worse prognosis than tracheal
stenosis, a possible increase in the rate of post-tracheostomy is reported to be greater than those associated with post-
stomal stenosis is an acceptable trade-off. intubation LTS41, with dysphonia being present in as many
If patients are to undergo a microlaryngoscopy, as 70% of patients with inhalation injuries 16–25 years after
tracheobronchoscopy or oesophagoscopy, this should be the initial injury.42
within 24 hours of injury. Beyond this period, oedema The more severe cases of caustic ingestion may end
and ulceration are more marked and instrumentation may up with completely stenosed larynges and stenosis of
exacerbate subsequent problems. The upper aerodigestive the pharynx and oesophageal inlet. The swallow and
tract should be irrigated in cases of caustic injury to secretions may be restored to some degree with colonic
remove any residual substances. Further treatment is interposition or free jejunal flaps to re-establish a conduit
dependent on the nature and extent of injuries found and from the pharynx to the stomach. However, even though
the consequences of healing and scarring. the laryngeal stenosis may be just at the level of the
supraglottis, attempts to improve the airway will often lead
Sequalae of caustic/thermal laryngeal injuries to chronic aspiration. Most of these patients will retain a
Caustic and thermal injuries (Figure 9.9) can cause tracheostomy and where there is no voice a laryngectomy
laryngeal and tracheal airway strictures, whose severity may be considered.

References
1 Darwin C (1859) (ed) On the Origin of Species. Facsimile 5 Luutilainen M, Vintturi J, Robinson S et al.
(1964) Havard University Press, Cambridge, MA. (2007) Laryngeal fractures: clinical findings and
2 Bhojani RA, Rosenbaum DH, Dikmen E et al. (2005) considerations on suboptimal outcome. Acta
Contemporary assessment of laryngotracheal trauma. Otolaryngol 128:213–218.
J Thorac Cardiovasc Surg 130:426–432. 6 Minard G, Kudsk KA, Croce MA et al. (1992)
3 Gussack GS, Jurkovich GJ, Luterman A (1986) Laryngotracheal trauma. Am Surg 58:181–187.
Laryngotracheal trauma: a protocol approach to a rare 7 Ford HR, Gardner MJ, Lynch JM (1995)
injury. Laryngoscope 96:660–665. Laryngotracheal disruption from blunt pediatric neck
4 Jewett BS, Shockley WW, Rutledge R (1999) injuries: impact of early recognition and intervention
External laryngeal trauma analysis of 392 patients. on outcome. J Pediatr Surg 30:331–334.
Arch Otolaryngol Head Neck Surg 125:877–880.

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 References

8 Close DM (1981) Traumatic avulsion of the larynx. 27 Hoffman JR, Mower WR, Wolfson AB et al. (2000)
J Laryngol Otol 95:1157–1158. Validity of a set of clinical criteria to rule out injury
9 Graham J, Dick R, Parnell D et al. (2006) to the cervical spine in patients with blunt trauma.
Clothesline  injury mechanism associated with National Emergency X-Radiography Utilization
all-terrain vehicle  use by children. Pediatr Emerg Study Group. New Engl J Med 343:94–99.
Care 22:45–47. 28 Fuhrman GM, Stieg FH, Buerk CA (1990) Blunt
10 Maxeiner H, Bockholdt B (2003) Homicidal and laryngeal trauma: classification and management
suicidal ligature strangulation: a comparison of the protocol. J Trauma 30:87–92.
post-mortem findings. Forensic Sci Int 14:60–66. 29 Lee WT, Eliashar R, Eliashar I (2006) Acute external
11 Rejali SD, Bennett JD, Upile T et al. (1998) Diagnostic laryngotracheal trauma: diagnosis and management.
pitfalls in sports related laryngeal injury. Br  J  Sports Ear Nose Throat J 85:184.
Med 32:180–181. 30 Mace A, Sandhu GS, Howard DJ (2005) Securing
12 Pennington CL (1972) External trauma of the larynx tracheal stents: a new and simple method. J  Laryngol
and trachea. Immediate treatment and management. Otol 119:207–208.
Ann Otol Rhinol Laryngol 81:546–554. 31 Sandhu G, Nouraei S (2010) Laryngeal and
13 Nahum AM, Siegel AW (1967) Biodynamics of injury esophageal trauma. In: Cummings Otolaryngology Head
to the larynx in automobile collisions. Ann Otol Rhinol & Neck Surgery, 5th edn. (ed. P Flint) Mosby Elsevier,
Laryngol 76:781–785. Philadelphia, pp. 933–942.
14 Becker M, Leuchter I, Platon A et al. (2014) Imaging of 32 Myer C, Orobello P, Cotton RT et al. (1987) Blunt
laryngeal trauma. Eur J Radiol 83(1):142–154. laryngeal trauma in children. Laryngoscope 97:1043–1048.
15 Mupparapu M, Vuppalapati A (2005) Ossification 33 Elmaraghy CA, Tanna N, Wiet GJ et al. (2007)
of laryngeal cartilages on lateral cephalometric Endoscopic management of blunt pediatric laryngeal
radiographs. Angle Orthod 75:196–201. trauma. Ann Otol Rhinol Laryngol 116:192–194.
16 Danic D, Prgomet D, Sekelj A et al. (2006) External 34 Nouraei SAR, Singh A, Patel A et al. (2006) Early
laryngotracheal trauma. Eur Arch Otorhinolaryngol endoscopic treatment of acute inflammatory airway
263:228–232. lesions improves the outcome postintubation airway
17 Bent JP, Silver JR, Porubsky ES (1993) Acute laryngeal stenosis. Laryngoscope 116:1417–1421.
trauma: a review of 77 patients. Arch Otolaryngol Head 35 Erdoğan E, Eroğlu E, Tekant G et al. (2003)
Neck Surg 109:441–449. Management of esophagogastric corrosive inuries in
18 Cohn AM, Larsonm DL (1976) Laryngeal review: a children. Eur J Pediatr Surg 13:289–293.
critical review. Arch Otolaryngol 102:166–170. 36 Arevalo-Silva C, Eliashar R, Wohlgelernter J et al.
19 Francis S, Gaspard DJ, Rogers N et al. (2002) Diagnosis (2006) Ingestion of caustic substances: a 15-year
and management of laryngotracheal trauma. J Natl experience. Laryngoscope 116:1422–426.
Med Assoc 94:21–24. 37 Nottet JB, Duruisseau O, Herve S et al. (1997)
20 Harris HH, Ainsworth JZ (1965) Immediate Inhalation burns: apropos of 198 cases. Incidence of
management of laryngeal and tracheal injuries. laryngotracheal involvement. Ann Otolaryngol Chir
Laryngoscope 75:1103–1115. Cervicofac 114:220–225.
21 Harris HH, Tobin HA (1970) Acute injuries of the 38 Ramasamy K, Gumaste VV (2003) Corrosive ingestion
larynx and trachea in 49 patients (observations over a in adults. J Clin Gastroenterol 37:119–124.
15-year period). Laryngoscope 80:1376–1384. 39 Madnani DD, Steele NP, de Vries E (2006) Factors that
22 Lambert GE, McMurry GT (1976) Laryngotracheal predict the need for intubation in patients with smoke
trauma: recognition and management. JACEP inhalation injury. Ear Nose Throat J 85:278–280.
5:883–887. 40 Lund T, Goodwin CW, McManus WF et al. (1999) Upper
23 Schaefer SD (1992) The acute management of airway sequelae in burn patients requiring endotracheal
external laryngeal trauma. A 27-year experience. Arch intubation or tracheostomy. Ann Surg 201:374–382.
Otolaryngol Head Neck Surg 118:598–604. 41 Gaissert HA, Lofgren RH, Grillo HC (1993) Upper
24 Shaia FT, Cassady CL (1972) Laryngeal trauma. Arch airway compromise after inhalation injury. Complex
Otolaryngol 95:104–108. strictures of the larynx and trachea and their
25 Maran A, Stell P, Murray J et al. (1981) Early management management. Ann Surg 218:672–678.
of laryngeal injuries. J Royal Soc Med 74:656–660. 42 Casper JK, Clark WR, Kelley RT et al. (2002) Laryngeal
26 Schaefer S (1982) Primary management of laryngeal and phonatory status after burn/inhalation injury: a long
trauma. Ann Otol Rhinol Laryngol 91:399–402. term follow-up study. J Burn Care Rehabil 23:235–243.

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 CHAPTER 10

Laryngotracheal stenosis
Guri Sandhu & S. Mahmoud Nouraei

Introduction
The larynx and tracheobronchial tree form a conduit and a dysfunctional larynx can affect swallowing safety.
between the external environment and the lungs, Due to medical advances, more patients are surviving
allowing for the transportation and exchange of gases and periods of ventilation on intensive care units (ICUs).1,2 As
the clearance of pulmonary secretions. In all mammals, a consequence, the incidence of laryngotracheal injury is
including the human infant, the pharyngeal airway is short probably increasing but remains unknown. Endotracheal
and the epiglottis and the soft palate are anatomically intubation injury is identified as the most common cause
related, allowing simultaneous swallowing and breathing. of acquired laryngotracheal stenosis (LTS) in the developed
The human larynx has evolved to protect the airway from world. Prospective studies have demonstrated some sort of
aspiration, perform a Valsalva manoeuvre and, more recently, intubation injury in all patients who have been ventilated.3
as the organ facilitating phonation. This requires the adult Although the risk of significant laryngeal injury correlates
larynx to sit lower in the neck, which allows humans to meet with duration of intubation, there does not appear to be
the requirements of complex speech through resonance and a safe limit and significant injuries have been observed
articulation. after only 8 hours of intubation in adults and 1 week in
One hundred years ago the principal causes of airway children.4 A significant airway injury has been described
stenosis were infections such as tuberculosis, diphtheria in up to 48% of patients at extubation on the ICU. Most
and syphilis. The patterns of airway injury changed during of these injuries resolve but in some patients healing by
the 20th century following the discovery of antimicrobials, fibrosis and contracture may produce symptoms weeks and
endotracheal tube anaesthesia and the development of months after discharge from the ICU. The incidence of
intensive care medicine. chronic airway stenosis following prolonged ventilation is
Airway stenosis can have a significant impact on the estimated at 5%.5
quality of life and sometimes on life itself. Abnormal The narrowest site of the paediatric larynx is the
narrowing of the laryngotracheal complex causes subglottis and consequently this is the principal site of LTS,
breathlessness, especially during physical activity. Retention whereas in adults, injuries are spread between the glottis, the
of pulmonary secretions may lead to lung infection or subglottis and the trachea.
collapse. Laryngeal stenosis can interfere with phonation

Physiology and anatomy of airway stenosis

Most surgeons size the airway using the Myer–Cotton as diameter decreases. The resistance to airflow is also
grading system (Figure 10.1), which is based on the surface proportional to the length of the stenosis. However, an area
area of the stenosis as a percentage of the normal airway.6 of airway stenosis also produces turbulence, which adds to
The Myer–Cotton system allows for easy stratification resistance but cannot easily be calculated.
of airway injury but does not take into account airflow
physiology. In laminar airflow, airway resistance is dictated 8nl
R=
by the diameter of the airway and by the density of the πr 4
inspired gas (Poiseuille’s law, see below). The fourth power
in the denominator means the resistance increases rapidly R = resistance; n = viscosity; l = length; r = radius.

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 Laryngotracheal stenosis

Grade I No obstruction 50% obstruction

Grade II 51% obstruction 70% obstruction

Grade III 71% obstruction 99% obstruction

Grade IV No detectable lumen

Figure 10.1 Myer–Cotton grading system for subglottic stenosis.

Paediatric laryngotracheal stenosis

Paediatric LTS is a well-researched area of laryngotracheal both. The procedure can be performed as a two-stage
airway compromise. The majority of cases are acquired, operation, where a stent is placed in  the  airway at
involve the subglottis and are due to periods of endotracheal reconstruction (first stage) with a covering tracheostomy.
tube ventilation.7 The stent and tracheostomy are removed at a second stage.
Treatment strategies include airway augmentation with In a single-stage procedure there is no tracheostomy;
rib grafts as well as tracheal and cricotracheal resections. instead, the child is kept ventilated with an endotracheal
Most cases of grade I and some smaller grade II stenoses do tube for a week. The endotracheal tube doubles as a stent.
not usually require airway surgery, as the child’s symptoms LTR is suited to grade II or III SGS with or without
will generally improve with growth. A distinction should minor glottic involvement. A partial cricotracheal
also be made between early inflammatory subglottic resection (PCTR) is indicated in cases of grades III and
stenosis (SGS) and a mature stenosis, which is comprised IV SGS and salvage surgery after failed LTR. An extended
principally of scar tissue. The former will often respond to partial cricotracheal resection (E-PCTR) includes, in
endoscopic surgery utilising injections of corticosteroids, addition, a posterior cricoid cartilage split with a costal
radial cuts with a sickle knife and gentle balloon cartilage interposition and stenting for 2–3 months.
dilatation.8 A  covering tracheostomy is usually indicated. E-PCTR
Laryngotracheal reconstruction (LTR) uses rib is also suitable for congenital laryngeal atresia and cases of
cartilage to augment the anterior or posterior airway, or transglottic stenosis.9

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 Diagnosis of laryngotracheal stenosis

Diagnosis of laryngotracheal stenosis

Generally, the diagnosis is made based on the history and sensitive to stenosis severity and can also be used to quantify
symptomology. The patient attending the airway clinic has treatment response.
in most cases already been diagnosed with airway stenosis CT scanning is the preferred imaging modality for
and is experiencing a variable degree of dyspnoea. As a part adults and children with airway damage, although some
of the history it is important to ask about the voice and authorities still use fluoroscopic techniques in children.The
swallowing, but also co-existing medical conditions such problem with assessing airway stenosis on a CT scan relates
as diabetes, vasculitis and other airway disorders such as to the fact that CT imaging is a form of sampling. Unless
chronic obstructive pulmonary disease and ‘true’ asthma. fine cuts are made through the airway at 1–2 mm, the apex
Obesity is associated with a poor outcome following airway of the stenosis may be missed and the degree of stenosis
surgery10 and the body mass index should be determined underestimated. Similarly, if there are secretions overlying
and, if appropriate, a dietetic referral made. the apex of the stenosis, the degree of stenosis may be
Clinical examination should assess the degree of stridor overestimated.
and chest-related recession.The chest and trachea should be Definitive airway assessment is at laryngotracheoscopy
auscultated. Flexible nasendoscopy should be used to exactly using either flexible or rigid endoscopy. This allows the
determine and document any limitations in vocal cord clinician to determine dynamic collapse as well accurate
movement, evidence of laryngopharyngeal reflux (LPR), lesional anatomy. The anatomical sites and pathologies
pooling of hypopharyngeal secretions and appearance of the of paediatric LTS can differ greatly from the adult group.
airway stenosis if visible. If there is a tracheostomy present, Ninety-five percent of paediatric stenosis is post intubation
the endoscope should be passed through this to look at the and 5% congenital.7 The variety of pathologies, based
lower airway. on 700 consecutive adult referrals to an airway reconstruction
If there is evidence of swallowing problems, the patient unit in the United Kingdom, is shown below:
should be referred for videofluoroscopy to determine
aspiration risk. Airway surgery in a patient with even ●● Acquired LTS (49.9%):
microaspiration is unlikely to be successful.10 ●● SGS (33.7%).
Flow-volume loops are the mainstay of diagnosis and ●● Tracheal stenosis (16.14%).
monitoring adult patients with LTS and should always ●● Bilateral vocal cord mobility impairment (BVCMI)
be requested as part of respiratory function testing. The (16.86%) (nerve injury, scar/fixation, rheumatoid arthritis).
flow-volume loop test begins from total lung capacity as ●● Wegener’s granulomatosis (10.14%).
a maximum effort expiration of the forced vital capacity, ●● Idiopathic SGS (9.00%).
which is then proceeded by a maximum effort inspiration ●● SGS (5.70%) (sarcoid, 2.6%; other, 3.14%).
back to total lung capacity. From a diagnostic perspective, ●● Previous papillomatosis treatment (2.43%).
flow-volume loops can distinguish between obstructive and ●● Glottic web (2.43%).
restrictive lung diseases, can characterise airway obstruction ●● Tracheomalacia (1.14%) (relapsing polychondritis,
as upper airway or lower airway, and can separate upper 0.67%).
airway obstruction into fixed obstruction, variable ●● Vascular lesion (1.0%).
extrathoracic obstruction and variable intrathoracic ●● Amyloidosis (0.86%).
obstruction (Figure 10.2). Flow-volume loops are highly ●● Congenital SGS (0.57%).

Expiration
Flow (L/Sec)

Figure 10.2 Patterns of flow-volume loops. These

graphically depict the rate of airflow on the y-axis and
Inspiration
the total volume expired (above) and inspired (below)
on the x-axis. The patient is asked to take the deepest
breath, apply the mouth to the device and breathe out
Normal COPD Fixed airway Variable Variable
as hard as possible and for as long as possible. This is obstrction extrathoracic intrathoracic
followed by a maximum and rapid inspiration. COPD, (intrathoracic or
chronic obstructive pulmonary disease. extratrachea)

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 Laryngotracheal stenosis

Anaesthesia in laryngotracheal stenosis

Endoscopic airway assessment is performed by respiratory ventilation devices have considerably reduced this risk and
physicians, thoracic surgeons and otolaryngologists. allow for shared airway techniques used in adult patients.11
Pulmonologists and thoracic surgeons are trained to use both It is not possible, however, to assess dynamic airway collapse
flexible and rigid bronchoscopes. Flexible bronchoscopy and vocal fold movement in a paralysed patient.
is usually performed in the spontaneously breathing and Prolonged spontaneous breathing anaesthetic techniques
sedated patient who has had topical anaesthetic applied to the are not possible in adult patients. Adults tend to lighten
upper aerodigestive tract.This technique allows assessment of from anaesthesia much more rapidly, with the associated
the dynamic airway, the trachea and bronchi with the ability risk of laryngospasm. Also, access to the larynx in an adult is
to perform the full spectrum of interventions. However, with much easier in a paralysed patient. Suspension laryngoscopy
a flexible bronchoscope placed through a narrow stenosis, is performed routinely by otolaryngologists for assessment
the patient’s airway becomes obstructed. Similarly, attempted of the supraglottic and glottic larynx. Laryngologists
dilatation of an airway stenosis leads to temporary airway are also comfortable operating on the subglottis via a
obstruction. The rigid ventilating bronchoscope requires microscope or rigid endoscope. The advantages of the
the patient to be paralysed and ventilated by a face mask microscope are binocular vision, depth of field and
or endotracheal tube until the bronchoscope is inserted. superior axial illumination and it allows two hands free for
For assessment of the airway beyond an area of stenosis, the instrumentation. Also, the laser can be used with a ‘line-of-
bronchoscope has to be forced through the stenosis. This sight’ technique through a micromanipulator attached to the
has the effect of dilating the stenosis, but also causes stripping microscope. Some otolaryngologists still use the ventilating
of the mucosa in a longitudinal fashion. bronchoscope for tracheal or  bronchial assessment and
Paediatric airway surgery performed by an surgery. Suspension laryngoscopy allows the use of both
otolaryngologist differs in that the child is usually breathing optical rigid endoscopes and flexible bronchoscopes to
spontaneously and oxygen or a combination of oxygen access the airway. The advantages are that the patient is
and an anaesthetic gas is delivered by a nasotracheal tube paralysed and the full spectrum of rigid instrumentation,
withdrawn into the hypopharynx. Endoscopes and dilators, lasers and stents can be inserted and used with
instrumentation can then be passed through the glottis to relative ease. As the patient is ventilated using a supraglottic
access the trachea and bronchi. Traditionally, jet ventilation jetting technique, lasers can also be used without the risk
in children has been associated with an unacceptable of fires, providing no flammable material is introduced into
incidence of a pneumothorax. However, some modern jet the airway.

Tracheobronchial stenting
Stents are named after a British dentist in the 19th century, patient co-morbidities that restrict reconstructive surgery
Charles Thomas Stent, who used impression material to or patient preference. Stents are also used temporarily
support surgical repairs. Stents are used by many different following airway surgery. All the currently available stents
surgical specialities and there has been a proliferation of are associated with a high incidence of complications.
devices for airway stenting. There is currently a variety of Uncovered metal stents are particularly problematic.
silicone and expandable metal stents. The metal stents can Although patients with metal stents enjoy immediate
be uncovered, covered or partially covered (hybrid). Wire palliation of  symptomatic tracheal stenosis, metal stents
stents tend to be covered with polyurethane, although are associated with a high incidence of obstruction
Teflon or silicone is used in some designs (Figure 10.3). with granulation.13 They are susceptible to metal fatigue
The next generation of stents will be reabsorbable or and fracture (Figure 10.4) and they have also been reported
bioengineered in other ways, negating the need for to have migrated into major intrathoracic vessels with
subsequent removal. disastrous consequences. Based on personal experience and
In benign and malignant disease, stents have been used a review of the literature14, the authors’ recommendation is
to palliate the effects of large airway obstruction caused that uncovered or hybrid metal stents should only be used
by extrinsic compression, endoluminal disease or loss in a select group of patients with a short life expectancy.
of cartilaginous support. Indications in benign disease If not removed within the first few weeks of deployment,
include long length stenoses, failed previous repair, they become a permanent fixture in the airway.

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 Post-intubation laryngotracheal stenosis

Figure 10.3 A selection of stents in current use. Left: a

Montgomery T-tube showing how a length can be cut and used as
Figure 10.4 A fractured covered wire stent used in a patient with
a stent providing it is sutured to the airway.12 Centre left: a Dumon
tracheomalacia.
silicone stent. Centre right: a covered wire stent. Right: woven
polyester in silicone stent.

Silicone stents also have complication rates, ranging from series. All patients with stents are prescribed daily saline
21.5%15 to 42%.16 There is a high incidence of bacterial nebulisers. Carbocysteine can be prescribed in those
colonisation of all stents, which can lead to granular patients where there is evidence of mucus plugging.
tissue formation17,18, the most common organisms being There is no research evidence to support the use of any of
Staphylococcus aureus and Pseudomonas aeruginosa in most these measures.

Post-intubation laryngotracheal stenosis

The risk factors for LTS following a period of ventilation BVCMI, due to glottis damage, is always a compromise
on the ICU include: sizing of endotracheal tubes, excessive between voice, airway and swallowing. Damage to the
lateral cuff pressure due to poor cuff pressure monitoring, subglottis or trachea can always be treated with a resection,
hypotension, local infection, gastro-oesophageal reflux, usually with no impact on vocal cord function.
duration of intubation, use of steroids (and other causes The early phase of the post-intubation airway stenosis
of compromised patient immunity), patient movement is characterised by mucosal ulceration and perichondritis
and agitation, tracheostomies and bilateral injuries to the followed by the formation of exophytic granulation tissue.
posterior vocal cords.The majority of patients ventilated on As healing progresses, granulation tissue is gradually replaced
ICUs do not appear to develop airway stenosis. Although with mature fibrotic tissue and the wound contracts,
there is no current research to support this, patients who giving rise to the classical picture of mature airway scar
tend to scar excessively following injury (for example, who (Figures 10.5a, b). It has been shown that inflammatory
develop excessive skin scarring), may self-select for airway conditions in the airway (Figures 10.6a, b) do respond to
stenosis. intralesional steroids.21
The use of appropriately sized ventilation tubes is Using suspension laryngoscopy and supraglottic jet
important not only in the paediatric population but also ventilation, up to 3 ml of methylprednisolone acetate
in adult patients where there is still a relationship between (40 mg/ml) can be injected into the stenosis. Radial cuts
patient height and tracheal diameter19 regardless of sex. are then made into the stenosis with the CO2 laser (8–10 W
The authors recommend early tracheostomy on the ICU continuous) delivered through the microscope using a
even though a multicentre study looking at early versus ‘line-of-sight’ technique. The lesion is then dilated using
late tracheostomy did not show any difference in morbidity a pulmonary balloon dilator to the size of the adjacent
or mortality.20 The reason is that the surgical repair of normal airway. With more mature and fibrotic lesions,

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 Laryngotracheal stenosis

a b
Figures 10.5a, b Tracheal stenosis (a) due to mature scar tissue and cartilage collapse can only be managed with an open procedure such as
a tracheal resection (b).

a b
Figures 10.6a, b Early inflammatory post-intubation subglottic stenosis (a) will respond to injection with corticosteroids, radial cuts with a
laser and pulmonary balloon dilatation. A view following endoscopic treatment is shown (b).

intralesional steroids are of limited value. In these cases, (Figure 10.7) leading to a ‘Lambda-shaped’ stenotic
radial cuts into the lesion are followed by balloon dilatation, deformity and airway compromise.22 The lesion usually
and topical mitomycin-C application may be considered. extends over 1–2 tracheal rings with normal proximal and
Endoscopic surgery is repeated every 3–4 weeks. Patients distal trachea.22 The trachealis is not involved and there
whose lesions prove recalcitrant to endoscopic therapy is usually a small anterior bridge not contributing to the
(which is usually evident by the third procedure) should stenosis. Tracheal resection and anastomosis has been
be treated with open LTR or tracheal resection techniques. recommended for this condition23, but this is a major
Where there is collapse and damage to the laryngotracheal operation with associated morbidity and a small mortality
cartilaginous support, open surgical techniques should be rate.
considered earlier, as endoscopic techniques are likely to The lesion can be treated using a CO2 laser, delivering
fail. The overall success rate of the endoscopic approach to 8–10 W continuously, deployed through a micromanipulator
airway stenosis is 72%. It is highly relevant that in one series attached to the microscope using a ‘line-of-sight’ technique.
all patients with a body mass index of greater than 45 failed The proximal and distal trachea is used as a guide to the limits
endoscopic airway surgery.10 of the resection and the collapsed cartilage is vaporised.
A less common variant of post-ventilation tracheal The resection can extend to the tracheal fascia if necessary
stenosis is seen in a small number of post-tracheostomy and any bulging of the trachealis can also be reduced with
patients. This is caused by over-resection or subsequent the laser (Figures 10.8a–c). A pulmonary balloon dilator
pressure necrosis of anterior tracheal rings due to a may be used to expand the airway. The mucosa over the
tracheostomy. At decannulation, there is scarring and trachealis and the apex of the Lambda must be preserved
contracture at the stoma site, which draws in the lateral because a circumferential injury with the laser will lead to
cartilage remnants as a result of the wound contracture further stenosis.

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 Idiopathic subglottic stenosis

Figure 10.7 Illustration showing the formation of a ‘lambdoid’ tracheal stenosis, through healing by contracture, drawing in remnants of
the tracheal cartilage at the stoma site.

a b c
Figures 10.8a–c ‘Lambdoid’ tracheal deformity before treatment (a) and after laser resection of encroaching cartilage remnants (b). There
has also been superficial lasering to the bulging trachealis. Note that there are strips of normal mucosa between each site that has been
lasered. The airway is shown some weeks later (c).

Idiopathic subglottic stenosis

Idiopathic SGS is a rare, slowly progressive, fibroin­ methylprednisolone (up to 120 mg), radial laser incisions
flammatory process of unknown aetiology leading to and dilatation (similar to as shown in Figure 10.7). Stenosis
narrowing of the airway in the subglottic region and usually recurs usually over a period of 6–12 months, at which time
involving the first and second tracheal rings. The condition surgery can be repeated. Cricotracheal resection has been
occurs predominantly in women, post puberty, but has been recommended26 but the high reported success rate in this
reported in males.24–27 The diagnosis is one of exclusion particular series has not been matched by other units.27
and the patient must not have been intubated, sustained Cricotracheal resection is challenging for lesions extending
neck trauma or had a significant respiratory tract infection up to the glottis, and when performed it removes part of the
in the preceding 2 years. Patients must also be investigated pitch elevation mechanism. The authors’ approach to open
for LPR, autoimmune disorders, including granulomatosis ‘curative’ surgery differs from the orthodoxy of cricotracheal
with polyangiitis, and have tissue sent for histology at each resection. A laryngofissure is performed to include the first
opportunity. Histology reveals a fibroinflammatory process. two tracheal cartilages. Next, a posterior cricoid split is also
It is not unusual for these patients to have been treated for performed taking care not to enter the hypopharynx. The
asthma, when the cause of their airflow restriction could majority of the stenosed mucosa is  removed  and  a piece
simply be determined using flow-volume loop studies of costal cartilage is placed in the posterior cricoid split to
(see Figure 10.2). act as a ‘spacer’ (Figures 10.9a–d). A closed laryngeal stent,
An endoscopic approach is recommended for the covered with a superficial skin graft (epidermal surface
majority of patients. Most patients respond to intralesional against stent), is held in place inside the larynx with a single,

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 Laryngotracheal stenosis

a   b

c   d
Figures 10.9a–d Technique for treating idiopathic subglottic stenosis even where there is disease extension up to the glottis. Following
laryngofissure, a piece of costal cartilage (a) is placed as a ‘spacer’ in a posterior cricoid split (b, c). The disease is resected and a closed skin-
covered stent (d) is left in place for 2 weeks.

strong, monofilament suture. The laryngofissure is closed flap. A temporary tracheostomy needs to be fashioned,
completely at the anterior commissure and above but left as the stent obstructs the airway. The stent is removed
separated below this by a few millimetres to allow one endoscopically at 2 weeks and the patient is decannulated
sternohyoid muscle to be sewn in as a vascular transposition the next day.28

Bilateral vocal cord mobility impairment

BVCMI usually leaves a patient with a reasonable voice but The interarytenoid region is normally the largest part of
some degree of dyspnoea, as the vocal cords tend to lie in the the glottic airway and surgery should therefore be aimed at
median or paramedian position. Bilateral abducted cords are improving this region. For bilateral denervation injuries, the
usually seen in neurological conditions and management is authors have had significant success with endoscopic partial
designed to prevent aspiration and is discussed elsewhere in posterior cordectomy and partial arytenoidectomy using
this text. the CO2 laser (Figures 10.10a, b).
There are three principal causes for BVCMI: The resection is usually unilateral but can be bilateral.
Mitomycin-C may be applied topically at the time of
●● Bilateral laryngeal denervation (thyroid surgery or neck surgery to reduce the tendency for the resection to fill in
and chest malignancy). with fibrosis and scar.The voice does become ‘breathier’ but
●● Bilateral cricoarytenoid joint (CAJ) fixation (rheumatoid remains functional. Destructive laryngeal surgery should
arthritis or trauma). only be considered when the possibility of spontaneous
●● Interarytenoid scarring (post intubation): nerve recovery has been ruled out. If there is the chance
●● Early inflammatory injury. of recovery of vocal cord function, then the temporary
●● Mature interarytenoid fibrotic scar. placement of a tracheostomy or the use of vocal cord suture

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 Bilateral vocal cord mobility impairment

lateralisation procedures may be considered for symptom (Figure  10.12a) must be recognised early and treated
palliation.29 Various reinnervation operations have been with corticosteroid injection and gentle reduction of
described; for example, anastomosing the ansa cervicalis or granulation tissue, otherwise there is the risk of scar
hypoglossal nerve to the recurrent laryngeal nerve or using tissue formation and fixation of vocal cord abduction.
muscle nerve pedicle flaps. A more promising technique Thin posterior glottis webs may be divided with a sickle
is the use of the accessory phrenic nerve anastomosed to knife (Note: never with the laser) and balloon dilatation
the posterior cricoarytenoid muscle.30 Other groups are or temporary suture lateralisation deployed. The repair
looking at reanimating the human larynx with implantable of dense posterior glottis scars is challenging. Lasers are
electrical stimulation devices31; however, this work is in generally ineffective. Posterior laryngeal mucosal flaps,
early stage clinical trials. advanced into the posterior glottis after division of the
With fixed CAJs the only surgical option is some form scar tissue, have been reported. The authors have had
of laser procedure to the posterior cord  or arytenoid, considerable success with the open placement of a costal
as described above (Figures 10.10a, b). Posterior cartilage derived ‘spacer’ within a posterior cricoid split
glottic injuries can result in interarytenoid scar tissue (a similar technique to that shown in Figures 10.9a–d).
(Figures  10.11a, b), which in turn can lead to CAJ These procedures all lead to a compromise between
ankylosis unless identified and treated early. voice, airway and swallowing. The prevention of these
The most common cause for this type of injury injuries, through early tracheostomies on the ICU, must
is endotracheal intubation. Inflammatory injuries be encouraged.

a   b
Figures 10.10a, b A partial right laser arytenoidectomy technique to treat a patient with airway compromise from bilateral recurrent
laryngeal nerve injuries.

a   b
Figures 10.11a, b Image (a) demonstrates a posterior glottic injury seen after extubation. Features are of granulation tissue, which if left
untreated can form scar tissue, which can permanently fix the cricoarytenoid joints (b).

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 Laryngotracheal stenosis

Inflammatory and autoimmune disorders

Granulomatosis with polyangiitis managed with intralesional steroid injections12, radial laser
cuts and dilatation (Figure  10.12b). The same technique
Granulomatosis with polyangiitis (formally Wegener’s
can be applied to the treatment of bronchial lesions. Even
granulomatosis) is perhaps the most common disorder
during periods of disease relapse it is possible to avoid
affecting the mucosa and connective tissue of the airway
tracheostomies or stents. In this condition, early endoscopic
resulting in stenosis. This condition, of unknown aetiology,
treatment of airway stenosis is advised partly because disease
is characterised by a necrotising vasculitis involving the
in this area can be more resistant to medical treatment and
respiratory tract, kidneys, skin, eyes and joints. One in
because the natural evolution of these lesions is to turn to
four patients will have laryngotracheal involvement
mature scar tissue. Old vasculitis-related airway injuries
(Figure 10.12a), although the nose and ears may be
consist predominantly of scar tissue and do not respond so
involved in up to 75% of cases. Biopsies cannot always
well to the endoscopic approach.32
differentiate inflammation from other causes. The most
useful serological test is cytoplasmic antineutrophil
cytoplasmic antibody, which is positive in over 90% Sarcoidosis
of patients with active disease. Corticosteroids are the Sarcoidosis is a non-caseating granulomatous condition
mainstay of treatment in combination with other immune of unknown aetiology. Although there is no cure,
modulating drugs. Subglottic and tracheal stenosis can be corticosteroids may control the rate of disease progression.

a   b
Figures 10.12a, b Typical appearance of a vasculitis of the airway (a). Typical appearance 2 weeks later following treatment with
corticosteroid injection, radial cuts and balloon dilatation (b).

a b c
Figures 10.13a–c Typical apearance of the supraglottic larynx in sarcoidosis (a). Treatment with corticosteroid injection and ‘pepper-pot’
lasering (b). Appearance 3 weeks later (c).

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 References

The larynx is involved in 1–5% of cases.16 The supraglottic laser debulking of laryngeal lesions can be effective in
larynx tends to be affected more often than the subglottis. restoring the airway.33 The authors have evolved a ‘pepper-
The laryngeal lesion is usually a pale pink, oedematous pot’ lasering pattern that reduces the bulk of sarcoid tissue
swelling that can pedunculate into the airway and produce without creating a circumferential injury in the laryngeal
stridor (Figure 10.13a). Intralesional steroids and CO2 inlet, which may risk stenosis (Figures 10.13b, c).

Discussion
In children, up to half the length of the trachea can be properties of tracheal cartilage could be used to provide
resected and there is also the option of slide tracheoplasty shape to muscle flaps for use as tracheal replacements. Bio-
procedures.34 In the adult patient, 4–6 cm of trachea can integrating stents could be an even simpler solution to the
be resected with primary anastomosis.The length resectable management of airway stenosis. Until these technologies are
decreases with age due to the progressive reduction in the proven and widely available, prevention of laryngotracheal
elasticity between the intercartilaginous tissues. For longer airway compromise is essential. This involves not just the
lengths of tracheal damage, failed resections and extensive early recognition and treatment of airway diseases, but also
tracheal malacia, there is no easy solution other than an understanding of the risk factors for airway injury on
palliation with stents or long-term tracheostomies. Tissue the ICU. More appropriate sizing of ventilation tubes and
engineering for tracheal replacement holds promise.35,36 monitoring cuff pressures may reduce the incidence of
Similarly, laryngeal transplantation may be the solution subglottic and tracheal stenosis, and it is anticipated that
to restoring the airway where this organ is damaged the incidence of glottic stenosis will be reduced in patients
beyond repair.37 The other area of research with potential destined for prolonged ventilation with the current practice
for future treatments is biotechnology. Biocompatible of early tracheostomy insertion.
and bio-integrating scaffolds that mimic the mechanical

References
1 Williams T, Dobb G, Finn J et al. (2005) Long-term placed between the vertically divided halves of the
survival from intensive care: a review. Intensive Care posterior lamina of the cricoid cartilage. Laryngoscope
Med 31:1306–1315. 101(12 Pt 2, suppl 56):1–34.
2 Intensive Care National Audit & Research Centre 8 Nouraei S, Singh A, Patel A et al. (2006) Early
United Kingdom (2011) Available from: http://www. endoscopic treatment of acute inflammatory airway
icnarc.org lesions improves the outcome of postintubation airway
3 House J, Noordzij J, Murgia B et al. (2010) Laryngeal stenosis. Laryngoscope 116:1417–1421.
injury from prolonged intubation: a prospective 9 Monnier P, Lang F, Chapuis G (1993) Partial cricoid
analysis of contributing factors. Laryngoscope 121: resection with primary tracheal anastamosis for
596–600. subglottic stenosis in infants and children. Laryngoscope
4 White R (1984) A prospective study of laryngotracheal 103:1273–1283.
sequelae in long-term intubation. Laryngoscope 9: 10 Nouraei S, Ghufoor K, Patel A et al. (2007) Outcome
367–377. of endoscopic treatment of adult postintubation
5 Esteller-More E, Ibanez J, Matino E et al. (2005) tracheal stenosis. Laryngoscope 117:1073–1079.
Prognostic factors in laryngotracheal injury following 11 Mausser G, Friedrich G, Schwarz G (2007) Airway
intubation and/or tracheotomy in ICU patients. Eur management and anesthesia in neonates, infants and
Arch Otorhinolaryngol 262:880–883. children during endolaryngeal surgery. Pediatric Anesth
6 Myer C, O’Connor D, Cotton R (1994) Proposed 17:942–947.
grading system for subglottic stenosis based on 12 Mace A, Sandhu G, Howard D (2005) Securing
endotracheal tube sizes. Ann Otol Rhinol Laryngol tracheal stents: a new and simple method. J Laryngol
103:319–323. Otol 119:207–208.
7 Cotton R (1991) The problem of paediatric 13 Ranu H, Madden B (2009) Endobronchial stenting
laryngotracheal stenosis: a clinical and experimental in the management of large airway pathology. Postgrad
study on the efficacy of autogenous cartilaginous grafts Med J 85:682–687.

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14 Mello-Filho F, Antonio S, Carrau R (2003) 26 Grillo H, Mark E, Mathisen DJ et al. (12993) Idiopathic
Endoscopically placed expandable metal tracheal laryngotracheal stenosis and its management. Ann
stents for the management of complicated tracheal Thorac Surg 56:80–87.
stenosis. Am J Otolaryngol 24:34–40. 27 Dedo H, Catten M (2001) Idiopathic progressive
15 Dumon J, Cavaliere S, Diaz-Jimenez J (1996) Seven- subglottic stenosis: findings and treatment in
year experience with the Dumon prosthesis. J Bronchol 52 patients. Ann Otol Rhinol Laryngol 110:305–311.
3:6–10. 28 Nouraei S, Sandhu G (2013) Outcome of a multimo-
16 Wood D, Yun-Hen Liu Y-H et al. (2003) Airway dality approach to the management of idiopathic sub-
stenting for malignant and benign tracheobronchial glottic stenosis. Laryngoscope 123:2474–2484.
stenosis. Ann Thorac Surg 76:167–174. 29 Van Griethuysen J, Al Yaghchi C, Sandhu G (2012)
17 Nouraei SAR, Petrou M, Randhawa PS et al. (2006) Use of bilateral suture lateralisation technique in
Bacterial colonization of airway stents: a promoter of severe paradoxical vocal fold movement. J Laryngol
granulation tissue formation following laryngotracheal Otol 126:328–330.
reconstruction. Arch Otolaryngol Head Neck Surg 30 Marie J-P (2009) Nerve reconstruction. In: Surgery
132:1086–1090. of Larynx and Trachea. (eds. M Remacle, H Eckel)
18 Noppen M, Pierard D, Meysman M (1999) Bacterial Springer-Verlag, Berlin, pp. 279–294.
colonization of central airways after stenting. Am J 31 Zealear D, Billante C, Courey M et al. (2003)
Respir Crit Care Med 160:672–677. Reanimation of the paralysed human larynx with an
19 Griscom N, Wohl M (1985) Dimensions of the implantable electrical stimulation device. Laryngoscope
growing trachea related to body height. Am Rev Respir 113:1149–1156.
Dis 131:840–844. 32 Nouraei S, Obholzer R, Ind P et al. (2008) Results
20 Young D, Harrison D, Cuthbertson B et al. (2013) Effect of endoscopic surgery and intralesional steroids for
of early vs late tracheostomy placement on survival in airway compromise due to tracheobronchial Wegener’s
patients receiving mechanical ventilation: the TracMan granulomatosis. Thorax 63:49–52.
randomised trial. J Am Med Assoc 309:2121–2129. 33 Butler C,Nouraei SAR,Mace A et al.(2010) Endoscopic
21 Lorenz R (2003) Adult laryngotracheal stenosis: airway management of laryngeal sarcoidosis. Arch
etiology and surgical management. Curr Opin Otolaryngol Head Neck Surg 136:251–255.
Otolaryngol Head Neck Surg 11:467–472. 34 Tsang V, Murday A, Gillbe C et al. (1989) Slide
22 Nouraei S, Kapoor K, Ghufoor K et al. (2007) Results tracheoplasty for congenital funnel-shaped tracheal
of endoscopic tracheoplasty for treating tracheostomy- stenosis. Ann Thorac Surg 48:632–635.
related airway stenosis. Clin Otolaryngol 32:471–475. 35 Macchiarini P, Jungebluth P, Go T et al. (2008) Clinical
23 Grillo H (2003) Postintubation stenosis. In: Surgery transplantation of a tissue engineered airway. Lancet
of the Trachea and Bronchi. (ed. H Grillo) Decker Inc., 372:2023–2030.
Hamilton, pp. 301–331. 36 Delaere P, Vranckx J, Verleden G et al. (2010) Tracheal
24 Benjamin B, Jacobson I, Eckstein R (1997) Idiopathic allotransplantation after withdrawal of immunosuppres-
subglottic stenosis: diagnosis and endoscopic laser sive therapy. N Engl J Med 362:138–145.
treatment. Ann Otol Rhinol Laryngol 106:770–774. 37 Strome M, Stein J, Esclamado R et al. (2001) Laryngeal
25 Valdez T, Shapshay SM (2002) Idiopathic subglottic transplantation and 40 month follow-up. N Engl J Med
stenosis revisited. Ann Otol Rhinol Laryngol 111: 690–695. 344:1676–1679.

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 CHAPTER 11

Extra-oesophageal reflux
James O’Hara

Laryngopharyngeal reflux
Introduction would target those patients who truly merit treatment and
avoid injudicious ‘empirical’ treatment in those that do not.
Laryngopharyngeal reflux (LPR) is a controversial subject.
The ubiquitous use of the term LPR may imply that the
condition is well defined. However, given the evidence,
Aetiology/pathogenesis
LPR may be better considered as a group of chronic It is postulated that the upper respiratory tract is more
upper respiratory symptoms for which reflux of gastric susceptible to damage by gastric contents than the stomach
contents has been popularised as a cause. Symptoms and oesophagus. Originally it was felt that targeting the
attributable to LPR include globus pharyngeus, dysphonia, refluxing gastric acid would relieve symptoms. In addition
throat clearing, cough, excessive phlegm, throat pain and to the direct effects of reflux, it has been postulated that
post-nasal secretions. These symptoms have often been laryngeal cells may have the potential to produce gastric
oversimplified into separate entities.The reality is that there acid through a H+/K+ ATPase pump.6 The role of pepsin,
is overlap between them. Chronic throat symptoms are very a proteolytic enzyme active in lower pH, and bile salts
common; in one study 6% of middle-aged females had a has been raised. Acidified pepsin appears to cause damage
persistent feeling of something in the throat in the previous to intercellular spaces.7 Raising the pH of refluxate may
3 months1, while an English study of primary care attenders therefore be protective. Johnston et al. have shown that
suggested that as many as 25% had recent experience of pepsin is taken up into posterior cricoid cells even in non-
persistent upper respiratory symptoms.2 Fifty per cent of acidic conditions.8 They postulate that this intracellular
patients attending a specialist voice clinic were deemed to pepsin could then be the cause of cell damage following
have underlying reflux.3 reactivation in intracellular environments of lower pH.
Treating LPR with gastric acid suppression has been This mechanism may explain why patients continue to get
in vogue for over a decade, on the basis that recurring symptoms of LPR when on maximal acid suppression and
symptoms are atypical manifestations of gastro-oesophageal also raises the question of non-acidic reflux and its role in
reflux disease (GORD). Much of this practice results from a symptoms.
number of uncontrolled case series demonstrating symptom The vast majority of patients with chronic upper
response to gastric acid suppression. From a purely pragmatic respiratory symptoms will be assessed and treated
viewpoint, there is level 3 evidence (case series4) to support pragmatically in primary care or in a specialist
this treatment rationale and indeed patients’ symptoms otolaryngology/voice clinic. While specialist investigations
do improve with treatment and time. However, there has exist and will be discussed, patients’ symptoms and clinical
been a failure of level 1 evidence (randomised controlled findings tend to guide treatment.
trials [RCTs] and meta-analyses of RCTs) to demonstrate
the benefit of gastric acid suppression over placebo. The Symptom questionnaires
evidence behind LPR was presented at the Evidence Based A number of self-report patient questionnaires have been
Medicine (EBM) Conference: Extra-oesophageal Reflux – advocated. The most common appears to be the Reflux
Separating Myth and Evidence, in Edinburgh in 2011.5 The Symptom Index (RSI), a nine-item questionnaire validated
basis for a ‘diagnosis’ of LPR relies upon symptoms, signs or for patients with LPR ‘diagnosed’ by dual-probe pH
objective demonstration of reflux. As will become evident, manometry (Table 11.1).9 The authors suggested a cut-off
LPR remains a condition of clinical suspicion as signs and of greater than 13 to signify LPR. A further option is the
objective investigations do not correlate strongly with Glasgow and Edinburgh Throat Scale (GETS), originally
symptoms. The author’s own personal view is that LPR designed to assess globus symptoms (Table 11.2).10 Both
does exist and plays a role in symptoms for some patients but these questionnaires were shown to have good internal
not all. Improved characterisation of reflux-related disease consistency in a study of over 300 patients.11 Both were

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 Extra-oesophageal reflux

Table 11.1  The Reflux Symptom Index

Within the last month how did the following problems affect you? 0 = no problem;  5 = severe problem
Hoarseness or a problem with your voice 0 1 2 3 4 5
Clearing your throat 0 1 2 3 4 5
Excess throat mucus or feeling of post-nasal drip 0 1 2 3 4 5
Difficulty swallowing food, liquids or tablets 0 1 2 3 4 5
Coughing after eating or lying down 0 1 2 3 4 5
Breathing difficulties or choking episodes 0 1 2 3 4 5
Troublesome or annoying cough 0 1 2 3 4 5
Sensation of something sticking in your throat or of a lump in your throat 0 1 2 3 4 5
Heartburn, indigestion or stomach acid coming up 0 1 2 3 4 5

Table 11.2  The Glasgow Edinburgh Throat Scale

0 = none; 7 = unbearable
Feeling of something stuck in the throat 0 1 2 3 4 5 6 7
Pain in the throat 0 1 2 3 4 5 6 7
Discomfort/irritation in the throat 0 1 2 3 4 5 6 7
Difficulty swallowing food 0 1 2 3 4 5 6 7
Throat closing off 0 1 2 3 4 5 6 7
Swelling in the throat 0 1 2 3 4 5 6 7
Phlegm down the throat 0 1 2 3 4 5 6 7
Can’t empty the throat when swallowing 0 1 2 3 4 5 6 7
Want to swallow all the time 0 1 2 3 4 5 6 7
Food sticking when swallowing 0 1 2 3 4 5 6 7
None All the time
How much time do you spend thinking about your throat? 0 1 2 3 4 5 6 7
Not at all Extremely
At present, how annoying do you find your throat sensation? 0 1 2 3 4 5 6 7

shown to have two principal domains: (1) cough and The need for an improved tool has led to the
blockage and (2) globus, post-nasal drip or throat clearing. emergence of the Comprehensive Reflux Symptom Scale
This trial noted that the single ‘reflux’ symptom of the (CReSS)13, a 34-item questionnaire with oesophageal,
RSI, ‘heartburn or indigestion’, did not correlate well upper airway and pharyngeal subscales (Table 11.3).
with throat symptoms. Indeed, it has been suggested that The greater level of detail of the CReSS and the likely
improvement in symptoms during clinical trials of acid better discrimination of normal from abnormal scores
suppression, when measured on composite scoring systems, at baseline may facilitate improved characterisation of
may be as a result of improved classical heartburn symptoms symptoms that respond to acid suppression. The CReSS
rather than throat symptoms.5 Utilising the RSI, Kamani has been investigated in 532 participants: 103 healthy
et al.12 received 378 responses from 2,000 questionnaires volunteers (mean  score 6.5,  sd 8), 175  throat clinic
sent to a UK population. Taking an RSI score of greater attenders (32, sd 22) and 254 attenders for gastrointestinal
than 10 to signify LPR, they found the prevalence to be endoscopy (40, sd 26)14.
34%. Interestingly, they found that three-quarters of patients The Laryngopharyngeal Reflux: Health-Related Quality
scoring highly on the ‘heartburn’ score had ‘LPR’ as of Life instrument was tested alongside the 36-item Short
opposed to one-quarter in those who did not score highly Form Health Survey, the Voice Handicap Index and the
on the heartburn score. Quality of Life in Reflux and Dyspepsia questionnaire.15

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 Laryngopharyngeal reflux

Table 11.3  The Comprehensive Reflux Symptom Scale

Within the last month, how did the following problems affect you? Please tick the box that best fits
0 = no 5 = severe
Symptom problem 1 2 3 4 problem
Heartburn
Pressure in chest
Regurgitation
Acid/sour taste in mouth
Gurgling stomach
Pressure/lump in throat
Difficulty swallowing food
Difficulty swallowing liquids
Nausea
Pain in throat
Vomiting
Bloating
Belching
Flatulence
Hiccups
Decreased appetite
Rush of saliva into mouth
Feeling full too early in a meal
Bad breath
Back pain
Choking
Coughing when upright
Coughing after eating
Coughing when lying down
Wheezing
Difficulty breathing
Hoarseness
Throat clearing
Excess mucus
Mucus dripping down back of throat
Feeling things stuck in throat
Indigestion
Stomach acid coming up
Other – please describe

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 Extra-oesophageal reflux

It is a 43-item questionnaire with voice, cough, clear throat, manometry in patients with granuloma than healthy
swallow and overall impact domains. (Note the lack of volunteers.18 Pseudosulcus is another physical finding
emphasis on heartburn.) Its use is limited in the literature widely linked to LPR (Figure 11.2). However, there is
but it does exist as a valid, reliable and responsive tool to variation in the evidence; the  sensitivity and specificity
assess quality of life in LPR. for observing reflux on pH manometry in the presence
of pseudosulcus is 30–70% and 67–70%, respectively.16
Clinical findings While those patients with observed reflux on pH
Mucosal changes in the upper respiratory tract are manometry almost always have symptoms, it is difficult to
evident during fibreoptic examination. A review followed establish whether the third of patients with false-positive
the EBM conference, with all evidence of level 3.16 pseudosulcus in respect to pH manometry have symptoms.
Inflammation may present as vocal cord oedema, This illustrates the main concern with diagnosing LPR;
erythema, posterior commissure hypertrophy thick which is most predictive of reflux as a cause: symptoms,
mucus, diffuse oedema and pseudosulcus (infraglottic clinical findings or objective assessment of reflux episodes?
oedema spreading from the anterior to the posterior
commissures).These findings form the basis of the Reflux
Finding Score (RFS), devised by the group publishing
the RSI (Table 11.4).17 The review noted that individual
signs suggestive of LPR can be found in 64–93% of
healthy volunteers and 17–85% of patients with GORD.16
Five signs were only noted in 3% of healthy volunteers.
The RFS was originally tested on 40 pH manometry-
proven refluxers and 40 patients without symptoms who did
not undergo manometry. The authors conclude a cut-off of
greater than 7 as being ‘diagnostic’ for LPR. While the RFS
correlates well with the RSI and has good sensitivity (88%)
with pH manometry, it has low specificity (38%). In other
words, a low RFS is unlikely to be associated with a significant
pH manometry test, but a high RFS will only be associated Figure 11.1 Endoscopic view of the larynx demonstrating a vocal
with a positive pH manometry test in roughly a third of granuloma.
patients.
Laryngeal granuloma (Figure 11.1) is commonly
associated with LPR but there is little evidence to support
this.16 One study has been identified that demonstrates
significantly higher episodes of reflux on dual probe

Table 11.4  The Reflux Finding Score

Physical finding Score
Pseudosulcus 0 = absent 2 = present
Ventricular obliteration 2 = partial 4 = complete
Erythema/hyperaemia 2 = arytenoids only 4 = complete
Vocal cord oedema 1 = mild 2 = moderate
3 = severe 4 = polypoid
Diffuse laryngeal 1 = mild 2 = moderate
oedema 3 = severe 4 = obstructing
Posterior commissure 1 = mild 2 = moderate
hypertrophy 3 = severe 4 = obstructing
Granuloma/granulation 0 = absent 2 = present
Figure 11.2 Endoscopic view of the glottis demonstrating
Thick endolaryngeal 0 = absent 2 = present
a pseudosulcus of the vocal fold believed to be due to
mucus laryngopharyngeal reflux.

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 Laryngopharyngeal reflux

Diagnosis improvement in visual analogue scores was noted with

speech therapy.
Ambulatory oesophageal pH monitoring is seen as the
standard investigation for documenting GORD. Dual Acid suppression
probe 24-hour pH manometry allows analysis of acid
There is a paucity of evidence for anything other than
reflux events at just above the lower and upper oesophageal
PPIs. Over half of UK otolaryngologists prescribe PPIs
sphincters. However, its routine use in the diagnosis of LPR
for persistent throat symptoms in the absence of structural
is questionable19; evidence is conflicting as to whether
pathology.25 The message has also filtered through to
pharyngeal reflux episodes differ between controls and
primary care that PPIs are a reasonable ‘empirical’ treatment.
patients with LPR. Up to 50% of asymptomatic controls
PPIs cost the NHS in England £425 million in 2006 and
have between one and 17 episodes of LPR (pH <4) in
globally this was £7 billion.26 The advice given from
24 hours.5 Multichannel intraluminal impedance utilises a
uncontrolled studies in treating LPR is to use a twice daily
series of electrodes on a catheter within the oesophagus to
regimen and consider higher dosage than for GORD.
measure impedance (differing resistance) to detect air/gas
Karkos and Wilson’s systematic review of studies
or fluid bolus within the oesophagus. When combined
between 1994 and 200427 showed that while uncontrolled
with pH manometry this allows analysis of both acid
prospective case series demonstrated significant
and non-acid reflux episodes20 and is seen as the most
improvements in symptoms following PPI therapy, no
sensitive tool to document reflux episodes.21 It may also
statistical differences were found in the five RCTs of PPIs
be useful in assessing patients on acid-suppression, with
versus placebo. A significant placebo effect was noted, with
over 50% of persistently symptomatic patients on twice
both treatment and placebo groups showing improved
daily proton pump inhibitor (PPI) therapy noted to have
symptoms at follow-up. Gatta  et al. performed a meta-
non-acid reflux events.22 A more recent innovation is the
analysis of five RCTs published prior to 2005.28 They too
less invasive pharyngeal probe used to measure the pH in
concluded that high-dose PPIs were no more effective
the aerosolised environment of the pharynx (Restech®
than placebo for LPR symptoms. Qadeer et al.29 found a
Pharyngeal  pH probe). However, poor correlation
non-significant symptom reduction with PPIs compared
was found between pH manometry/impedance and
with placebo in eight RCTs. Common findings amongst
pharyngeal pH levels.21 Given the lack of consistency
the individual trials were: predominantly small sample sizes,
between investigations and symptoms, it is difficult to
variable quality, selection bias, differing treatment regimens
view any of these investigations as anything other than
and variable outcome measures.5 The only substantial sized
‘research in progress’.
RCT included in these meta-analyses was performed
by Vaezi et al.30 One-hundred and forty-five patients
Management were randomised to 40 mg esomeprazole twice daily or
Lifestyle placebo for 16 weeks. Five symptoms of throat clearing,
cough, globus, sore throat and hoarseness were recorded
No specific studies have investigated the role of lifestyle on a seven-point Likert scale. No statistically significant
modification in LPR.5 While initial advice suggested difference was found between the PPI group and placebo.
LPR to be different to classical GORD, more studies are A single well-designed RCT has demonstrated improved
demonstrating an overlap in the  symptoms.12 It would post-nasal drainage with lansoprazole 30 mg twice daily.31
therefore seem sensible to offer patients relevant advice to Excluding patients with signs of chronic rhinosinusitis,
avoid factors associated with GORD: eating for 3  hours 75 patients were randomised, with symptoms recorded
prior to sleep, overnight snacking, excessive alcohol, on a visual analogue score. The presence of heartburn,
smoking, lack of exercise, quick eating and obesity.23 regurgitation or objective assessment of reflux did not
predict response to treatment.
Speech therapy A small RCT (n = 40) found no significant improvement
Again, no studies have addressed this in LPR.5 However, in globus symptoms with lansoprazole compared with
high-quality speech therapy was employed in the no placebo, assessed using the GETS.32 Despite the lack of
treatment arm of the RCT investigating alginate therapy level 1 evidence to support PPI therapy in all but post-
for LPR. The no treatment arm showed a significant nasal drainage, case series continue to be published claiming
improvement in symptoms at 2 months compared with benefit.33 Lee et al.34 assessed the efficacy of 10–20 mg
baseline, albeit less so than in the treatment arm. A small rabeprazole twice daily in 455 patients treated in 40
RCT (n = 40) compared speech therapy with nurse led hospitals between 2007 and 2008. The mean RSI improved
reassurance in the treatment of globus.24 A significant from 15.1 at baseline to 5.9 at 12 weeks and the mean RFS

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 Extra-oesophageal reflux

improved from 9.1 to 4.5. Globus, hoarseness and throat from 23.9 in the GA group and 24.6 in the no-treatment
clearing were the symptoms most responsive to therapy. group to 11.2 and 16.8 at 2 months, with scores of 11.2
When considering case series evidence readers should and 18.3 at 6 months.
question the natural resolution of symptoms with time, the An unpublished subgroup of a larger study performed
positive placebo effect and the effect of being involved in a a similarly designed analysis comparing GA plus
trial. The other consideration the advocates of PPI therapy esomeprazole 40 mg twice daily versus esomeprazole
may quote is whether the current level 1 evidence is flawed; 40 mg twice daily alone (n = 19).40 At no stage of the
patients without true LPR included in RCTs may dilute 6-month follow up did the PPI alone group achieve an
the effect of PPIs in those that do. Surely that would also improvement in RSI or RFS compared with baseline. GA
be the case in non-controlled studies? Would improved plus PPI showed improved RSI and RFS scores at 4 and
characterisation of the disease identify particular groups 6 months.
of patients more likely to respond to therapy? While PPIs There may be a benefit of GA in LPR that requires
are considered to be generally efficacious and to have low confirmation in a larger, placebo-controlled RCT setting.
toxicity26, it is not just the cost of overprescription that is While GA is the only alginate licensed for use in LPR
of concern. Rebound hypersecretion of gastric acid on in the UK, it must be remembered that no trials have
withdrawal is a real phenomenon inducing heartburn been performed using other alginates. GA is unique in
symptoms.5 Other side-effects of PPIs include osteoporosis, containing a higher concentration of sodium alginate,
reduction of the effects of anti-platelet medication along with potassium bicarbonate, to help form the CO2
for cardiac disease, pneumonia and Clostridium difficle raft. However, many other alginate products contain
infection.35 additional acid neutralisation in the form of calcium
There is very little evidence for anything other than carbonate. Further work needs to be performed to establish
PPIs. A single small, unpowered controlled trial found no the most efficacious and cost-effective alginate formulation.
difference in treatment outcomes between an H2 antagonist It is interesting to note how little attention alginates have
versus placebo.36 A single observational study demonstrated received in the LPR literature and readers may wish to
the positive use of H2 antagonists within the setting of a question the role of the pharmaceutical industry in the
departmental protocol.37 available evidence.

Alginates Surgery
Alginates are seaweed compounds that form a raft on The role of endoscopic fundoplication is established
gastric contents. A buoyant CO2 retaining gel contacts the for GORD but is less clear in the management of LPR.
gastric contents preventing reflux. In-vitro experiments Van  der Westhuizen et al. received 244 out of 611
have shown removal of pepsin and bile salts from the questionnaires from patients treated between 1998 and
refluxate.38 There is a single randomised, open, parallel 2008.41 The majority of patients reported heartburn and
study of Gaviscon Advance (GA), which contains sodium regurgitation preoperatively, but one-third to two-thirds of
alginate and potassium bicarbonate, 10 ml four times daily patients reported symptoms attributable to LPR. Although
versus ‘no treatment’ (n = 49).39 Although no placebo the authors conclude that surgery is effective for most LPR
medication could be identified as appropriate and the ‘no symptoms, classical GORD symptoms of heartburn and
treatment’ group received high-quality speech therapy regurgitation improved the most, with throat clearing least
input, the methodology is sound. Both groups showed likely to improve. Wassenaar found that antireflux surgery
an improvement in RSI and RFS at 2 months, with a eradicated the preoperative findings of pepsin in laryngeal
significant additional benefit noted in the GA group. mucosa in seven out of eight patients.42 In 10 LPR patients
The  benefit in RSI persisted until 6 months, again to a unresponsive to PPI therapy, fundoplication was not
greater extent with GA, whereas RFS remained improved found to be any more beneficial than continued medical
at 6  months in the GA group alone. The RSI improved therapy.43

Summary
There are unanswered questions over LPR as a pathology. There is a lack of clarity as to how symptoms, signs and
Symptom profiling has been overly simplistic and investigations correlate. RCTs have failed to demonstrate
improvements with acid suppression may have been the positive effect of PPIs observed in the large number of
exaggerated by the effect on classical GORD symptoms. case series. Improved characterisation of symptoms in the

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 References

setting of a larger multicentre RCT may help identify those an alternative to PPIs and potentially cover both acid and
patients most responsive to acid suppression and avoid the non-acid reflux, but there appears to be a lack of wider
widespread use of ‘empirical’ treatment. Alginates may offer research interest in this treatment.

References
1 Deary IJ, Wilson JA, Kelly SW (1995) Globus 13 Papakonstantinou L, Leslie P, Gray J et al. (2009)
pharyngis, personality, and psychological distress in Laryngopharyngeal reflux: a prospective analysis of
the general population. Psychosomatics 36(6):570–577. a 34-item symptom questionnaire. Clin Otolaryngol
2 Lowden M, McGlashan JA, Steel A et al. 34(5):455–459.
(2009) Prevalence of symptoms suggestive of 14 Powell J, Ali Nikkar JD, Janet A. et al. (2012)
extra-oesophageal reflux in a general practice Extraesophageal reflux: throat and gastrointestinal
population in the UK. Logoped Phoniatr Vocol patients. Otolaryngol Head Neck Surg 147(S2):73.
34(1):32–35. 15 Carrau RL, Khidr A, Gold KF et al. (2005) Validation
3 Koufman JA, Amin MR, Panetti M (2000) Prevalence of a quality-of-life instrument for laryngopharyngeal
of reflux in 113 consecutive patients with laryngeal reflux. Arch Otolaryngol Head Neck Surg 131(4):
and voice disorders. Otolaryngol Head Neck Surg 315–320.
123(4):385–388. [Erratum appears in Otolaryngol 16 Powell J, Cocks HC (2013) Mucosal changes in
Head Neck Surg 2001 124(1):104] laryngopharyngeal reflux–prevalence, sensitivity,
4 Harbour R, Miller J (2001) A new system for grading specificity and assessment. Laryngoscope 123(4):
recommendations in evidence based guidelines. Brit 985–991.
Med J 323(7308):334–336. 17 Belafsky PC, Postma GN, Koufman JA (2001) The
5 Ah-See K, Wilson J (2012) Extra-oesophageal reflux: validity and reliability of the reflux finding score
state of the knowledge base. Clin Otolaryngol 37(1): (RFS). Laryngoscope 111(8):1313–1317.
9–16. 18 Ylitalo R, Ramel S (2002) Extraesophageal reflux
6 Altman KW, Haines GK 3rd, Hammer ND et al. (2003) in patients with contact granuloma: a prospective
The H+/K+-ATPase (proton) pump is expressed in controlled study. Ann Otol Rhinol Laryngol 111(5 Pt 1):
human laryngeal submucosal glands. Laryngoscope 441–446.
113(11):1927–1930. 19 Abou-Ismail A,Vaezi MF (2001) Evaluation of patients
7 Franchi A, Brogelli B, Massi D et al. (2007) Dilation with suspected laryngopharyngeal reflux: a  practical
of intercellular spaces is associated with laryngo- approach. Curr Gastroenterol Rep 13(3):213–218.
pharyngeal reflux: an ultrastructural morphometric 20 Tutuian R, Castell DO (2003) Use of multichannel
analysis of laryngeal epithelium. Eur Arch intraluminal impedance to document proximal
Otorhinolaryngol 264(8):907–911. esophageal and pharyngeal nonacidic reflux episodes.
8 Johnston N, Wells CW, Samuels TL et al. (2010) Am J Med 115(Suppl 3A):119S–123S.
Rationale for targeting pepsin in the treatment 21 Becker V, Graf S, Schlag C et al. (2012) First agreement
of reflux disease. Ann Oto Rhinol Laryngol 119(8): analysis and day-to-day comparison of pharyngeal
547–558. pH monitoring with pH/impedance monitoring in
9 Belafsky PC, Postma GN, Koufman JA (2002) Validity patients with suspected laryngopharyngeal reflux.
and reliability of the reflux symptom index (RSI). J Gastrointest Surg 16(6):1096–1101.
J Voice 16(2):274–277. 22 Carroll TL, Fedore LW, Aldahlawi MM (2012) pH
10 Deary IJ, Wilson JA, Harris MB et al. (1995) Globus Impedance and high-resolution manometry in
pharyngis: development of a symptom assessment laryngopharyngeal reflux disease high-dose proton
scale. J Psychosom Res 39(2):203–213. pump inhibitor failures. Laryngoscope 122(11):
11 Cathcart RA, Steen N, Natesh BG et al. (2011) Non- 2473–2481.
voice-related throat symptoms: comparative analysis 23 Yamamichi N, Mochizuki S, Asada-Hirayama I et al.
of laryngopharyngeal reflux and globus pharyngeus (2012) Lifestyle factors affecting gastroesophageal reflux
scales. J Laryngol Otol 125(1):59–64. disease symptoms: a cross-sectional study of healthy
12 Kamani T, Penney S, Mitra I et al. (2012) The prevalence 19,864 adults using FSSG scores. BMC Medicine 10:45.
of laryngopharyngeal reflux in the English population. 24 Khalil HS, Bridger MW, Hilton-Pierce M et al. (2003)
Eur Arch Otorhinolaryngol 269(10):2219–2225. The use of speech therapy in the treatment of globus

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pharyngeus patients. A randomised controlled trial. 35 Madanick RD (2011) Proton pump inhibitor side
Rev Laryngol Otol Rhinol (Bord) 124(3):187–190. effects and drug interactions: much ado about nothing?
25 Karkos PD, Benton J, Leong SC et al. (2007) Trends in Cleve Clin J Med 78(1):39–49.
laryngopharyngeal reflux: a British ENT survey. Eur 36 Kibblewhite DJ, Morrison MD (1990) A double-blind
Arch Otorrhinolaryngol 264(5):513–517. controlled study of the efficacy of cimetidine in the
26 Forgacs I, Loganayagam A (2008) Overprescribing treatment of the cervical symptoms of gastroesophageal
proton pump inhibitors. Brit Med J 336(7634):2–3. reflux. J Otolaryngol 19(2):103–109.
27 Karkos PD, Wilson JA (2006) Empiric treatment of 37 Hanson DG, Kamel PL, Kahrilas PJ (1995) Outcomes
laryngopharyngeal reflux with proton pump inhibitors: of antireflux therapy for the treatment of chronic
a systematic review. Laryngoscope 116(1):144–148. laryngitis. Ann Otol Rhinol Laryngol 104(7):550–555.
28 Gatta L,Vaira D, Sorrenti G et al. (2007) Meta-analysis: 38 Strugala V, Avis J, Jolliffe IG et al. (2009) The role of
the efficacy of proton pump inhibitors for laryngeal an alginate suspension on pepsin and bile acids: key
symptoms attributed to gastro-oesophageal reflux aggressors in the gastric refluxate. Does this have
disease. Aliment Pharmacol Ther 25(4):385–392. implications for the treatment of gastro-oesophageal
29 Qadeer MA, Phillips CO, Lopez AR et al. (2006) reflux disease? J Pharm Pharmacol 60(8):1021–1028.
Proton pump inhibitor therapy for suspected GERD- 39 McGlashan JA, Johnstone LM, Sykes J et al. (2009)
related chronic laryngitis: a meta-analysis of randomized The value of a liquid alginate suspension (Gaviscon
controlled trials. Am J Gastroenterol 101(11):2646–2654. Advance) in the management of laryngopharyngeal
30 Vaezi MF, Richter JE, Stasney CR et al. (2006) reflux. Eur Arch Otorhinolaryngology 266(2):243–251.
Treatment of chronic posterior laryngitis with 40 Strugala V, Dettmar PW (2010) Alginate in the
esomeprazole. Laryngoscope 116(2):254–260. treatment of exrta-oesophageal reflux. In: Effects,
31 Vaezi MF, Hagaman DD, Slaughter JC et al. (2010) Diagnosis and Management of Extra-Esophgeal Reflux.
Proton pump inhibitor therapy improves symptoms in (eds. N Johnston, RJ Toohill) Nova Science Publishers,
postnasal drainage. Gastroenterology 139(6):1887–1893. New York, pp. 145–168.
32 Dumper J, Mechor B, Chau J et al. (2008) Lansoprazole 41 van der Westhuizen L,Von SJ,Wilkerson BJ et al. (2011)
in globus pharyngeus: double-blind, randomized, Impact of Nissen fundoplication on laryngopharyngeal
placebo-controlled trial. J Otolaryngol Head Neck Surg reflux symptoms. Am Surg 77(7):878–882.
37(5):657–663. 42 Wassenaar E, Johnston N, Merati A et al. (2011)
33 Naiboglu B, Durmus R, Tek A et al. (2011) Do the Pepsin detection in patients with laryngopharyngeal
laryngopharyngeal symptoms and signs ameliorate reflux before and after fundoplication. Surg Endosc
by empiric treatment in patients with suspected 25(12):3870–3876.
laryngopharyngeal reflux? Auris Nasus Larynx 38(5): 43 Swoger J, Ponsky J, Hicks DM et al. (2006) Surgical
622–627. fundoplication in laryngopharyngeal reflux unresponsive
34 Lee YS, Choi SH, Son YI et al. (2011) Prospective, to aggressive acid suppression: a controlled study. Clin
observational study using rabeprazole in 455 patients Gastroenterol Hepatol 4(4):433–441.
with laryngopharyngeal reflux disease. Eur Arch
Otorhinolaryngol 268(6):863–869.

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 CHAPTER 12

Infections of the larynx

Sachin Gandhi & Nick Gibbins

Introduction
Infections of the larynx are common; most people will a compromised airway, but knowledge of the underlying
experience one at some point. However, some may be life pathological process is key to successful treatment. This
threatening and others can easily be mistaken for malignancy. chapter covers the acute and chronic infections that may be
Quick, deliberate action may save the life of a patient with seen by the clinician.

Acute infections
Endoscopic evaluation of the adult larynx will show a
Laryngotracheobronchitis (croup) normal supraglottis but an inflamed larynx and subglottis.

Aetiology/pathogenesis Management
Croup is a viral infection and is the most common cause of The majority of cases are mild and can be treated in the
airway obstruction in children between the ages of 6 months community. However, if serious enough to require hospital
and 6 years.1 It is most commonly caused by parainfluenza treatment, oxygen, nebulised adrenaline and steroids,
viruses I and II and paramyxovirus but many other viruses and systemic steroids should be given in a calm and
have been implicated. Symptoms occur primarily due to quiet environment. Antibiotics should be given to cover
subglottic oedema but also oedema of the larynx and bronchi. secondary infection and to avoid bacterial tracheitis, which
Croup in the adult population is rare and immuno­ can be rapidly fatal. Ribavirin has been shown to be effective
compromise must be considered. It is more severe in nature against both respiratory syncytial virus and parainfluenza
with 100% of patients having subglottic narrowing compared virus in vitro but there is no evidence currently for its use
with approximately 25% of children.2,3 in vivo.4

Clinical findings
Croup is often preceded by an otherwise unremarkable
upper respiratory tract infection and so the symptoms are
of a slow onset over a few days. Symptoms typically last 5–7
days. Children present with a barking cough and hoarseness
but subglottic oedema may cause stridor.
Stridor is initially inspiratory in nature. However, if the
condition progresses, the stridor may become biphasic. In
combination with other signs of respiratory distress, this
signifies a severe airway compromise and must be treated
urgently and in an appropriate place of safety. As with any
airway emergency, deterioration can be rapid and fatal.

Diagnosis
Diagnosis in children is clinical. However, radiographs of
the neck may show narrowing of the subglottis (steeple
sign; Figure 12.1). This will also exclude foreign body Figure 12.1 Radiograph showing the steeple sign (arrow) in a
inhalation. Mucus sampling from the nasopharynx for viral patient with laryngotracheobronchitis (croup). (Image from
antigen detection may help isolate the causative organism. http://radiopaedia.org with the consent of Dr Frank Gaillard)

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The introduction of glucocorticoid steroid for the suctioning of tracheal secretions. Patients do not respond to
treatment of croup has resulted in a significant reduction in nebulised adrenaline11 or steroids12 but high-dose, broad-
hospital admissions and improved outcomes for children.5 spectrum antibiotics are given.
The first randomised clinical trial of steroids versus placebo Acute complications are numerous and include
in 1979 showed a significant improvement in symptoms cardiorespiratory arrest, acute respiratory distress syndrome,
and outcome6 that has been confirmed by a Cochrane toxic shock syndrome and renal failure. Historically, both
database review in 2011.7 Systemic steroids take a few morbidity and mortality was high but more recently
hours to have an effect so simultaneous nebulised steroids mortality has dropped towards 0%. It has been suggested
and adrenaline should be given. This has an immediate that improving survival is due to a changing disease pattern,
effect. In the 1.5% of patients who do not improve with but it is more likely to represent improvement in intensive
medical treatment, intubation is required until the oedema care management.13
resolves.
Epiglottitis/supraglottitis
Bacterial tracheitis
Thankfully, the incidence of childhood epiglottitis has
Aetiology/pathogenesis dropped dramatically since the introduction of the
H. influenzae type B (Hib) vaccination. In the UK this was
First described in 19798, bacterial tracheitis – bacterial instigated in 1992 and in the USA in 1985, but preceding
laryngotracheobronchitis, pseudomembranous croup, these dates 1 in 600 children developed some sort of Hib
neonatal necrotising tracheobronchitis – is a rare but serious disease by their fifth birthday.14,15 H. influenzae may also be
and potentially fatal infection of the trachea that is thought responsible for meningitis, arthritis, pneumonia, cellulitis
to be caused by secondary bacterial infection following a and osteomyelitis.16
viral upper respiratory tract infection. Acute epiglottitis is a fulminating infection that can cause
The age at presentation is much more wide-ranging rapid, progressive airway obstruction. The majority of the
than with croup but a seasonal link suggests a respiratory infection and inflammation affects the elastic cartilage of
viral link. Approximately one-third of patients have a virus the epiglottis and the infective organism is Hib.
found with immunofluoresence testing.The most common After the introduction of vaccination, a change in the
bacterial organism cultured from the mucopus found age profile of patients has occurred, with the majority of
inferior to the subglottic oedema is Staphylococcus aureus9 epiglottitis cases now seen in the adult population. The
but Haemophilus influenzae and Streptococcus pnuemoniae10 infection and inflammation are more widespread, affecting
are also described. the whole supraglottis – termed supraglottitis – and
the causative organism is most likely to be a Streptococcus
Clinical findings species.17–19 The drop in childhood infection rates is not
The onset of symptoms is similar to croup but is more rapid. seen worldwide as vaccination against Hib infection is not
Its rapidity is similar to epiglottitis, with sepsis and stridor universal.20
but without associated dysphagia or drooling.
Clinical findings
Diagnosis The classic presentation of epiglottitis is of a septic, pale,
Endoscopy is required to make the diagnosis. A direct tired child aged 3–6 years with stridor, drooling, dysphonia
view will confirm ulceration of the tracheal mucosa and and odynophagia. The child uses respiratory accessory
copious mucopus causing partial tracheal obstruction. muscles and sits separated from their parents with no
Radiographs should not be taken as the airway is complaint (separation sign), leaning forward on their hands
considered precipitous and delays in transferring the in the tripod position.
patient to the radiology department may trigger airway The adult presentation is more varied and symptoms may
collapse. be non-specific. Peak incidence seems to be in the third
decade21 and the male to female ratio is 2–3:1.22 Features
Management may resemble those of an upper respiratory tract infection,
Prompt diagnosis and intensive medical therapy are required pharyngitis or tonsillitis. However, a key feature that must
if significant morbidity and mortality are to be avoided. Up raise suspicion and trigger the need for indirect laryngoscopy
to 91% of patients require intubation but tracheostomy is anterior neck pain disproportionate to the examination
is rarely required. A definitive, safe airway allows regular findings.23

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 Acute infections

Diagnosis debris, the affected patient has coughing fits. This spreads
the bacteria in aerosolised, droplet form.
Diagnosis of the child is clinical and any attempt to examine
the oral cavity or oropharynx should not be attempted
Clinical findings
while the patient is awake, as this may precipitate airway
collapse. Visualisation of the airway should be undertaken Patients’ symptoms are similar to that of a standard viral upper
urgently in theatre with both otolaryngology and paediatric respiratory tract infection, the difference being the prolonged
anaesthetic/intensive care personnel present. coughing fits 1–2 weeks after the start of symptoms. As the
Diagnosis in the adult patient is somewhat easier as patient reaches the end of the coughing fit, they gasp to
flexible indirect laryngoscopy is possible. This will confirm inhale, giving the characteristic whooping noise.
gross erythema and oedema of the supraglottis. The presence of the whoop or post-tussive emesis
Imaging prior to obtaining a definitive airway is increases the likelihood of a diagnosis of pertussis; however,
contraindicated, but for historical interest a lateral the absence of a whoop does not mean that the patient does
radiograph of the neck in a patient with epiglottitis will not have pertussis.27 The disease is generally milder in adults
show the oedematous epiglottis as a ‘thumb print’ sign. and the main symptom may be a prolonged cough and
Supraglottitis does not have specific findings on radiography. therefore its incidence may be underestimated.28
Swabs can be taken from the nasopharynx, oropharynx,
sputum and blood to determine the causative organism in
Diagnosis
the event of an unusual pathogen, but this will not affect the The diagnosis is clinical; however, a nasopharyngeal swab or
immediate management. serum assay may confirm this.

Management Management
If there is danger of airway collapse, endotracheal intubation Meta-analysis has shown that antibiotics are effective in
and intensive care admission is required. If intubation is eliminating the bacterium but do not affect the course of
not possible, a ventilating bronchoscope may be passed to the illness.29 Erythromycin for 14 days has been the standard
maintain the airway until a tracheostomy has been inserted. treatment. However, 3 days of azithromycin or 7 days of
High-dose intravenous antibiotics are required. In some clarithromycin (7 days of trimethoprim/sulphamethoxazole
studies over 50% of Hib strains are now postulated to be for those unable to take a macrolide) are as effective, with
resistant to ampicillin24, so a third generation cephalosporin fewer side-effects, and have been recommended.There is no
is the treatment of choice. Resolution of symptoms, evidence for prophylaxis.30
typically over 2–3 days, leads to reduction of supraglottic
swelling, allowing extubation and discharge from hospital.
It is of note that there has been no change in the
Diphtheria
presenting symptoms or the speed of progression of
the airway compromise despite the introduction of the
Aetiology/pathogenesis
vaccination programme. It is essential that reduced clinical Diphtheria, caused by Corynebacterium diphtheriae, is an
experience is not accompanied by a rise in mortality for illness with high incidence and mortality globally. It has
affected children.25 been all but eliminated in the UK with the introduction of
a mass screening programme approximately 60 years ago.
However, the combination of epidemic re-emergences in
Whooping cough Russia and the former Soviet States in the 1990s and the
ease of continental travel urges caution to the clinician
Aetiology/pathogenesis presented with a patient with a severe sore throat. At
Whooping cough, caused by Bordetella pertussis, is a present, only sporadic cases are seen in Europe, but
notifiable disease that is vaccinated against in the UK and toxigenic strains are still seen around the world.31,32 It is a
other developed countries at 2, 3 and 4 months of age. testament to the severity of the disease that the first Nobel
This vaccination programme has had a dramatic effect on prize for Medicine was awarded to Emil von Behring in
the numbers of patients infected.26 B. pertussis is a gram- 1901 for developing a serum to treat diphtheria.33
negative, aerobic coccobacillus whose effects are a result of
both endo- and exotoxin production. Once adherent to a Clinical findings
pulmonary epithelial cell it produces a tracheal cytotoxin, The illness causes a severe sore throat with malaise  and
stopping the cilia from beating. Unable to clear pulmonary pyrexia. Nasal discharge has been described. Characteristically,

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 Infections of the larynx

a grey membrane is seen in the oropharynx with associated In the professional voice user it may be necessary to
cervical lymphadenopathy. Different strains of C. diphtheriae try and alleviate symptoms rapidly to allow an upcoming
have varying levels of toxogenicity and the degree of illness performance. It is most important that any treatment must
depends on this and the host response. Corynebacterium ulcerans be balanced against the risk of causing further laryngeal
infections are now more common in the UK than C. diphtheriae, damage when masking symptoms with medication. No-
with similar signs, symptoms and high fatality rates.34 one will thank you for a short-term gain followed by a
long-term vocal problem that may have been avoidable with
Diagnosis voice rest and cancelling an engagement. Patients should be
A throat swab and a sample of membrane should be sent for warned against the use of non-steroidal anti-inflammatory
microscopy, culture and sensitivities. Positive isolates must drugs as there is an increased risk of haemorrhage in the
be sent to a reference laboratory for detection of exotoxin.35 acutely inflamed vocal fold.
Steroids have been the mainstay of treatment in this group
Management of patients and they have been given orally, by injection or
Treatment is with benzylpenicillin and antitoxin. inhaled. The basic science of the anti-inflammatory properties
Appropriate airway management should be undertaken of steroids on the laryngeal mucosa was confirmed in 2014.36
(intubation may be necessary) and close contacts and Patients who were given oral hydrocortisone following
relatives immunised. induced phonotrauma had half the level of pro-inflammatory
markers and 6.3-fold increase in anti-inflammatory cytokine
IL-10 than patients in the control group.
Acute laryngitis Injected steroids will start to have an effect within a
couple of hours, oral steroids within a day. However, these
Aetiology/pathogenesis must be used in conjunction with voice rest and the patient
Laryngitis is simply inflammation of the laryngeal epithelium. re-examined prior to full voice use. The patient must be
More specifically, it refers to an engorgement of the superficial aware of the risks of voice use in this early stage including
layer of lamina propria (Reinke’s space) with inflammatory vocal fold haemorrhage, scarring and tearing. A study
cells, increasing the mass of the vocal fold and preventing comparing inhaled and oral steroids in patients with acute
normal vibration.The most common cause of acute laryngitis dysphonia (but without a placebo group) showed better
is a viral infection but, as with any other anatomical space, oedema reduction with inhaled steroids but no difference
infections may also be bacterial or fungal. Mechanical trauma between the groups in terms of voice outcomes37, and
(e.g. vocal misuse, persistent cough) and other reasons for a paediatric study of croup showed  no difference in
acute onset of hoarseness must also be excluded. outcomes between nebulised, oral or parenteral steroids.38
Although this did not study voice outcomes specifically, it
Clinical findings does suggest that steroids in any form may be of benefit to
Acute laryngitis refers to symptoms lasting less than 3 weeks the acutely inflamed larynx.
(chronic laryngitis to those lasting more than 3 weeks). Antibiotics have not been shown to be effective in the
Whether acute or chronic the patient will be hoarse, have a treatment of acute viral laryngitis and are not recommended.39
sore throat and may have associated dysphagia. However, if there is any suspicion of bacterial infection, a
broad-spectrum antibiotic could be used. Fungal infections
Management should be suspected in immunocompromised patients or
The treatment for acute laryngitis is largely supportive, the those using long-term inhaled steroids. A systemic anti-
mainstay being absolute voice rest, with additional advice fungal agent should be considered, the patient’s technique for
to drink a minimum of 2 litres of water per day and steam inhaling steroids addressed and, if not previously addressed,
inhalations to avoid dryness of the laryngeal mucosa. their immune status investigated.

Chronic infections
Chronic infections of the larynx are probably more of for patients to undergo aggressive surgical treatment
common than generally appreciated. Laryngologists for conditions that could have been treated medically
should have an understanding of these conditions and or conservatively. Pathogens that can cause chronic
their insidious onset and progression. A gradual onset of laryngeal infections are broadly divided into bacterial
symptoms can mimic malignancy and it is not unheard and fungal.

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 Chronic infections

expose pulmonary changes on chest radiographs and

Bacterial infections identify abnormal cervical lymph nodes on ultrasound
scan. Cytology may identify granulomata on fine
Tuberculosis needle aspiration of abnormal lymph nodes or in a
sputum specimen. Histological examination following
Aetiology/pathogenesis microlaryngoscopy and biopsy will confirm the diagnosis.
Tuberculosis still remains the commonest cause of chronic Recent advances in the detection of acid-fast bacilli, such
granulomatous infection of larynx. It is usually secondary as MGIT-960 (Mycobacteria Growth Indicator Tube) and
to pulmonary tuberculosis but primary cases have also been TB-PCR, may aid diagnosis.
reported.40 It should be noted that although multi-drug resistant
tuberculosis is still rare, there are case reports of this disease
Clinical findings presenting in the larynx and its occurrence may increase.42
Symptoms include progressive dysphonia, pain on Management
phonation (odynophonia), dysphagia and dry cough. It is
usual for systemic symptoms including anorexia, weight Treatment involves combination therapy with four drugs
loss, evening hyperthermia and night sweats to be present. in an intensive phase that includes isoniazid, rifampicin,
Cervical lymphadenopathy is common. ethambutol and pyrazinamide for 2 months, followed by a
2-drug therapy (isoniazid and rifampicin) for 4 months.
Diagnosis
The most common laryngoscopic finding is of erythematous Syphilis
swelling of the posterior third of the true vocal folds,
arytenoids and interarytenoid space (Figures  12.2a, b). Aetiology/pathogenesis
The next most frequently affected areas are the ventricular Syphilis of the larynx is rare but there are sporadic reports of
folds (false cords) and aryepiglottic folds. Rarely, the involvement by tertiary syphilis.43
epiglottis can be affected.41
Diagnosis is by a combination of haematological, Clinical findings
radiological and cytological/histological investigations. Persistent dysphonia is the presenting feature. Laryngoscopy
Haematological findings include lymphocytosis and reveals erythematous nodules or ulceration that commonly
raised erythrocyte sedimentation rate. Radiology may affect the anterior part of the vocal folds and epiglottis.

a   b
Figures 12.2a, b Endoscopic views of severe tuberculosis of the larynx with marked interarytenoid oedema and mucus (a) and classic
tuberculosis of the larynx affecting the vocal folds, arytenoids and interarytenoid space (b).

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 Infections of the larynx

Diagnosis dapsone 100 mg once daily, rifampicin 600 mg once

monthly, clofazimine 50 mg once daily and 300 mg once
Diagnosis is confirmed by a serumVenereal Disease Research
monthly, all for 1 year.45
Laboratory (VDRL) test. This test needs to be repeated at
6-month to 1-year intervals to rule out any recurrence. A
patient testing VDRL positive needs to be confirmed by Scleroma
Treponema pallidum particle haemagglutination assay, which
has a higher specificity. Aetiology/pathogenesis
Scleroma of the larynx is found in a subset of patients
Management with rhinoscleroma and is a disease is caused by Klebsiella
Treatment is with benzylpenicillin, 2–4 million IU rhinoscleromatis, which is a subspecies of Klebsiella pneumoniae.
intramuscularly once per week for 3 weeks. All patients with scleroma of the larynx have rhinoscleroma,
but only 40% of those with rhinoscleroma have an affected
Leprosy larynx.46
Scleroma is known to progress through three stages: a
Aetiology/pathogenesis catarrhal phase, a granulomatous phase and the cicatrising
Leprosy of the larynx is rare. However, it is the second most phase. Each phase affects the larynx in different ways.47
common site of leprosy in the head and neck after the nose.44 The infection is passed from the nose posteriorly to the
larynx via post-nasal drip in the catarrhal phase. It causes
Clinical findings oedema and erythema of the true vocal folds, false cords
Patient presents with symptoms of dysphonia, dysphagia and arytenoids. This is followed by the granulomatous
and cough. Unlike tuberculosis, there is hardly any phase in which granulomata are seen, typical of the disease
odynophonia. (Figure 12.3a).This in turn heals by scar formation during
the cicatrising phase.
Diagnosis
Laryngoscopy reveals nodular oedema of the glottis and Clinical findings
supraglottis. A sputum sample contains acid-fast  bacilli During the catarrhal phase patients complain of throat
that help in the diagnosis. Biopsy and histopathological pain, hoarseness, dysphagia and odynophonia along with
examination shows characteristic ‘foam cells’. concurrent nasal symptoms. The symptoms continue
through the granulomatous phase with the possible
Management addition of stridor due to mass effect. The cicatrising phase
According to the WHO guidelines, treatment of can lead to web formation or laryngotracheal stenosis (LTS)
multibacillary leprosy is in the form of multi-drug therapy; (Figure 12.3b), which may give the patient stridor.

a   b
Figures 12.3a, b Endoscopic view of scleroma changes in the larynx (a). Granulomata are seen on the right vocal fold and in the
interarytenoid space. An example of subglottic/tracheal stenosis in scleroma (b).

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 Chronic infections

Diagnosis
Diagnosis is made from the history and presence of
concurrent nasal and laryngeal signs and symptoms. Biopsy
from this region shows typical ‘Mikulicz cells’.

Management
Treatment is with levofloxacin 500 mg once daily or
rifampicin 450–600 mg for 4–6 weeks. It may need to be
prolonged for 6–12 weeks in recurrent cases. Surgically, the
granulomata can be excised using a CO2 laser to reduce the
mass effect. In cases of LTS, excision and reconstruction in a
specialist centre may be required.

Fungal infections Figure 12.4 Endoscopic view of candidiasis of the larynx. Note the
Most fungal infections are opportunistic and are seen in similarity to keratosis. This condition may also cause generalised
inflammation without leukoplakia.
immunocompromised individuals. Susceptible patients
include those with acquired immunodeficiency syndrome
(AIDS), uncontrolled diabetes, organ transplant patients on cotton wool appearance may or may not be seen. It is
immunosuppressive medication, prolonged ICU care with important to think of this condition as it can mimic
long-term broad-spectrum antibiotics, those at the extremes malignancies. In those patients who have already had
of age, and in patients after irradiation for laryngeal cancers. radiotherapy, it may resemble a recurrence. Diagnosis is
Occasionally, fungi may affect immunologically competent confirmed by sending the tissue for fungal stain, fungal
individuals locally rather than systemically, for example in culture and histopathological examination. This shows
those with asthma using regular inhaled steroids. pseudoepithelial hyperplasia, pseudohyphae and rarely
Diagnosis is with tissue biopsy for histology or acanthosis.
bronchoscopic brushings for microscopy, culture and
sensitivities. Microscopy can be done within a few hours; Management
however, culture takes longer (up to 3 weeks). The treatment of choice is administration of a systemic
antifungal. Commonly, fluconazole is used at a dose of
400 mg or itraconazole 100 mg once daily for 2 weeks.
Candidiasis
Aetiology/pathogenesis Aspergillosis
Candidiasis is the most common of the fungal infections
and is caused by Candida albicans. It is usually seen in Aetiology/pathogenesis
patients using inhaled steroids or in those having undergone The most common causes of fungal infection in humans
radiotherapy for head and neck malignancies. The severity are Aspergillus fumigates and Aspergillus flavus. Patients usually
of this condition is greater in immunocompromised become infected by inhaling fungal spores, but entry may
individuals.48 also be via tracheostomy tube or stoma.49

Clinical findings Clinical findings

Patients present with dysphonia, dysphagia and a sore Aspergillus spp. are known to form granulomata and so
throat. Candidiasis commonly involves the epiglottis presentation may be as a mass effect.They are more invasive
and aryepiglottic folds but rarely the true vocal folds. In in the immunocompromised patient.
post-irradiation patients the site of infection is that of the
primary tumour. Diagnosis
Macroscopically, Aspergillus spp. form greenish or blackish
Diagnosis fungal spores that can be seen on laryngoscopic examination.
Laryngoscopic findings range from white patch to Diagnosis is relatively straightforward based on fungal stains.
ulcerations and granulations (Figure 12.4). The classic Confirmation is with tissue culture and histopathology.

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 Infections of the larynx

Management Management
Treatment is with the systemic antifungal voriconazole Treatment is with intravenous amphotericin B 0.6–1 mg/
200 mg three times a day for 24 hours followed by twice a day kg/day. A less nephrotoxic type, liposomal amphotericin B,
for 6–12 weeks. Itraconazole100 mg twice daily for 6 weeks can be used at a dose of 3–5 mg/kg given for 6–12 weeks.
can be used as an alternative. Aspergillosis has a tendency to Oral voriconazole has been tried with limited success.
recur and more prolonged courses may be required.

Histoplasmosis Less common fungal infections

Histoplasmosis is a chronic granulomatous disease caused Blastomycosis
by Histoplasma capsulatum. Though immunologically
competent hosts can be affected, more severe infection is Blastomycosis is caused by the diamorphic fungus
found in the immunocompromised patient. The larynx is Blastomyces dermatides. The lungs and skin are the most
usually a secondary infection after the lower respiratory common sites and infection of the larynx may be secondary
tract or as a part of disseminated disease, but primary to pulmonary involvement.51
involvement can also rarely happen.50 Infection is The usual symptom is of prolonged dysphonia.
contracted via inhalation of spores. Laryngoscopic examination shows typical exophytic
granular nodules. In some cases ulcerations are also
Clinical findings seen. It may readily be mistaken for verrucous/invasive
Clinical features are very non-specific in the form of change carcinoma.
of voice and sore throat. The condition can be diagnosed on histopathology or
fungal stains and culture, and it is treated with itraconazole
Diagnosis for 6 weeks.
Diagnosis remains a challenge as laryngoscopy shows
mucosal ulcerations, chronic inflammation and granuloma Cryptococcosis
formation. These can mimic tuberculosis or malignancy
(Figure 12.5a).A biopsy from the tissue shows granulomata Caused by Cryptococcus neoformans, this infection usually
and pseudoepitheliomatous hyperplasia. Tissue can also affects patients with AIDS. It is more commonly known
be sent for periodic acid-Schiff stain and silver stain to cause meningitis and involvement of the larynx is a rare
and will show intracellular yeast buds (Figure  12.5b). feature.
The precise  species can be confirmed by culture. Chest The clinical course remains similar to that of blastomycosis
radiographs may show multiple small calcifications. and the treatment is intravenous amphotericin B for 2 weeks.

a   b
Figures 12.5a, b Endoscopic view of histoplasmosis of the larynx (a). Histoplasmosis (b). There is granulomatous inflammation and a giant
cell with intracytoplasmic fungi (arrow). (H&E, ×40)

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 Summary

Coccidioidomycosis histopathology, which show classical septate hyphae of

mucor.
This fungus also infects the lungs via inhaled spores of Prior to 1955 and the introduction of amphotericin,
Coccidiodes immitis/posadasii and is far more common in invasive mucor had a 100% mortality rate. Now, treatment
children.52 Infection manifests itself with typical granuloma is with thorough débridement coupled with a high dose of
formation. Fungal stains show coccidioidal spherules filled intravenous amphotericin B (1 mg/kg/day) for 6–12 weeks.
with numerous endospheres. In refractory cases local infiltration of amphotericin B has
Intravenous amphotericin B for 2–4 weeks remains the been advocated. Occasionally, combination of amphotericin
treatment of choice. B with oral posaconazole 400 mg twice daily shows good
results. It is essential to have rigid glycaemic control.
Rhinosporidiosis
Actinomycosis
Rhinosporidiosis is caused by Rhinosporidium seeberi. T   his
organism belongs to the class Mesomycetozoea, which lies The causative organism of actinomycosis is Actinomyces
between fungi and animal. It is most commonly found in israeli. It is a filamentous intermediate between bacteria
Southern Asia.53 The nose is the commonest site of infection and fungi. It is part of the normal flora of the tonsils and
but laryngeal involvement is also known.54 Presentation is in gingival but may become invasive.56
form of mulberry-shaped nodules, usually on the arytenoids Actinomyces israeli invades and multiplies in necrotic
and vocal folds. tissue. Though the most common site is skin and bones,
Treatment consists of excision of the nodules. Dapsone infrequently the larynx can also be involved. Presentation is
is effective in some cases, with a dosage of 100 mg daily for with progressive dysphonia. Laryngoscopy may or may not
4–6 weeks. reveal the characteristic ‘sulphur granules’. If left untreated,
laryngeal actinomycoses may rupture through the skin.
Diagnosis is made by tissue biopsy. There are classical
Mucormycosis filamentous and granular forms of actinomycosis. The
Mucormycosis is an invasive fungal infection seen in culture is difficult and requires 2–3 weeks to grow.
immunocompromised hosts, particularly in diabetics. The The treatment of choice is intravenous penicillin 10–20
causative organism is Mucor from the order Mucorales.55 The million units for 4–6 weeks, followed by oral penicillin
larynx is usually involved only as a part of pulmonary or head 2–4 g/day for 6–12 months.
and neck mucor. Spread is vascular via septic fungal thrombi.
When not treated aggressively and controlled, the condition Chronic laryngitis
is rapidly progressive with a high mortality rate. In the larynx,
the supraglottis and subglottis are commonly involved, with Chronic laryngitis is a secondary response to external
classical blackening and charring of the affected tissue. factors such as cigarette smoke, allergens, environmental
Aside from symptoms arising from infected areas, the pollutants or laryngopharyngeal reflux. Identifying and
patient will have dysphonia with breathlessness in later either removing or treating the primary source is the
stages. Diagnosis is confirmed by tissue fungal stains and mainstay of treatment.

Summary
As with infections elsewhere, patients’ symptoms may be (dysphonia, weight loss, sore throat) and signs (ulceration,
acute or chronic, mild or severe. Unlike infections in other erythema) frequently mimic malignancy and this must be
parts of the body, those in the larynx can have acutely excluded. While investigating the patient with laryngeal
catastrophic consequences with loss of the airway. Severe or pharyngeal symptoms, the diagnostician should keep
acute infections of the larynx are thankfully infrequent, the possibility of a chronic infection in mind, especially
but the clinician must always be aware of the potentially in immunocompromised patients. Tissue biopsy and
precipitous airway in a patient with a laryngeal infection. histopathological investigation remain the gold standard
Most chronic infections of the larynx on the for diagnosis on which management is based.
other hand have an insidious onset. Both symptoms

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 Infections of the larynx

Laryngeal infections in the antibiotic and vaccination eras

We live in an antibiotic era.57 However, we may also be outcomes of which have now been condemned, and the
approaching the end of this era as bacteria continually evolve backing by certain ill-informed celebrities, the number
means of resistance to the range of antibiotics currently of children not being vaccinated is growing. In 2011, an
available. Prior to the widespread introduction of penicillin outbreak of measles in Minnesota61 was traced back to a
in the 1940s, bacterial laryngeal infections were feared. single unvaccinated child returning from holiday in Kenya,
An article published in 1977 summed up the feeling of where the disease had been contracted. Three thousand
clinicians at the time when it stated that “…acute epiglottitis individuals were exposed and 21 cases reported. Of those
is the most treacherous inflammatory process that can affect cases, 16 were not vaccinated, nine of whom were eligible
the respiratory tract. It can be a cause of sudden death in for the MMR vaccine. Of those nine, seven were not
children”.58 Haemophilus was also the most common cause vaccinated because of parental safety concerns.
of meningitis in childhood, and a common cause of cellulitis At the time of writing (June 2014) the state of California
and osteomyelitis, conditions that have been eradicated in the USA is experiencing a whooping cough epidemic.62
thanks to vaccination. W  hooping cough was also a significant The California Department of Public Health (CDPH)
cause of infant morbidity and mortality, with the majority of stated on their website on 13th June 2014 that more than
hospitalisations in children under 6 months of age.These are 800 new cases had been reported in the previous two weeks.
serious pathogens causing serious diseases. In the first half of 2014, 3,458 cases had been reported, more
However, vaccination against B. pertussis, introduced in than the whole of 2013.
the 1950s in the UK, and against Hib, in 1992, dramatically Vaccines work to reduce the incidence of infections.
reduced the incidence of these infections. Prior to the However, they also work because of the concept of herd
1950s, whooping cough notifications in the UK exceeded immunity. Vaccines are not always 100% effective so it is
120,000 annually. By 1972, vaccination uptake was at still possible for a vaccinated child to become infected if
80% and notifications were down to 2,069. Then, in a exposed to a pathogen. This is partly why epiglottitis in
process that we are to see repeated over time, professional the USA continues to be a clinical entity.63–65 Reliance
and public anxiety grew over the safety and efficacy of on the whole community to be vaccinated limits the
the vaccines, despite the numbers stated above. What potential for spread but does not eliminate it. This level
followed was a drop in vaccination rates and consequently of herd immunity is important for those children who
major epidemics in the UK in 1977–79 and 1981–83. cannot have the vaccinations due to immunocompromise
This resulted in 200,000 extra notifications and over 100 or allergies. Currently, epiglottitis and whooping cough
deaths over this time period. Uptake increased as general are rare. Indeed, they are rare enough that they need to be
confidence in the vaccine increased and coverage is now at continually mentioned when educating trainees, as failure
over 96%.59,60 to recognise the signs and symptoms may be fatal. However,
However, within a generation the collective memory if vaccination rates fall, we may see a return to the ‘bad old
of the dangers and mortality rates of these infections has days’ that current junior doctors will not have experienced.
faded and an anti-vaccination lobby has grown, not only If this coincides with the end of the antibiotic era, or
to the infections mentioned but also to others that are even partial resistance to antibiotic treatment, then the
now routinely vaccinated against including measles and precipitously ill child with airway compromise may once
mumps. Unfortunately, as  a  result of publications, the again become commonplace.

References
1 Leung AK, Kellner JD, Johnson DW (2004) Viral 4 Wendt CH, Hertz MI (1995) Respiratory syncitial
croup: a current perspective. J Pediatr Health Care virus and parainfluenza virus infections in the
18(6):297–301. immunocompromised host. Semin Respir Infect
2 Woo PCY, Young K, Tsang KWT, Ooi CGC, Peiris 10(4):224–231.
M, Yuen K (2000) Adult croup: a rare but more 5 Rajapaksa S, Starr M (2010) Croup – assessment and
severe condition. Respiration 67:684–688. management. Aust Fam Physician 39(5):280–282.
3 Postma DS, Jones RO, Pillsbury HC (1984) Severe 6 Leipzig B, Oski FA, Cummings CW et al. (1979) A
hospitalized croup: treatment trends and prognosis. prospective randomized study to determine the efficacy
Laryngoscope 94:1170–1175. of steroids in treatment of croup. J Pediatr 94(2):194–196.

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 References

7 Russell KF, Liang Y, O’Gorman K et al. (2011) 22 Lon SA, Lateef M, Sajad M (2006) Acute epiglottitis:
Glucocorticoids for croup. Cochrane Database Syst a review of 50 patients. Indian J Otolaryngol Head Neck
Rev Accessed Jan 19th 2011. doi:10.1002/14651858. Surg 58(2):178–180.
CD001955.pub3. 23 Al-Qudah M, Sheety S, Alomari M et al. (2010) Acute
8 Jones R, Santos JI, Overall JC (1979) Bacterial adult supraglottitis: current management and treament.
tracheitis. JAMA 242(8):721–726. South Med J 103(8):800–804.
9 Bernstein T, Brilli R, Jacobs B (1998) Is bacterial 24 Del Carmen Otero M, Sanchis N, Modesto V et al.
tracheitis changing? A 14-month experience in a (1997) Acute epiglottitis caused by Haemophilus
pediatric intensive care unit. Clin Infect Dis 27(3): influenzae type B in children: presentation of 21 cases.
458–462. Enferm Infecc Microbiol Clin 15(9):462–467.
10 Orenstein JB, Tomsen JR, Baker SB (1991) 25 Leighton S (2009) Acute laryngeal infections. In: Scott-
Pnuemococcal bacterial tracheitis. Am J Emerg Med Brown’s Otorhinolaryngology, Head and Neck Surgery, 7th
9(3):243–245. edn., Vol. 1. (eds. MJ Gleeson, RC Clarke) Hodder
11 Donnelly BW, McMillan JA, Weiner LB (1990) Arnold, London, pp. 1127–1134.
Bactieral tracheitis: report of eight new cases and 26 McVernon J, Slack MPE, Ramsay ME (2006)
review. Rev Infect Dis 12(5):729–735. Changes  in the epidemiology of epiglottitis
12 Eckel HE,Widemann B, Damm M et al. (1993) Airway following the introduction of Haemophilus influenzae
endoscopy in the diagnosis and treatment of bacterial type B (Hib) conjugate vaccines in England: a
tracheitis in children. Int J Pediatr Otorhinolaryngol comparison of two data sources. Epidemiol Infect
27:147–157. 134(3):570–572.
13 Tebruegge M, Pantazidou A, Thorburn K et al. (2009) 27 Cornia PB, Hersh AL, Lipsky BA et al. (2010) Does this
Bacterial tracheitis: a multi-centre perspective. Scand J coughing adolescent or adult patient have pertussis?
Infect Dis 41(8):548–557. JAMA 304(8):890–896.
14 Booy R, Moxon ER (1993) Immunisation of infants 28 Senzilet LD, Halperin SA, Spika JS et al. (2001)
against Haemophilus influenzae type b in the UK. Arch Pertussis is a frequent cause of prolonged cough
Dis Child 69:1251–1254. illness in adults and adolescents. Clin Infect Dis 32:
15 Booy R, Hodgson SA, Slack MP et al. (1993) Invasive 1691–1697.
Haemophilus influenzae type b disease in the Oxford 29 Pillay V, Swingler G (2008) Symptomatic treatment of
region (1985–91). Arch Dis Child 69:225–228. the cough in whooping cough. [Protocol]. Cochrane
16 Janai H, Stutman HR, Marks MI (1990) Invasive Database Syst Rev 4:CD003257.
Haemophilus influenzea type B infections: a continuing 30 Altunaiji S, Kukuruzovic R, Curtis N et al. (2005)
challenge. Am J Infect Control 18(3):160–166. Antibiotics for whooping cough (pertussis). Cochrane
17 Bizaki AJ, Numminen J, Vasama JP et al. (2011) Acute Database Syst Rev 25(1):CD004404.
supraglottitis in adults in Finland: review and analysis 31 Zakikhany K, Efstratiou A (2012) Diphtheria in
of 308 cases. Laryngoscope 121(10):2107–2113. Europe: current problems and new challenges. Future
18 Briem B, Thorvardsson O, Petersen H (2009) Acute Microbiol 7(5):595–607.
epiglottitis in Iceland 1983–2005. Auris Nasus Larynx 32 Mattos-Guaraldi AL, Moreira LO, Damasco PV et al.
36(1):46–52. (2003) Diphtheria remains a threat to health in the
19 Wood N, Menzies R, McIntyre P (2005) Epiglottitis developing world – an overview. Mem Inst Oswaldo
in Sydney before and after the introduction of Cruz 98(8):987–993.
vaccination against Haemophilus influenzae type B 33 http://www.nobelprize.org/nobel_prizes/medicine/
disease. Intern Med J 35(9):530–535. laureates/1901/
20 Peltola H (2000) Worldwide Haemophilus influenzae 34 Wagner KS, White JM, Crowcroft NS et al. (2010)
type B disease at the beginning of the 21st century: Diphtheria in the United Kingdom, 1986–2008: the
global analysis of the disease 25 years after the use increasing role of Corynebacterium ulcerans. Epidemiol
of the polysaccharide vaccine and a decade after Infect 138(11):1519–1530.
the advent of conjugates. Clin Microbiol Rev 13(2): 35 Efstratiou A, Engler KH, Mazurova IK et al. (2000)
302–317. Current approaches to the laboratory diagnosis of
21 Qazi IM, Jafar AM, Hadi KA et al. (2009) Acute diphtheria. J Infect Dis 181:S138–145.
epiglottitis: a retrospective review of 47 patients in 36 Ingle JW, Heou LB, Li NY et al. (2014) Role of steroids
Kuwait. Indian J Otolaryngol Head Neck Surg 61(4): in acute phonotrauma: a basic science investigation.
301–305. Laryngoscope 124(4):921–927.

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37 De Souza A, de Campos Duprat A, Costa RC et al. of two cases and review of literature. Ann Otol Rhinol
(2013) Use of inhaled versus oral steroids for acute Laryngol 109:281–286.
dysphonia. Raz J Otorhinolaryngol 79(2):196–202. 52 Allen JE, Belafsky PC (2011) Laryngeal
38 Cetinkaya F,Tufekci BS, Kutluk G (2004) A comparison coccidioidomycosis with vocal fold paralysis. Ear Nose
of nebulized budesonide, and intramuscular, and oral Throat J 90(5):E1–5.
dexamethasone for treatment of croup. Int J Paediatr 53 Madana J, Yolmo D, Gopalakrishnan S et al. (2010)
Otorhinolaryngol 68(4):453–456. Rhinosporidiosis of the upper airways and trachea.
39 Reveiz L, Cardona AF (2013) Antibiotics for acute J Laryngol Otol 124(10):1139–1141.
laryngitis in adults. Cochrane Database Syst Rev 3: 54 Daharwal A, Banjara H, Singh D et al. (2011) A rare
CD004783. case of laryngeal rhinosporidiosis. J Laryngol Voice
40 Mehndiratta A, Bhat P, D’Costa L et al. (1997) 1:30–32.
Primary tuberculosis of larynx. Indian J Tuberc 44:211. 55 James WD, Berger TG, Elston DMD (2011) Andrews’
41 Gandhi S, Kulkarni S, Mishra P et al. (2012) Diseases of the Skin: Clinical Dermatology, 11th  edn.
Tuberculosis of larynx revisited: a report on clinical Saunders Elsevier, St. Louis.
characteristics in 10 cases. Indian J Otolaryngol Head 56 Khademi B, Dastgheib-Hosseini S, Ashraf M (2011)
Neck Surg 64(3):244–247. Vocal cord actinomycosis: a case report. Iranian
42 Mukherjee S, Sengupta A, Chakraborty J (2001) J Otorhinolaryngol 23:49–52.
Laryngeal tuberculosis in MDR-TB presenting as 57 Aminov RI (2010) A brief history of the antibiotic
laryngeal carcinoma. Indian J Otolaryngol Head Neck era: lessons learned and challenges for the future. Front
Surg 53(4):321–322. Microbiol 1:134.
43 Spinato L,Verougstraete, Bisschop P (2007) Laryngeal 58 Baxter JD, Pashley NR (1977) Acute epigolttitis –
syphilis: a case report. Rev Otol-Rhinol-Laryngol (Fr) 25 years’ experience in management, The Montreal
93:358–360. Children’s Hospital. J Otolaryngol 6(6):473–476.
44 Soni NK (1992) Leprosy of the larynx. J Laryngol Otol 59 Heath PT, McVernon J (2002) The UK Hib vaccine
106(6):518–520. experience. Arch Dis Child 86:396–399.
45 WHO guidelines found at: http://www.who.int/lep/ 60 Immunisation against infections disease - the Green
mdt/regimens/en/index.html Book. Dept of Health (latest edition).
46 De Champs C, Vellin JF, Diancourt L et al. (2005) 61 Gahr P, DeVries AS,Wallace G et al. (2014) An outbreak
Laryngeal scleroma associated with Klebsiella pneumonae of measles in an undervaccinated community. Pediatrics
subsp. ozaenae. J Clin Microbiol 43(11):5811–5813. 134(1):e220–228.
47 Soni NK (1997) Scleroma of the larynx. J Laryngol 62 http://www.cdph.ca.gov/Pages/NR14-056.aspx
Otol 111(5):438–440. 63 Guardini E, Bliss M, Harley E (2010) Supraglottitis
48 Malays J (2001) A case of isolated laryngeal in the era following widespread immunization
candidiasis mimicking laryngeal carcinoma in an against Haemophilus influenzae type B: evolving
immunocompetent individual. Med Sci 18(3):75–78. principles in diagnosis and management. Laryngoscope
49 Ladage DP, Wankhade AB, Mali RJ et al. (2012) 120(11):2138–2138.
Aspergillosis of larynx with involvement of epiglottis 64 Shah RK, Stocks C (2010) Epiglottitis in the United
in immunocompetent patient, a rare observation. States: national trends, variances, prognosis, and
Images Pathol 2(1):35–37. management. Laryngoscope 120(6):1256–1262.
50 Wolf J, Blumberg HM, Leonard MK (2004) Laryngeal 65 Campbell H, Amirthalingam G, Andrews N et al.
histoplasmosis. Am J Med Sci 327(3):160–162. (2012) Accelerating control of pertussis in England
51 Hanson J, Spector G, El-Mofty SK (2000) Laryngeal and Wales. Emerg Infect Dis 18(1):38–47.
blastomycosis: a commonly missed diagnosis. Report

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 CHAPTER 13

Recurrent respiratory papillomatosis

Adam Donne

Introduction
Recurrent respiratory papillomatosis (RRP) is a condition It is still a difficult condition to treat and typically requires
in which viral-induced warts grow within the larynx and significant operative time to control. RRP is relatively
elsewhere in the airway. It affects both children and adults uncommon; it may therefore be reasonable to ‘pool’ cases to
and behaves somewhat differently in these groups. In the develop expertise in management in order to give the best
paediatric population, it is generally more locally aggressive. outcomes for patients.

Epidemiology
RRP is caused by the human papillomavirus (HPV). HPV prevalence, which is present in different geographical
There are approximately 120 different types of HPV, regions of the world, although the prevalence rates do vary
and the nomenclature is based on the sequence of one of significantly.2
the two surface proteins called L1. The predominant HPV The fundamental question is why is there so much
types in RRP are HPV-6 and -11, which are actually very HPV yet so little RRP? The reality is that the majority
similar.1 HPV-6 and -11 are also categorised as ‘low-risk’ of humans have probably had at least a transient HPV
HPV. This implies they have a low risk of developing a infection. In some, the virus is cleared, in others it remains
malignancy when they infect a cell. This is in contrast to as a dormant commensal, and in a small proportion it results
the ‘high-risk’ types HPV-16 and -18, which have a much in a persistent infection with wart/papilloma formation.
greater risk of malignant change. HPV-16 and -18 are Persistent infection may be related to (as yet unspecified)
increasingly important aetiological agents in head and neck differences in host immunity and this may in turn be due
squamous cell carcinoma development, particularly in the to the host’s genetic make-up. Alternatively, there may be
oropharynx. In clinical practice, HPV-positive malignancy viral factors. Indeed there are 19 variants of HPV-6 and 10
responds differently to irradiation and chemotherapy; this variants of HPV-11.The variants have been shown to differ
finding is having profound implications for the treatment of in their activity (at least in vitro) and this may explain why
oropharyngeal cancer. some have more aggressive disease than others for the same
As the name suggests, HPV only affects humans and HPV type.3 Furthermore, it is clear that in cervical disease
not other animals. HPV infects any human anatomical site there is a worse prognosis if there are multiple different
that has stratified epithelium. Typically, the genital tract is HPV types present.4 It is reasonable to assume this to be the
affected by HPV-6 and -11 where it can result in genital same for RRP, as up to seven different types of HPV have
warts (condylomata accuminata). In fact 10–25% of women been identified in papillomas from RRP patients.5
on cervical screening have been identified as having HPV Although there is conflicting evidence, most researchers
present. Furthermore, there appears to be an age-related feel that HPV-11 causes more aggressive disease than HPV-6.

Clinical presentation
The literature indicates that RRP can present very publications on this area. Airway obstruction is obviously
early, even in neonates.6 The commonest presentation is important, as the usual airway medications (nebulised
hoarseness but in infants stridor with significant airway adrenaline and steroids) do not improve the airway in RRP.
obstruction is not unusual. Despite hoarseness being the The average age of presentation of a child is 4 years but
most common concern, surgeons are generally more adults present between 20 and 30 years of age.
concerned with maintaining a patent airway (in children) The link between genital tract HPV infection and
rather than the quality of voice, as judged by the paucity of RRP is important, as juvenile-onset RRP is acquired

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 Recurrent respiratory papillomatosis

through vertical transmission. As indicated above, significant The transmission of RRP in adults is thought to be
numbers of women of child bearing age have HPV in predominantly horizontal rather than delayed activation of
their genital tract. Up to 50% of children born to mothers dormant HPV acquired at birth.13 Horizontal transmission is
with genital warts have demonstrable HPV in their indicated as risk factors for adult-onset RRP include higher
nasopharyngeal aspirates at birth7, yet the risk of these risk with increasing numbers of sexual partners, the average
children developing RRP is only 1 in 400.8 Genital warts age of onset is between 20 and 30 years and higher reported
are a relatively common condition but the prevalence of frequency of oral sexual activity compared with controls.14
RRP is 4.3/100,000 and 3.6/100,000 in US and Danish The factor that triggers HPV-containing normal
studies, respectively.9,10 mucosa to develop papilloma remains unknown.  The
Should caesarian section be offered to mothers with ability to clear and control HPV is immunological and
genital warts? As previously indicated, the risk of developing human immunodeficiency virus (HIV) infection allows
RRP is 1 in 400, yet others suggest it may be double that some indication of this. Seventy-nine percent of HIV-
at 7 per 1,000 children and the risk increases if the delivery positive women in one study have been shown to be HPV
time is prolonged beyond 10 hours.11 However, caesarian positive on vaginal lavage, and a larger variety of HPV types
section does not appear to decrease the RRP risk and the were identified.15 Other immunocompromised states such
procedure has its own inherent risks. Infant death rate in as organ transplantation have also resulted in activation of
the first 28 days following caesarian section, for babies who latent HPV. In a study of renal transplantation patients, 48%
have no particular known risk, has been reported to be were found to have warts and the prevalence increased with
1.77 per 1,000 live births.12 duration of immunosuppression.16

Natural history
There are differences between juvenile-onset and adult- condition than HPV-6. The onset of puberty is not
onset RRP. The condition tends to be more aggressive associated with disease remission; however, hormonal
in children. This is exemplified by the average numbers influences may be more important in HPV-11-associated
of surgeries required before remission is achieved: 13 in disease. RRP due to HPV-11 has been shown to accelerate
children versus six in adults.17 Patients who present at an during pregnancy compared with HPV-6 disease.22
earlier age tend to have a more aggressive condition with Even after remission, HPV DNA can still persist in the
more recurrences and more sites affected.18,19 It has been mucosa, which appears histologically normal.23,24 This may
reported that only 33% of children went into remission explain why papillomas sometimes recur following a period
if they initially presented before 5 years of age compared of remission.
with 46% in the older age profile.20 More recent work has Disease remission remains highly variable, although
indicated that age of onset is more important than HPV laryngeal disease is likely to undergo remission whereas
type21 and HPV-11 probably results in a more aggressive bronchopulmonary disease is often fatal.25

Diagnosis
The diagnosis of RRP is often suspected in a clinic setting for Head and Neck carcinoma, by comparison, indicates
with the benefit of laryngoscopy. Most children can be treatment strategy.
persuaded to allow placement of a flexible laryngoscope to At each and every subsequent MLTB the same process
allow a provisional diagnosis. However, all patients must have of assessment and histology should be followed. The
a full microlaryngoscopy and tracheobronchoscopy (MLTB) rationale for this is that lower airway lesions may occur and
to attain a full airway assessment and a histological diagnosis. be overlooked. The value of serial histology is that routine
There are numerous grading systems for RRP – the microlaryngoscopy cannot detect malignant change within
Derkay system is probably the most popular. The limitation a papillomatous lesion, but might be suspected if the vascular
of all the staging systems is that they do not directly imply architecture deviates from the typical punctate appearance
prognosis or outcome, apart from the obvious negative (Figure 13.1).
prognostic indicator of papillomas below the level of The appearance of the vessels within papillomas changes
the subglottis. This limitation is at least partly due to the with the application of 1 in 10,000 adrenaline. This can be
unpredictability of the condition. The TNM Classification used to aid the ‘on the theatre table’ diagnosis.

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 Management

Figure 13.1 Endoscopic image of laryngeal papillomas with the punctate vascular pattern.

Management
As there is no cure for RRP, the mainstay of treatment difficulty in removing the papillomas. The argument for
remains surgical. Surgical treatment includes cold steel, not intubating is that there is a theoretical risk of trauma
microdebrider, laser and coblation. The microdebrider to the subglottic mucosa, hence the potential for papilloma
is a similar size to the latest laryngeal coblator wand formation. Intubation is reserved if oxygen desaturation
(Figure 13.2). Before papillomas are to be removed, occurs.
liberal application of 1 in 10,000 adrenaline on Neuro Lasers have previously been used widely. However, due to
Patties™ is helpful. The key to surgical clearance is to the collateral thermal damage to adjacent unaffected tissue,
protect the underlying normal structures, as the condition voice quality following laser treatment has been shown to be
(in most cases) will resolve, leaving a potentially scarred worse than with cold steel alone.26 As such there has been
larynx if deep dissection is performed. The laryngoscope a move away from laser use. The exception is for tracheal
is suspended in the usual way for microlaryngeal surgery. papillomas when access by other methods can be difficult.
For the experienced laryngologist, spontaneous breathing A laser delivered through laser fibre (typically through the
ventilation is best in children in order to fully assess the suction port of a ventilating bronchoscope) can be very
airway without the impedance of an endotracheal tube. effective. Clearly, all laser safety precautions must be taken.
However, the anaesthetic should not be so ‘light’ that The laryngeal microdebrider can also be used in the
the vocal cords are moving significantly, with resultant upper trachea to mid trachea and is mainly limited by
the available space at the glottis. It is probably the most
widespread method of cold steel surgery. In the larynx,
the microdebrider is best used with relatively low suction
pressure, otherwise adjacent normal soft tissue of the larynx
is sucked into the device with resultant risk of damage
to these unaffected structures. This risk is particularly
important in the larynx of an infant, where there is inherent
flaccidity of the supraglottic structures.
The laryngeal microdebrider can be used in the forward
rotating setting (rather than oscillating) with the mouth
of the shaver facing parallel to the normal vocal cord.
This allows the most delicate shave without damage to
Figure 13.2 Relative sizes of a laryngeal microdebrider (top) and underlying structures. The speed of the microdebrider is
a modern laryngeal coblator wand (bottom). best used at 500–600 rpm. The speed is variable as pedal

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 Recurrent respiratory papillomatosis

pressure corresponds to speed. This aspect of control is largest reported study of RRP patients (1,193) identified a
important to safe papilloma removal. If the papillomas are malignant transformation rate in children of 1%.9 The rate
extensive, a good strategy is to clear one side and then apply in adults is up to 6%.30  Why is the rate so high in adults?
adrenaline before starting the contralateral side. This allows This is unknown; however, smoking is an independent risk
better haemostasis. for malignant change and may be significant. Furthermore,
From the parents’ point of view, the main postoperative adults have more chance of exposure to other HPV types, of
criterion of successful surgery is the immediate voice which some could be high-risk.
outcome. Clearly as much visible papilloma should be Dysplasia is not an uncommon finding with RRP
removed as possible.The voice will tend to be strongest when and requires simple monitoring. This highlights the need
the vocal folds have flat glottic surfaces postoperatively; an for taking a biopsy at each and every MLTB. There are
irregular profile will not result in an adequate voice. Surgeons no guidelines for the management of carcinoma in situ
are rightly cautious of anterior commissure papillomas, (CIS) and invasive carcinoma specifically associated with
as removal from this site may result in webbing despite RRP. All patients should be appropriately discussed in
extremely careful removal. Theoretically, this can be reduced a Head and Neck oncology multidisciplinary team. In
by not allowing the apposition of two raw surfaces. This can many situations, the CIS would probably be fully excised
be difficult to achieve with extensive papillomatosis, which with complete clearance of the papilloma. However, if the
most commonly affects the anterior commissure. environment for transformation is present, the CIS will
A practical concern is when to offer the second and theoretically recur.
subsequent follow-ups. There are no guidelines for this and
different groups approach the problem in different ways: Adjuvant therapies
follow-up MLTB at regular intervals, follow-up depending When should adjuvant therapies be considered? The RRP
on symptoms, or a hybrid of the two. A sensible approach taskforce (USA) suggests this to be when more than four
is to perform a second MLTB approximately 4–6 weeks surgeries per annum for two successive years are required
after the initial surgery in an attempt to quantify the to maintain a safe airway or when papillomas have spread
aggressiveness of the disease. Clearly this may be shortened beyond the larynx.30a This figure puts most children in this
if extensive papillomas were initially present and there category; however, it would be prudent to suggest caution
had been a significant airway risk. Unfortunately, children with children, as adjuvant therapies have potential risks.
do still die of airway obstruction due to either delay in In the US, approximately 20% of paediatric cases receive
treatment or superadded infection (e.g. upper respiratory adjuvant therapy.31
tract infection).27 Early direct access to the specialist service Historically, many different adjuvant therapies have
is therefore encouraged. been used for RRP, including arsenic32 and formalin.33
Unsurprisingly, these adjuvants are no longer used;
nonetheless, even contemporary drugs are a subject of
Tracheostomy debate and concern.
Tracheostomy is occasionally performed with very severe
RRP where the airway is difficult to control. However, Cidofovir
papillomas tend to occur around the tracheostomy site
Cidofovir [(S)-1-(3-hydroxy-2-phosphonylmethoxypropyl)
in 50%23 and there is risk of distal (pulmonary) spread, so
cytosine] is a nucleoside analogue of deoxycytidine
repeated MLTB is the preferred option. Both tracheostomy
monophosphate and as such is a prodrug. Once inside a cell it
and pulmonary papillomatosis have a significant mortality.
undergoes a two-stage phosphorylation process. At this point
The rate of tracheostomy in children with RRP has been
the chemical structure resembles that of a nucleotide (which is
reported to be higher than in adults and reflects the more
the building block of DNA). It may then be incorporated into
aggressive paediatric condition.
host cell or virus DNA synthesis. Once two molecules have
been incorporated, DNA synthesis stops.34
Malignant change Cidofovir has been licensed for use in cytomegalovirus
HPV is a DNA virus that may exist either inside the cell, (CMV) retinitis of AIDS as a second-line treatment. CMV
but not integrated into the host DNA (episomal), or has its own viral DNA polymerase, which more avidly
integrated. The latter triggers malignant transformation incorporates cidofovir than human DNA polymerase.
in high-risk HPV28 but integration does not guarantee However, HPV does not have its own viral DNA
malignant change.29 HPV-6 and -11 can result in malignant polymerase and sabotages the function of the human host
transformation and this rate is higher for HPV-11. The polymerase.The mechanism of action of cidofovir in RRP

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 Conclusion

is related to the kinetics of DNA synthesis: if the HPV- between published reports. More than 70% of patients
infected papillomas are growing more rapidly than normal show a positive response to alpha interferon. A review of
mucosal cells infected with dormant HPV, cidofovir will four reports42–45 totalling 127 patients demonstrates 35%
have more potential for incorporation into the papilloma. complete response, 38% partial response, 21% to have a
There is evidence that cidofovir is useful against high- minimal response and 5.5% no response. Grouping these
risk HPV-related tumours and it was probably this that data shows 73% to have a response and approximately 27%
prompted the use of cidofovir for RRP. Direct comparison to have minimal or no response. This group compares well
of cidofovir effects of closely related cell lines transfected with a separate large uncontrolled study of 169 patients in
with HPV-6 and HPV-16 genes demonstrate a smaller which 73% had complete remission and the remainder had
effect on the former cell line.35 a significant reduction in the number and size of lesions.46
Cidofovir has been used around the world by many The effectiveness of alpha interferon therefore appears
groups and numerous protocols for use have been to be similar to cidofovir. A major difficulty with alpha
documented. An average typical cidofovir protocol would interferon therapy is that systemic treatment is required;
be the direct injection of 5 mg/ml into the larynx on a there are significant side-effects and monitoring of
monthly basis for 3 months. If the interval is too short, it blood counts and liver function is required.47 There are
has been observed that papillomas may be stimulated to numerous protocols ranging from 6 months to 2 years. The
grow.36 This observation fits with laboratory studies that RRP taskforce guidelines state: “5 million units per metre
indicate low doses of cidofovir to cells containing HPV squared body surface area by subcutaneous injection daily
genes can stimulate growth37 and this may in part explain for 30 days and then 3 times weekly for at least a 6 months
some of the differences in clinical outcomes. The dosing trial. The dose can be reduced to 3 million units/metre2
regimen is therefore of critical importance. 3 times a week if side-effects are severe” (http://www.
The overall clinical effectiveness of cidofovir is around 60% rrpf.org/RRPTaskForceGuidelines.html). The value
total response, 29% partial response and the remainder no of a gradual reduction in dose is to prevent recurrence/
response or progression.38 There have been concerns regarding rebound. The newer peg-interferon alfa-2a (Pegasys®,
the safety of cidofovir, initially highlighted by the carcinogenic Roche) has a longer half-life and requires less frequent
effects in rats during toxicology studies. One report suggests administration (once weekly) and has fewer side-effects.48
that cidofovir can induce the genes that are associated with HPV-6 may to be more sensitive to alpha interferon
malignancy in human cells in  vitro.37 A recent multicentre therapy and this may demonstrate the value of HPV typing
opinion states that the clinical rate of malignant transformation of all patients.49
with cidofovir use does not currently appear to be higher than
expected without cidofovir.39 A recent survey of opinions Vaccines
has demonstrated that cidofovir continues to be used despite Both therapeutic and prophylactic vaccines exist. The
manufacturers’ concerns.40 It is appropriate that patients therapeutic vaccines are still undergoing a process of
consent to knowledge of potential malignant transformation. trial. Gardasil® is currently the only prophylactic vaccine
designed against HPV-6 and -11 (in addition to HPV-16
Alpha interferon and -18). Some studies have suggested that Gardasil may
reduce RRP burden.50,51 Studies are currently underway to
Alpha interferons are naturally occurring polypeptides that
investigate this further. Gardasil is relatively safe, but should
have antiviral and anti-proliferative effects due to immune
not be given during pregnancy.
modulation. They have been used for RRP and the effect
Numerous other adjuvant therapies have been reported;
is dose-dependent.41 The heterogeneity of the studies
however, numbers in each of the reports have been too
performed make it difficult to make direct comparisons
small to make a recommendation.

Conclusion
RRP remains a difficult condition to treat, with surgery within the larynx; to do so would jeopardise the voice in
representing the mainstay of management. Repeated the long term when remission finally occurs.
surgery should be aimed at maintaining an adequate airway Numerous adjuvant therapies have been proposed but all
and achieving an improvement in voice. Surgical excision have their own concerns. Cidofovir is currently the most
(by whichever method is chosen) should be performed popular, with reasonably good outcomes, but concerns
judiciously, with care taken not to damage deep structures regarding long-term safety exist.

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References
1 Donne AJ, Hampson L, Homer JJ et al. (2010) The role 15 Broker TR, Jin G, Croom-Rivers A et al. (2001) Viral
of HPV type in Recurrent Respiratory Papillomatosis. latency-the papillomavirus model. Dev Biol (Basel)
Int J Pediatr Otorhinolaryngol 74(1):7–14. 106:443–451.
2 de Sanjose S, Diaz M, Castellsague X et al. (2007) 16 Rudlinger R,Smith IW,Bunney MH et al.(1986) Human
Worldwide prevalence and genotype distribution of papillomavirus infections in a group of renal transplant
cervical human papillomavirus DNA in women with recipients. Br J Dermatol 115(6):681–692.
normal cytology: a meta-analysis. Lancet Infect Dis 17 Benjamin B, Parsons DS (1988) Recurrent respiratory
7(7):453–459. papillomatosis: a 10 year study. J Laryngol Otol
3 Heinzel PA, Chan SY, Ho L et al. (1995) Variation of 102(11):1022–1028.
human papillomavirus type 6 (HPV-6) and HPV- 18 Gabbott M, Cossart YE, Kan A et al. (1997) Human
11 genomes sampled throughout the world. J Clin papillomavirus and host variables as predictors
Microbiol 33(7):1746–1754. of clinical course in patients with juvenile-onset
4 Spinillo A, Dal BB, Alberizzi P et al. (2009) Clustering recurrent respiratory papillomatosis. J Clin Microbiol
patterns of human papillomavirus genotypes in 35(12):3098–3103.
multiple infections. Virus Res 142(1–2):154–159. 19 Armstrong LR, Derkay CS, Reeves WC (1999) Initial
5 Penaloza-Plascencia M, Montoya-Fuentes H, Flores- results from the national registry for juvenile-onset
Martinez et al. (2000) Molecular identification of 7 recurrent respiratory papillomatosis. RRP Task Force.
human papillomavirus types in recurrent respiratory Arch Otolaryngol Head Neck Surg 125(7):743–748.
papillomatosis. Arch Otolaryngol Head Neck Surg 20 Evans JN (1996) Recurrent respiratory papillomatosis.
126(9):1119–1123. In: Scott Brown’s Otolaryngology: Paediatric Otolaryngology,
6 Loyo M, Pai SI, Netto GJ et al. (2008) Aggressive 6th edn., Vol. 6. (eds. D Adams, M Cinnamond) CRC
recurrent respiratory papillomatosis in a neonate. Int J Press, Boco Raton, pp. 1–5.
Pediatr Otorhinolaryngol 72(6):917–920. 21 Buchinsky FJ, Donfack J, Derkay CS et al. (2008)
7 Sedlacek TV, Lindheim S, Eder C et al. (1989) Age of child, more than HPV type, is associated with
Mechanism for human papillomavirus transmission at clinical course in recurrent respiratory papillomatosis.
birth. Am J Obstet Gynecol 161(1):55–59. PloS One 3(5):e2263.
8 Shah K, Kashima H, Polk BF et al. (1986) Rarity of 22 Gerein V, Soldatski IL, Babkina N et al. (2006) Children
cesarean delivery in cases of juvenile-onset respiratory and partners of patients with recurrent respiratory
papillomatosis. Obstet Gynecol 68(6):795–799. papillomatosis have no evidence of the disease during
9 Derkay CS (1995) Task force on recurrent respiratory long-term observation. Int J Pediatr Otorhinolaryngol
papillomas. A preliminary report. Arch Otolaryngol 70(12):2061–2066.
Head Neck Surg 121(12):1386–1391. 23 Cole RR, Myer CM III, Cotton RT (1989)
10 Lindeberg H, Elbrond O (1990) Laryngeal papillomas: Tracheotomy in children with recurrent respiratory
the epidemiology in a Danish subpopulation papillomatosis. Head Neck 11(3):226–230.
1965–1984. Clin Otolaryngol Allied Sci 15(2):125–131. 24 Shapiro AM, Rimell FL, Shoemaker D et al. (1996)
11 Silverberg MJ, Thorsen P, Lindeberg H et al. (2003) Tracheotomy in children with juvenile-onset
Condyloma in pregnancy is strongly predictive of recurrent respiratory papillomatosis: the Children’s
juvenile-onset recurrent respiratory papillomatosis. Hospital of Pittsburgh experience. Ann Otol Rhinol
Obstet Gynecol 101(4):645–652. Laryngol 105(1):1–5.
12 MacDorman MF, Declercq E, Menacker F et al. (2006) 25 Soldatski IL, Onufrieva EK, Steklov AM et al. (2005)
Infant and neonatal mortality for primary cesarean Tracheal, bronchial, and pulmonary papillomatosis in
and vaginal births to women with “no indicated children. Laryngoscope 115(10):1848–1854.
risk,” United States, 1998–2001 birth cohorts. Birth 26 Holler T, Allegro J, Chadha NK et al. (2009) Voice
33(3):175–182. outcomes following repeated surgical resection of
13 Doyle DJ, Gianoli GJ, Espinola T et al. (1994) laryngeal papillomata in children. Otolaryngol Head
Recurrent respiratory papillomatosis: juvenile versus Neck Surg 141(4):522–526.
adult forms. Laryngoscope 104(5 Pt 1):523–527. 27 Carroll CD, Saunders NC (2002) Respiratory
14 Kashima H, Mounts P, Leventhal B et al. (1993) Sites papillomatosis: a rare cause of collapse in a young adult
of predilection in recurrent respiratory papillomatosis. presenting to the emergency department. Emerg Med J
Ann Otol Rhinol Laryngol 102(8 Pt 1):580–583. 19(4):362–365.

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28 Schneider-Maunoury S, Croissant O, Orth G (1987) 41 MulloolyVM,Abramson AL, Steinberg BM et al. (1988)

Integration of human papillomavirus type 16 DNA Clinical effects of alpha-interferon dose variation on
sequences: a possible early event in the progression of laryngeal papillomas. Laryngoscope 98(12):1324–1329.
genital tumors. J Virol 61(10): 3295–3298. 42 Avidano MA, Singleton GT (1995) Adjuvant drug
29 Choo KB, Pan CC, Liu MS et al. (1987) Presence strategies in the treatment of recurrent respiratory
of episomal and integrated human papillomavirus papillomatosis. Otolaryngol Head Neck Surg 112(2):
DNA sequences in cervical carcinoma. J Med Virol 197–202.
21(2):101–107. 43 Benjamin BN, Gatenby PA, Kitchen R et al. (1988)
30 Hartley C, Hamilton J, Birzgalis AR et al. (1994) Alpha-interferon (Wellferon) as an adjunct to standard
Recurrent respiratory papillomatosis: the Manchester surgical therapy in the management of recurrent
experience, 1974–1992. J Laryngol Otol 108(3):​226–229. respiratory papillomatosis. Ann Otol Rhinol Laryngol
30a http://www.rrpf.org/RRPTaskForceGuidelines.html 97(4 Pt 1):376–380.
31 Schraff S, Derkay CS, Burke B et al. (2004) American 44 Lusk RP, McCabe BF, Mixon JH (1987) Three-
Society of Pediatric Otolaryngology members’ year experience of treating recurrent respiratory
experience with recurrent respiratory papillomatosis papilloma with interferon. Ann Otol Rhinol Laryngol
and the use of adjuvant therapy. Arch Otolaryngol Head 96(2 Pt 1):158–162.
Neck Surg 130(9):1039–1042. 45 Leventhal BG, Kashima HK, Mounts P et al. (1991) Long-
32 Thomson S (1910) Papilloma of the larynx in a boy aged term response of recurrent respiratory papillomatosis
6(1/2), of four years’ duration, cured by tracheotomy to treatment with lymphoblastoid interferon alfa-N1.
and repeated operations by direct laryngoscopy. Proc R Papilloma Study Group. N Engl J Med 325(9):613–617.
Soc Med 3(Laryngol Sect): 11–12. 46 Nodarse-Cuni H, Iznaga-Marin N, Viera-Alvarez D
33 Bronner A (1906) Notes on an unusual case of et al. (2004) Interferon alpha-2b as adjuvant treatment
papilloma of the larynx in a child treated by the local of recurrent respiratory papillomatosis in Cuba:
application of formalin. Br Med J 2(2395):1448. National Programme (1994–1999 report). J Laryngol
34 De Clercq E (2004) Antivirals and antiviral strategies. Otol 118(9):681–687.
Nat Rev Microbiol 2(9):704–720. 47 Crockett DM, McCabe BF, Lusk RP et al. (1987) Side
35 Donne AJ, Hampson L, He XT et al. (2007) Effects of effects and toxicity of interferon in the treatment of
cidofovir on a novel cell-based test system for recurrent recurrent respiratory papillomatosis. Ann Otol Rhinol
respiratory papillomatosis. Head Neck 29(8):741–750. Laryngol 96(5):601–607.
36 Albright JT, Pransky SM (2003) Update on the use 48 Gallagher TQ, Derkay CS (2009) Pharmacotherapy
of cidofovir for managing recurrent respiratory of recurrent respiratory papillomatosis: an expert
papillomatosis. ENT News 12(1):71–73. opinion. Expert Opin Pharmacother 10(4):645–655.
37 Donne AJ, Hampson L, He XT et al. (2009) Potential 49 Szeps M, Dahlgren L, Aaltonen LM et al. (2005)
risk factors associated with the use of cidofovir to treat Human papillomavirus, viral load and proliferation
benign human papillomavirus-related disease. Antivir rate in recurrent respiratory papillomatosis in
Ther 14(7):939–952. response to alpha interferon treatment. J Gen Virol
38 Donne AJ, Rothera MP, Homer JJ (2008) Scientific 86(Pt 6):1695–1702.
and clinical aspects of the use of cidofovir in recurrent 50 Mudry P,Vavrina M, Mazanek P et al. (2011) Recurrent
respiratory papillomatosis. Int J Pediatr Otorhinolaryngol laryngeal papillomatosis: successful treatment with
72(7):939–944. human papillomavirus vaccination. Arch Dis Child
39 Tjon Pian Gi RE, Ilmarinen T, van den Heuvel ER et al. 96(5):476–477.
(2013) Safety of intralesional cidofovir in patients with 51 Forster G, Boltze C, Seidel J et al. (2008) Juvenile
recurrent respiratory papillomatosis: an international laryngeal papillomatosis: immunisation with the
retrospective study on 635 RRP patients. Eur Arch polyvalent vaccine gardasil. Laryngorhinootologie
Otorhinolaryngol 270(5):1679–1687. 87(11):796–799.
40 Derkay CS,Volsky PG, Rosen CA et al. (2013) Current
use of intralesional cidofovir for recurrent respiratory
papillomatosis. Laryngoscope 123(3):705–712.

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 CHAPTER 14

Inflammatory disorders of the larynx

Ivor Kwame

Introduction
The fact that the larynx is a fibroelastic osseocartilaginous and neurologically intact and well-coordinated. Dysphonia
structure whose main function is airway protection has can therefore be a sensitive early manifestation of laryngeal
already been discussed. The larynx is also important for inflammation and dysfunction due to a myriad of different
phonation and plays a key role in the Valsalva manoeuvre, conditions.
which allows the elevation of intrathoracic pressure with This chapter will provide an overview of the main
subsequent ability to strain. pathophysiology of a number of different rare but important
In health, adult vocal cords vibrate at 100–250 cycles inflammatory disorders of the larynx and highlight current
per second during phonation. In order to do this the entire recommendations for management strategies.
architecture of the vocal apparatus needs to be mechanically

Granulomatosis with polyangiitis

Granulomatosis with polyangiitis (GPA, formerly known as The detectable presence or absence of circulatory
Wegener’s granulomatosis) is a potentially life-threatening, c-ANCA neither confirms nor excludes a diagnosis of
necrotising, autoimmune anti-neutrophil cytoplasmic GPA.5 c-ANCA can be elevated in a number of other
antibody (ANCA)-associated small vessel vasculitis. It can conditions and patients with GPA may never show
affect multiple systems including, typically, the kidneys c-ANCA positivity or demonstrate intermittent c-ANCA
and lungs. In general there is a slight male to female positivity at different time points along the course of their
preponderance of 1.5:1 in adults and while GPA can present illness, for reasons that are beyond the scope of this chapter.
in all ages and ethnicities, the majority of cases globally
involve patients between their third and fifth decade, who are Clinical findings
of Northern European extraction.1 Many patients also have Perilaryngeal manifestations of GPA typically include exertional
otolaryngological manifestations affecting the nose, larynx dypnoea, dysphonia and inspiratory stridor. Coughing on
and subglottis, as well as the ear, in independent orders of swallowing may also be a feature. Fibreoptic endoscopic
frequency.2,3 No progressive pattern of organ involvement assessment of the larynx may reveal apparently normal vocal
has been demonstrated and patients may present with cords, but more commonly reveal non-specific perilaryngeal
dysphonia, dyspnoea and/or dysphagia due to perilaryngeal hyperaemia with evidence of subglottic inflammation, with or
involvement as the first manifestations of GPA. without crusting. Evidence of a varying degree of subglottic
stenosis (SGS) may also be present, which may be graded using
Aetiology/pathogenesis the Cotton–Myer classification as I–IV based on whether
While the underlying aetiology remains uncertain, it is there is up to 50% occlusion, 51–70% occlusion, 71–99% or
thought that the destructive pattern of disease in GPA is total occlusion, respectively.6
due to an auto-amplifying inflammatory feedback loop,
where cytoplasmic anti-neutrophil cytoplasmic antibodies Diagnosis
(c-ANCAs) target neutrophil proteinase 3 (PR3) enzymes, Haematological investigations typically include tests
resulting in cell degranulation and the release of mediators for systemic inflammation, such as the erythrocyte
including oxygen free radicals, with associated local tissue sedimentation rate, renal involvement, an autoantibody
destruction. Local activated neutrophils produce further screen, including ANCA, and tests to exclude other rare
surface PR3, which induces upregulation of c-ANCA, with causes of inflammation. Spirometry with flow-volume
a subsequent ANCA-driven ongoing inflammatory state loops is less frequently carried out but may corroborate
featuring tissue injury, secondary infection and scarring.4 evidence of SGS with patterns typical of an underlying

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reason, as a small number of cases are ANCA negative at

presentation, diagnosis of GPA is sometimes made on the
clinical picture, and histology is often non-diagnostic.

Management
Because of the multisystem involvement in GPA, a
multidisciplinary approach is advocated, featuring screening
and management as appropriate. Systematic treatment
with combinations of cytotoxic agents, B-cell depleting
monoclonal antibodies and immunosuppressants may yield
good multisystem control of GPA and yet have a variable effect
on laryngeal manifestations, in which case targeted surgery
may still be required. Laryngeal surgery tends to be directed
to encroaching airway threats due either to restricted vocal
Figure 14.1 Endoscopic view of a patient with subglottic
granulomatosis with polyangiitis.
cord abduction or SGS.While tracheostomy can be performed
to bypass restrictions at the glottis and subglottis, endoscopic
fixed airway stenosis (see Figure 10.2). Imaging may also treatment should be employed early in the disease, avoiding the
be considered in the form of a plain chest radiograph or need for tracheostomy or stenting, as associated scarring may
fine-cut CT of the laryngotracheobronchial tree, which damage the airway further. Endoscopic airway management
may further highlight other sites of airway narrowing and can target disease at the level of the glottis, subglottis or
perhaps uncover evidence of pulmonary involvement. tracheobronchial tree. Where restricted vocal cord abduction
Definitive assessment is achieved with suspension is the issue, partial posterior cordotomy may be performed
laryngoscopy with rigid or flexible endoscopy of the with the aid of a CO2 laser via suspension microlaryngoscopy
large airways. This will also allow biopsies of the disease and jet ventilation. For subglottic disease, suspension
process (Figure 14.1). While the presence of giant cells microlaryngoscopy is also employed along with intralesional
with evidence of granulomata, inflammatory infiltrate steroid injection, radial CO2 laser cuts and balloon dilatation.7
and necrosis surrounding blood vessels is the classical Further interventions to address SGS include airway
histological manifestation of GPA, biopsies frequently stenting and laryngofissure with open airway reconstructive
yield non-specific signs of chronic inflammation. For this surgery, as detailed in Chapter 10 (Laryngotracheal stenosis).

Sarcoidosis
Aetiology/pathogenesis due to sarcoidosis affecting laryngeal nerve supply either
locally or in the central nervous system.10 Tracheobronchial
Sarcoidosis is a chronic, multisystem, autoimmune, non-
sarcoidosis is seen in more aggressive forms of the disease.
caseating, granulomatous, inflammatory disorder that
The underlying aetiology of sarcoidosis is
preferentially affects the lungs and perihilar lymph nodes.
unknown, but is believed to be due to excessive helper
It may also target numerous other sites including joints,
T  lymphocyte activation, in response to an exogenous
skin, heart, nerves, eyes, nose and larynx.7 Sarcoidosis was
agent, in genetically susceptible individuals. This leads to
first formally described by Caesar Boeck in Denmark in
immune dysregulation with resultant inflammation and
1899.8,9 It preferentially affects females rather than males
accumulation of non-caseating granulomata at affected
by 2:1, typically between their second and fifth decade and
sites. It is thought that part of the granulomatous process
while it can affect individuals of all ethnicity, it does have a
in sarcoidosis involves the direct synthesis of angiotensin-
propensity for people of African descent.9
converting enzyme (ACE), hence its elevated but non-
It is more common for the otolaryngologist to encounter
diagnostic serum levels.11
a patient with sarcoidosis who has nasal manifestations,
but patients may co-present or present with isolated,
potentially life-threatening upper airway involvement. In Clinical findings
general, perilaryngeal involvement tends to involve the Perilaryngeal involvement typically presents with
supraglottis and, less frequently, the vocal folds directly. dysphonia, dyspnoea, dysphagia and varying degrees of
Vocal cord paralysis is possible and is more commonly stridor. The onset is usually insidious with slow progression

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 Amyloidosis

Figure 14.3 Appearance of laryngeal infection with

mycobacterium tuberculosis.

involvement. Biopsy from an involved organ should reveal

non-caseating granuloma. It is also important to exclude
other treatable forms of granulomatous conditions, such
as mycobacterial infections (Figure 14.3).
Figure 14.2 View of laryngeal sarcoidosis, showing involvement of
the epiglottis, aryepiglottic folds and arytenoid mucosa.
Management
A multidisciplinary approach is advocated, with particular
and may be against a background of general lethargy. importance on working collaboratively with a chest
Fibreoptic laryngeal inspection typically reveals a thickened, physician. The main treatment options are long-term
oedematous pattern of inflammation involving the systemic immunosuppression.
arytenoids, aryepiglottic folds and epiglottis. The epiglottis Upper airway involvement can be successfully treated
may also be curled.The affected mucosa is classically pale or with intralesional steroids and the use of the CO2 laser
pink (Figure 14.2). via suspension microlaryngoscopy, where up to 120 mg
of methylprednisolone can be injected locally.12  The CO2
Diagnosis laser is used at 8 watts continuously to create multiple
Investigations are routinely carried out to check for closely related narrowed needle-point-like pits throughout
elevated calcium, serum ACE and signs of general the affected mucosa, giving a ‘pepper-pot’ pattern of laser
inflammation, such as an erythrocyte sedimentation burns. This mucosal sparing approach heals by scarring and
rate. A chest radiograph is important to exclude hilar contracts, reducing overall volume. Pedunculated lesions
lymphadenopathy or other pulmonary involvement. An violating the airway can be excised with the CO2 laser. (See
electrocardiogram may also be necessary to exclude cardiac p. 163 for further details regarding surgical management.)

Amyloidosis
Aetiology/pathogenesis The abnormal accumulation of these resistant proteins
leads to progressive organ dysfunction due principally to
Amyloidosis is a benign, chronic, inflammatory condition
volumetric expansion with associated pressure effects on
characterised by extracellular deposition of insoluble protein
local healthy tissues. In general, amyloidosis preferentially
fibrils, resistant to complete proteolysis, which aggregate
affects males rather than females by 2:1, typically between
in and around one or more organs. A number of different
their fifth and sixth decade.12 It can affect multiple systems
unrelated proteins may form the problematic misfolded
including cardiovascular, cutaneous, endocrine and both
classical beta-pleated sheets characteristic of amyloidosis
the peripheral and central nervous systems. In the larynx
and are frequently derived from immunoglobulins.

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 Inflammatory disorders of the larynx

amyloidosis can manifest as benign proteinaceous masses in

the supraglottis, at the level of the vocal cords or below.
It has already been established that amyloidosis is the
accumulation of a number of different subclasses of proteins
that form insoluble misfolded beta-pleated sheets that
proteases are unable to completely eliminate. Nomenclature
has now changed from earlier classifications describing
amyloidosis as either local disease, restricted to one organ,
or systemic to now being classed by the type of protein that
has undergone amyloid transformation.
There are over 50 recognised different types of amyloid
proteins.13, 14 It remains unclear why the proteins undergo
the beta-pleated sheet formation. Proteases are only able to
partly digest amyloid proteins, exposing the hydrophobic and
hydrophilic components, and so they progressively accumulate
in and around normal tissues as insoluble aggregates, slowly Figure 14.4 Amyloidosis involving the glottis and subglottis.
expanding and/or compressing the affected organ(s).
Clinical findings A serum amyloid P component scan is one such test, whereby
Symptoms will vary with the sites of perilaryngeal radiolabelled protein is injected into patients to locate areas of
involvement but will typically feature progressive dyspnoea amyloid deposition.
and dysphonia. Endoscopically, amyloid may present with
supraglottic masses, such as in the ventricles. Amyloidosis Management
may also present as a growth at any point along the vocal Management of laryngeal amyloidosis should be directed
fold or as a concentric narrowing (Figure 14.4), of the at the site of involvement. Amyloid-associated swelling can
subglottis.15 be treated as a benign tumour and excised with the CO2
laser or ‘cold steel’ phonomicrosurgery techniques. More
Diagnosis aggressive localised disease, where surgery may be damaging
The mainstay of diagnosis is obtaining a biopsy from an to laryngeal function (such as shown in Figure 14.4), may
affected site. Amyloidosis displays a pathognomonic apple be treated with radiotherapy and systemic involvement may
green birefringence on microscopy under polarised light after respond in varying degrees to chemotherapeutics. Hence
being stained with Congo red dye.14 Other investigations a collaborative multidisciplinary approach is essential. (See
should focus around excluding other system involvement. p. 57 for further discussion on amyloidosis.)

Mucous membrane pemphigoid

Aetiology/pathogenesis vulgaris, an intradermal desquamating condition that
classically affects the oral cavity.15,16 These disorders do
Mucous membrane pemphigoid (MMP), also known
share some similarities with MMP but differ in that MMP
as cicatricial pemphigoid, is a chronic relapsing-
preferentially affects the subepithelium of mucosa as a
remitting autoimmune disease that features subepithelial
chronic condition.15,16
mucocutaneous blisters with subsequent scarring, which
While the underlying aetiology remains uncertain, it has
can affect multiple sites, including eyes, oral cavity,
been established that autoantibody formation to components
genitalia and skin. It can also present with life-threatening
of the basement membrane induces an immune response at
involvement of the upper airways and aerodigestive
affected sites, leading to cleavage of the basement membrane
tract and usually affects older adults with equal gender
with disruption of the dermal–epidermal layer.15,16 The
distribution.15
separation leads to blistering and inflammation in the
There are a number of other similar blistering
subepithelial plane, which eventually heals with inefficient
autoimmune conditions whose details are beyond the
scaring. The scar formation, or cicatrisation, leads to restriction
scope of this chapter, such as bullous pemphigoid, which
and progressive loss of function at affected sites.
primarily forms tense cutaneous bullae, and pemphigus

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 Immunoglobulin G4-related disease

a b c
Figures 14.5a–c Mucous membrane pemphigoid (a) causing pharyngeal strictures, ulceration and inflammation. Radial CO2 laser cuts
and dilatation reveals vocal folds and oesophageal inlet (b). Appearance after response to medical treatment (c).

Clinical findings Management

Patients with upper airway MMP present with progressive MMP is difficult to treat. Current long-term systemic
dysphonia, dyspnoea and stridor.15,17 They may also be treatments include immunsupression, in combination
dysphagic. Fibreoptic assessment may reveal hyperaemia, with chemotherapeutics and compound antibiotics and
ulcers, blisters or evidence of strictures or scaring of the antibacterials such as dapsone, which themselves carry
supraglottis, subglottis or vocal cords directly. increased morbidity with prolonged use.18 Due to the
propensity for scarring, surgical intervention at the larynx
can be controversial, with concern that surgical injury may
Diagnosis potentiate further scarring and stricturing.
CT or MRI imaging of patients is helpful in assessing the The disease appears to more commonly involve the
extent of disease manifestation. Biopsy of laryngeal lesions supraglottic larynx with associated pharyngeal strictures
will reveal subepithelial blistering and immunoflourescence (Figures 14.5a–c). Surgery ideally should only be considered
studies will demonstrate autoantibody (IgG, IgA) deposition when medical treatment has proved ineffective. Endoscopic
along with complement on the epithelial basement CO2 laser cuts through the bands of scar and gentle
membrane layer.16 As this is not pathognomonic of MMP, balloon dilatation may relieve the need for tracheostomy17,
diagnosis incorporates this along with clinical presentation and intermittent endoscopic dilation of the pharynx, either
and features.16 with serial bougies or balloon, may help with dysphagia.

Immunoglobulin G4-related disease

Aetiology/pathogenesis sites.20,21 A wide range of affected sites has been reported
including the head and neck, thorax, retroperitoneum
The G4 subclass of immunoglobulins are glycoproteins
and hepatopancreatobiliary system. IgG4 disease has been
that are involved in mounting an antimicrobial immune
demonstrated in the upper airway as a fibroinflammatory
response. Immunoglobulin G4 (IgG4)-related diseases
pseudotumour of the glottis and subglottis.22
are a collection of multisystem inflammatory autoimmune
The underlying aetiology of IgG4 proliferation remains
processes that are typified by sclerosis with a dense
unclear; however, its accumulation at affected sites induces
inappropriate accumulation of IgG4 at affected sites.19,20
inflammation and fibrosis.19–23 This leads to progressive
The condition was well recognised in the pancreas but
tissue dysfunction, which may be partly reversible with
as extrapancreatic features continued to be reported,
appropriate treatment.
IgG4-related autoimmune disease became recognised as a
multisystem disorder in 2003.19
Most epidemiology and demographic studies to date have Clinical findings
focussed mainly on pancreatic patients, where it preferentially There is limited reported evidence of laryngeal
affects middle aged to older men, but age and gender manifestations, but it may present in isolation with
distribution is assumed to vary with pattern of affected progressive dysphonia, stridor and dysnoea.22

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 Inflammatory disorders of the larynx

Diagnosis Management
Circulating concentrations of IgG4 in the blood may While IgG4 disease may initially appear as a tumourous
be elevated or normal in affected cases, so the hallmark mass, it consistently responds well to systemic corticosteroids,
of diagnosis remains tissue biopsy.20,23 The general which underscores the importance of satisfactorily obtaining
immunohistological pattern of IgG4 manifestation is of a tissue diagnosis. Laryngeal manifestations may be managed
diffuse, sclerosing inflammation with an abundant, storiform with CO2 laser, topical intralesional steroids and balloon
(whirling irregular patterned) lymphoplasmic infiltrate, dilatation.22
abundant IgG4-positive plasma cells and T lymphocytes at
affected sites, alongside features of obliterative phlebitis and
a mild to moderate tissue eosinophilia.

Idiopathic inflammatory disorder of the larynx

Aetiology/pathogenesis examination classically reveals a degree of scarring that may
be of the subglottis in isolation or span from the glottis to
Idiopathic inflammatory disorder of the larynx is a diagnosis
the upper trachea.24–29
of exclusion for an isolated benign fibroinflammatory
condition of unknown aetiology that affects the larynx.
Diagnosis
It features chronic inflammation of the glottis and SGS
without history of previous laryngeal trauma or insult, The mainstay of investigations is to exclude other
including no previous history of laryngeal intubation. It inflammatory disorders that can affect the larynx, as discussed
primarily affects women of Northern European extraction earlier in this chapter, including serial blood tests for ACE
who are in in their third to fifth decade.24 and ANCA. Biopsy shows non-specific inflammation.
There are no particularly distinguishing features of this
condition. Indeed, diagnosis is made on clinical grounds, Management
with appropriate history and immunohistological studies Asymptomatic stridor can be managed conservatively.
showing generalised non-specific fibrosis without any Control of limited disease can be achieved with simple
of the characteristic features of other inflammatory balloon dilatation or steroid injection, cruciate CO2 laser
conditions.24–29 cuts and balloon dilation (Figures 14.6a, b). This may be
necessary on a repeated basis to obviate the need for long-
Clinical findings term tracheostomy.25–29 Patients with aggressive recurrent or
Patients present with dysphonia, dyspnoea and a variable extensive scarring may require open airway laryngotracheal
degree of stridor without history of previous laryngeal reconstruction utilising a variety of techniques, as detailed
intubation, injury or surgery. Fibreoptic laryngeal in Chapter 10 (Laryngotracheal stenosis).25–29

a   b
Figures 14.6a, b Idiopathic subglottic stenosis before treatment (a) and after steroid injection, radial CO2 laser cuts and balloon dilatation (b).

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 References

References
1 Lane SE, Watts R, Scott DGI (2005) Epidemiology of 17 Higgins TS, Cohen JC, Sinacori JT (2010) Laryngeal
systemic vasculitis. Curr Rheumatol Rep 7:270–275. mucous membrane pemphigoid: a  systematic  review
2 Srouji I, Andrews P, Edwards C et al. (2007) Patterns of and pooled-data analysis. Laryngoscope 120(3):
presentation and diagnosis of patients with Wegener’s 529–536.
granulomatosis: ENT aspects. J Laryngol Otol 121: 18 Kirtschig G, Murrell D, Wojnarowska F et al. (2002)
653–658. Interventions for mucous membrane pemphigoid/
3 Langford C, Sneller M, Hallahan C et al. (1996) Clinical cicatricial pemphigoid and epidermolysis bullosa
features and therapeutic management of  subglottic acquisita: a systematic literature review. Arch Dermatol
stenosis in patients with Wegener’s granulomatosis. 138(3):380–384.
Arthritis Rheum 39:1754–1760. 19 Kamisawa T, Funata N, Hayashi Y et al. (2003) A
4 Hoffman GS, Kerr GS, Leavitt RY et al. (1992) new clinicopathological entity of IgG4-related
Wegener granulomatosis: an analysis of 158 patients. autoimmune disease. J Gastroenterol 38:982–984.
Ann Intern Med 116:488–498. 20 Stone JH, Zen Y, Deshpande V (2012) Mechanisms
5 Seo P, Stone J (2004) The antineutrophil cytoplasmic of disease: IgG4-related disease. N Eng J Med 366(6):
antibody-associated vasculitides. Am J Med 117:39–50. 539–551.
6 Myer C, O’Connor D, Cotton R (1994) Proposed 21 Zen Y, Nakanuma Y (2010) IgG4-related disease: a
grading system for subglottic stenosis based on cross-sectional study of 114 cases. Am J Surg Pathol
endotracheal tube sizes. Ann Otol Rhinol Laryngol 34(12):1812.
103:319–323. 22 Virk JS, Stamatoglou C, Kwame I (2012) IgG4-
7 Sandhu GS, Howard DJ (2006) Acquired sclerosing pseudotumor of the trachea: a case report
Laryngopharyngeal Stenosis, 3rd edn. (eds. J Rubin, and review of the literature. Arch Otolaryngol Head
R Sataloff, G Korovin) Plural Publishing, Abingdon. Neck Surg 138(9):864–866.
8 Maier L (1997) Sarcoidosis. N Engl J Med 336(17): 23 Carruthers MN, Khosroshahi A,Augustin T et al. (2014)
1224–1234. The diagnostic utility of serum IgG4 concentrations
9 Black J (1973) Sarcoidosis of the nose. Proc R Soc Med in IgG4-related disease. Ann Rheum Dis doi:10.1136/
66(7):669–675. annrheumdis-2013-204907.
10 Devine KD (1965) Sarcoidosis and sarcoidosis of the 24 Liberman M, Mathisen DJ (2009) Treatment of
larynx. Laryngoscope 75:533–569. idiopathic laryngotracheal stenosis. Semin Thorac
11 Baudin B (2005) Angiotensin I-converting enzyme Cardiovasc Surg 21(3):278–283.
(ACE) for sarcoidosis diagnosis. Pathol Biol (Paris) 25 Benjamin B, Jacobson I, Eckstein R (1997) Idiopathic
53(3):183–188. subglottic stenosis: diagnosis and endoscopic laser
12 Butler CR, Nouraei SAR, Mace AD et al. (2010) treatment. Ann Otol Rhinol Laryngol 106:770–774.
Endoscopic management of laryngeal sarcoidosis. Arch 26 Grillo H, Mark E, Mathisen DJ et al. (1993) Idiopathic
Otolaryngol Head Neck Surg 136:251–255. laryngotracheal stenosis and its management. Ann
13 Gallivan G, Helen K (2010) Gallivan laryngeal Thorac Surg 56:80–87.
amyloidosis causing hoarseness and airway obstruction. 27 Valdez T, Shapshay SM (2002) Idiopathic subglottic
J Voice 24(2):235–239. stenosis revisited. Ann Otol Rhinol Laryngol 111:
14 Daudia A, Motamed M (2000) Primary amyloidosis of 690–695.
the larynx. Postgrad Med J 76:364–372. 28 Dedo H, Catten M (2001) Idiopathic progressive
15 Bergstrom L (1987) Cicatricial pemphigoid of upper subglottic stenosis: findings and treatment in
digestive and respiratory tract. Clin Dermatol 5: 52 patients. Ann Otol Rhinol Laryngol 110:305–311.
36–42. 29 Giudice M, Piazza C, Foccoli P et al. (2003) Idiopathic
16 Scully C, Muzio LL (2008) Oral mucosal diseases: subglottic stenosis: management by endoscopic and
mucous membrane pemphigoid. Brit J Oral Maxillofac open neck surgery in a series of 30 patients. Eur Arch
Surg 46:358–366. Otorhinolaryngol 260:235–238.

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 CHAPTER 15

Dysplastic lesions of the larynx

Taran S. Tatla

Definition and histological classification

Historically, laryngeal dysplasia (pre-malignant disease) has lesions of the laryngeal mucosa within which invasive
been observed and defined by the technical limitations of laryngeal SCC may arise.
the available optical systems at the time. To the naked eye, Kleinsasser2 described the first systematic classification
these lesions when illuminated with white light in  vivo for pre-cancerous, dysplastic lesions of the larynx: class 1:
appear white – hence the term ‘leukoplakia laryngis’ simple squamous hyperplasia; class 2: hyperplasia with
as first described by Pierce in 1920.1 The visible white atypia; and class 3: CIS. Histologically, initial microscopic
characteristic is usually a feature of keratin production from cellular changes occur within the basal epithelial layer, with
cells in the lesion and this can be associated with a number gradual extension of the dysplasia superficially towards the
of benign, pre-malignant and malignant disease states, surface of the lesion and laterally in all directions within
including hyperplasia +/− keratosis (squamous metaplasia), the epithelium. The altered epithelium shows a variety
dysplasia, carcinoma in situ (CIS) and invasive squamous of cellular and architectural changes for which a large
cell carcinoma (SCC) in the larynx (Figures 15.1a–i). variety of grading and classification systems have been
Through the 20th century, histological classification of established worldwide. The subjectivity afforded to the
laryngeal lesions has evolved through observation of these pathologist reporting (resulting in both inter- and intra-
lesions ex vivo with the conventional transmitted light observer variability3,4), as well as the lack of consensus for
microscope. The non-discriminatory white appearance a universally accepted classification system, has invited
macroscopically has been augmented by higher power much debate and criticism, often preventing published
magnification and microscopic characterisation, allowing research from being directly comparable5, as well as having
pathologists to describe the cellular appearances and significant therapeutic implications. The two main systems
morphological arrangements/derangements between used in recent years to define laryngeal pre-malignancy
cells within lesions. Their observations and illustrative are the World Health Organisation (WHO)6 classification
descriptions have allowed the realisation that certain and the Ljubljana classification of epithelial hyperplastic
‘leukoplakia’ lesions constitute pre-malignant (dysplastic) laryngeal lesions.7

Figure 15.1b Endoscopic view of left vocal cord leukoplakia in a

male smoker. Histology confirmed parakeratosis but no dysplasia
or malignancy.

Figure 15.1a Endoscopic view of a left vocal cord papillomatous

lesion in a male smoker with dysphonia. Histology confirmed mild
to moderate degree dysplasia with active inflammation alone.

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Figure 15.1c Endoscopic view of bilateral vocal cord lesions Figure 15.1d Endoscopic view of bilateral vocal cord lesions in
(left larger than right). Histology of left-sided biopsy confirmed a 29-year-old male with dysphonia. Histology confimed vocal
abnormal keratinising squamous mucosa, suspicous but not cord papillomatosis with no evidence for dysplasia or cancer
diagnostic for squamous neoplasia (dysplasia or carcinoma). (human papilloma virus negative).

Figure 15.1e Endoscopic view of bilateral vocal cord lesions Figure 15.1f Endoscopic view of bilateral vocal cord irregularity in a
straddling the anterior commissure in a 92-year-old non- 69-year-old male smoker and drinker with clinical laryngopharyngeal
smoker male with progressive severe dysphonia over a 2-year reflux disease. Histology of left vocal cord biopsy revealed mild to
period (lesions slightly enlarged on serial endoscopic views, but severe dysplasia associated with areas of focal ulceration. Lobules of
three repeated biopsies of right-sided lesion over this period squamous epithelium were noted in underlying stroma, suggesting
demonstrated focal inflammation, ulceration and mild to either well-differentiated invasive carcinoma or downgrowth
moderate dysplasia). regeneration phenomenon following repeated CO2 laser biopsy.

The WHO classification6 is almost universally used ●● Moderate dysplasia (architectural disturbance extending
in UK pathology departments and a consensus statement to middle third of epithelium with more marked nuclear
has recently been issued through the combination of a atypia than mild dysplasia and prominent nucleoli of
national pathology and otorhinolaryngology working party cells but no abnormal mitoses).
in support of this classification. The WHO classification ●● Severe dysplasia (greater than two-thirds of epithelium
defines dysplasia into four categories: showing architectural disturbance with associated
cytological atypia, marked nuclear abnormalities and
●● Squamous cell hyperplasia (increased cell numbers in loss of maturation of cells, nuclear polymorphism
the basal layers of epithelium) but architecture showing and mitoses often atypical and high up in the epithelium).
regular stratification with no cellular atypia; mild ●● CIS (almost or full-thickness architectural abnormalities
dysplasia (architectural disturbance in epithelium limited with pronounced cytological atypia, atypical mitotic
to lower third with some cytological atypia). figures and abnormal superficial mitoses).

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 Aetiology and pathogenesis

Figure 15.1g Endoscopic view of the larynx of the patient in Figure 15.1h Endoscopic view of a left vocal cord lesion in a
Figure 15.1f, taken 3 months earlier, when histology of left vocal 75-year-old male chronic smoker with dysphonia. Histology from
cord biopsy revealed difficult-to-grade dysplasia (at least mild to transoral CO2 laser excision confirmed a moderately differentiated
moderate). keratinising SCC measuring 12 mm in maximal extent and
infiltrating to a depth of 1 mm, reaching within 1 mm of the
anterior resection margin and focally to the deep margin of the
specimen. There was no associated dysplasia or CIS.

Figure 15.1i Endoscopic view of a left vocal cord lesion extending the length
of the left vocal cord, white light imaging differentiating distinct leuokoplakia
anteriorly with a thicker, ulcerative lesion in the mid-cord region. Histology from
transoral CO2 laser excision confirmed a moderately differentiated SCC arising in
the left mid glottis, invading to a depth of 3 mm. Anterior left vocal cord biopsies
showed no evidence for dysplasia or malignancy.

In the latter, it is theorised that malignant transformation of the same risk for developing invasive carcinoma as CIS and
cells has occurred but basement membrane and subepithelial therefore the two are often grouped together for clinical
invasion is not present. Severe dysplasia is thought to have management purposes.

Aetiology and pathogenesis

The multi-step carcinogenesis model has been dysplasia that does not follow the mild-moderate-severe
proposed to account for the aetiology and natural paradigm) shows surface maturation accompanied by
history of laryngeal dysplasia, mucosal cells progressing basal epithelial and architectural atypia, which makes
stepwise from mild, moderate and severe dysplasia, conventional grading difficult. These dysplasias are
through CIS, before invasion through the basement common in the larynx and SCC can arise from these
membrane into deeper submucosal tissue (invasive SCC) lesions in the absence of full-thickness ‘conventional’
(Figures  15.2a–f  ). Keratinising dysplasia (a form of dysplasia (Figures 15.2e, f  ).

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 Dysplastic lesions of the larynx

Figure 15.2b Moderate dysplasia showing dysplasia involving the

lower two-thirds of the surface epithelium. H&E, ×200.
Figure 15.2a Mild dysplasia of vocal cord showing dysplastic
changes limited to the lower third of the epithelium. H&E, ×200.

Figure 15.2c Severe dysplasia/CIS involving the full thickness of the Figure 15.2d Severe dysplasia/CIS. There is loss of cell polarity,
epithelium. H&E, ×200. hyperchromasia, nuclear pleomorphism and prominence of
nucleoli. H&E, ×400.

Figure 15.2e Low-grade keratinising dysplasia. There is parakeratosis and

irregular epithelial hyperplasia. Surface maturation is preserved. Unlike
conventional dysplasia, keratinising dysplasia shows surface maturation
accompanied by basal epithelial and architectural atypia, which makes
conventional grading difficult. These dysplasias are common in the larynx and
do not often follow a continuum from mild to severe dysplasia. SCC can arise
from these lesions in the absence of full-thickness ‘conventional’ dysplasia.
H&E, ×200.

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 Diagnosis

with increasing severity/grade of dysplasia from 10.6%

for mild/moderate to 30.4% for severe/CIS.9 Malignant
transformation is shown to often occur late (mean interval
5.8 years, maximum 14 years) and without relation to the
grade of dysplasia, suggesting patients should be followed
up long term under regular out-patient surveillance.
Laryngeal dysplasia shows a male:female preponderance
of approx 3–4:1, with average  age  at  presentation of
52 years10, almost a decade earlier than the average age at
which laryngeal cancer is diagnosed.8 Although the meta-
analysis failed to demonstrate sufficient data in studies to
comment on risk factors, other studies unsurprisingly
demonstrate similar risk factors to laryngeal cancer
Figure 15.2f SCC arising from keratinising dysplasia. H&E, ×200. including heavy smoking and alcohol consumption and
low socioeconomic class/occupation.11 In a recent review
The incidence of laryngeal dysplasia is reported to be article of aetiological factors including viruses contributing
between 2 and 10 laryngeal lesions per 100,000 of the to the establishment of laryngeal dysplasia, the authors
population.8 A recent systematic review of case series and conclude there is at present little evidence base to suggest
meta-analysis has demonstrated that it carries a statistically a role for human papilloma virus as an oncogenic factor in
significant risk of malignant transformation, the risk tripling laryngeal carcinogenesis.12

Diagnosis
The current gold standard for the prediction of malignant Keratosis may be associated with moderate dysplasia
transformation (dysplasia to anaplasia) is ex-vivo histological and frequently is seen in severe dysplasia, as well as CIS
assessment following invasive biopsy, most commonly and frank invasive SCC. In fact it is the keratosis that often
performed using the WHO grading system. Although gives these lesions their ‘white’ appearance at endoscopy
malignant transformation appears to be highly correlated and microscopy; hence the term ‘leukoplakia’ – for
with the severity of dysplasia grade (11% in mild-moderate, ‘white plaque’. Cellular derangement with progressive
30% in severe/CIS), Weller et al.9 demonstrate in their transformation to malignancy results in architectural change
meta-analysis that even the best histological grading systems of the epithelium and its various sublayers at microscopy, as
are not highly accurate, as some cases of mild dysplasia well as molecular and spectral changes in tissue composition
do progress to cancer, whereas most severe dysplasia cases (as  witnessed  by  the keratin production). Some of these
remain static or even spontaneously regress. changes in biomolecules are not specific for cancer changes
(i.e. keratosis is not specific to SCC); however, others are
increasingly being shown to be specific to dysplasia and
Biomarkers, ‘optical biopsy’ and cancer cancer progression across anatomical systems15; these show
screening great promise as potential tumour beacons for ‘optical
Biomarkers of transformation, proteins or genes showing biopsy’ and multiorgan cancer screening.
correlative/quantitative changes in patterns of expression ‘Optical biopsy’ is a phrase coined in recent years, emerging
between dysplastic disease and fully transformed cancers from the development of a variety of emerging light-based
may be one possible method for improving diagnostic imaging technologies that, to date, have been primarily
accuracy.  Although a recent systematic review failed to employed in laboratory or pre-clinical environments.16,17
demonstrate any good present evidence base for the use of A  wealth of data has continued to emerge over the last
biomarkers in predicting the future behaviour of laryngeal decade on a number of optical techniques and tools related
dysplastic lesions13, immunohistochemistry studies have to ex-vivo disease recognition in excised tissue biopsies from
revealed putative biomarker molecules correlating with the larynx amongst other organs (for cancer and non-cancer
progressive transformation14, which invite the development discrimination), as well as optical imaging performed in vivo
of an appropriate optical imaging tool for screening and from animal and, increasingly, human clinical studies.The huge
diagnosis of high-risk laryngeal lesions for early therapeutic potential for such an optical imaging tool, if demonstrated
intervention. clinically for accuracy (sensitivity  and  specificity)

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 Dysplastic lesions of the larynx

approaching  the present histopathology gold standard, has high-resolution endoscopic technique, used widely to
encouraged multidisciplinary groups to emerge for the aid diagnosis of dysplastic intestinal lesions, which has
development and clinical translation of such technologies.18 recently been investigated in vivo for suspect laryngeal
Illustration of clinical utility for disease diagnosis, screening lesions to differentiate precancerous and malignant
and surveillance, as well as aiding stratification and personalised laryngeal disease.19  The modality is based on the fact
therapeutic strategies, remain the medium and long-term that the depth of light penetration depends on the light
objectives for these groups. wavelength; the longer the wavelength, the deeper the
A recent review of emerging specialised optical imaging penetration. NBI modifies the broadband white light of
techniques from which digital images (‘optical biopsies’) can a xenon lamp into two narrow band beams with central
be acquired at high micron level resolution, compares and wavelengths of 415 nm (narrow band blue) and 540 nm
contrasts the benefits of these techniques over conventional (narrow band green) (designed primarily to penetrate
transmitted light microscopy.16 New technologies applied mucosa and submucosa). When used in combination they
in this way include narrow band imaging (NBI), confocal provide high surface contrast, displaying morphology of
microscopy, optical coherence tomography, Raman superficial capillary networks and subepithelial vessels for
spectroscopy and wide-field fluorescence microscopy, in-vivo differentiation of non-malignant from malignant
amongst others. Many of these contemporary instruments laryngeal lesions. Ni  et  al.20 demonstrated that utilising
are able not only to offer imaging at high resolution non- white light modes and NBI modes in vivo during clinic-
invasively, but also allow users to interrogate molecular events based flexible nasendoscopy with topical local anaesthesia
and better image live cells without disruption of tissue. had a sensitivity of 88.9% and specificity of 93.2% in
A number of optical imaging technologies have detecting malignant lesions. This is significantly superior
emerged to provide potentially clinically useful to white light illumination alone and its routine use is
adjunctive endoscopic information to that provided by recommended for early detection of laryngeal cancer and
white light alone. NBI is a novel, commercially available, precancerous dysplastic lesions (Figures 15.3a–f).

a b
Figures 15.3a, b White light HDTV intraoperative 70° endoscopic image (a) and corresponding NBI image (b) of right vocal cord leuko/
erythroplakia. The NBI image is said to demonstrate the typical neoangiogenetic pattern (brown spotted areas, arrows) in the posterior
third of the vocal cord, which on histopathology was confirmed to be CIS. (Images courtesy Olympus and Dr Cesare Piazza)

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 Diagnosis

c d
Figures 15.3c, d White light HDTV intraoperative 30° rigid endoscopic image (c) and corresponding NBI image (d) of a sessile lesion of
the anterior right vocal cord. The NBI image is said to demonstrate the typical neoplastic vascular pattern, helping to demarcate a better
definition for the surgical resection margin. Histopathology confirmed this to be an invasive carcinoma that extended to the lateral aspect
of the resected specimen. (Images courtesy Olympus and Dr Cesare Piazza)

e f
Figures 15.3e, f White light HDTV intraoperative wide-field 0° rigid endoscopic image (e) of irregular vocal cords with corresponding NBI
image (f). Histopathology of biopsies taken from both vocal cords confirmed hyperplastic mucosa with mild parakeratosis associated
with mild to moderate degree dysplasia of the left vocal cord. Interestingly, at wide-field and close-up illumination in such hyperplastic
epithelium, the submucosal neovascular discrimination is not so obvious with NBI and it adds very little additional information to
characterise areas of dysplasia compared with the white light HDTV image.

Various other optical techniques are emerging as to around 90% (a statistically significant increase of
potential translative clinical tools with unique capabilities 12%). Others have explored potential additional benefits
for molecular imaging based on the interaction of visible to autofluorescence in applying aminolevulinic acid
and near-infrared light with tissue, each interrogating a topically to the laryngeal mucosa, to preferentially induce
disease-specific source of contrast affecting one or more fluorescence within neoplastic cells, but reports have
of the measurable properties  of light.17 This contrast been conflicting as to whether aminolevulinic acid-
may originate from endogenous or exogenous sources induced fluorescence spectroscopy adds any further
and be manifest in  the  wavelength, frequency, intensity diagnostic accuracy to autofluorescence alone in the
or polarisation state of the measured optical signal. larynx, particularly in the context of laryngeal dysplasia
Auto-fluorescence spectroscopy21 has shown increased and carcinoma.22 Optical coherence tomography18,
sensitivity for diagnosis of pre-malignant and malignant Raman spectroscopy23 and fluorescence lifetime imaging
laryngeal lesions when used as an endoscopic adjunct microscopy24 are other emerging techniques under
to white light illumination, improving sensitivity levels investigation (Figures 15.4a, b and 15.5a–e).

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 Dysplastic lesions of the larynx

Figures 15.4a, b Axial B-scan ex-vivo images of invasive laryngeal SCC taken with a 1300 nm time domain optical coherence tomography
(OCT) imaging system. Red outlines (partial and complete) of dark OCT contours correlate with stromal epithelial transitions of well-
differentiated SCC, whereas the green lines show bright OCT signal, which appears to correlate with mature surface keratin.

a   b
Figures 15.5a, b Wide-field fluorescence lifetime imaging microscopy (FLIM) (a), using a 440 nm portable FLIM assembly, of a salvage
total laryngectomy specimen (right glottis/supraglottis SCC) split in the midline posteriorly and splayed open (b). Ex-vivo FLIM imaging is
performed immediately upon resection in the dedicated optical imaging laboratory located within the operating theatre complex. (Images
taken by the author and Mr Hugh Sparks, Department of Photonics, Imperial College, London)

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 Management of laryngeal dysplasia

5 mm
c d e
Figures 15.5c–e Endoscopic 0° intraoperative image taken in the operating theatre of a left vocal cord SCC (c), ex-vivo white light image
of the same left vocal cord lesion following excision by transoral CO2 laser surgery (d) and ex-vivo FLIM map taken of the same lesion
immediately following excision (e). (Images taken by the author and Mr Hugh Sparks, Department of Photonics, Imperial College, London)

Management of laryngeal dysplasia

The lack of uniformity in classification to date and a It is recommended that surgeons managing dysplastic
dearth of good-quality prospective studies in relation to laryngeal lesions should be appropriately trained and
the diagnosis and management of dysplastic laryngeal preferably provide their services as part of a head and neck
lesions has been highlighted through systematic review and cancer multidisciplinary team (MDT). It is acknowledged
meta-analysis.9 Literature has been reviewed and assessed that in most cases, diagnosis and treatment of a leukoplakia
on the currently employed treatment strategies, namely lesion will be undertaken as one invasive surgical procedure
CO2 laser excision, radiotherapy, vocal cord stripping (to in order that appropriate histological reporting and
a lesser extent) and watchful waiting.25 The controversy diagnosis is achieved. This excision biopsy for diagnosis
and dilemma of management is illustrated well; maximising also constitutes the initial management (resection) of
the opportunity for cure of a condition that has significant the lesion and it is recommended that the overall ‘white
morbidity and mortality attached (particularly for severe light’ appearance (illuminated and magnified through
dysplasia/CIS) through adequate treatment needs to be theatre endoscopy or microscopy) of the lesion should
balanced with the potential functional sacrifice (voice be considered the most important factor in determining
and swallow) that may result from more radical treatment management. It is agreed that the management decision
options (vocal cord stripping, repeated CO2 laser excision, depends foremost on whether there are single or multiple
radiotherapy, etc). Sadri et al.25 report improved local leukoplakic lesions or widespread cohesive disease (as may
control rates for laryngeal dysplasia following radiotherapy be seen with mucosal field change). Single and multiple
(93.52%) compared with CO2 laser excision (80.88%) and foci should be completely excised to all visible margins
vocal cord stripping (77.37%). Given that most of the reports if possible, but in the presence of widespread, confluent
on the management of laryngeal dysplasia were case series, leukoplakia, histopathological mapping of the lesion with
they acknowledge that it is difficult to make therapeutic multiple biopsies should be initially performed, followed
recommendations on the basis of evidence to date and by staged resection if feasible. All biopsies, including those
certainly robust high-level evidence is presently unavailable from multiple foci, should be mounted, oriented and
to comment on functional outcomes comparing alternative presented on an anatomical template to the pathologist for
treatment approaches. photodocumentation prior to histological processing. The
A consensus document has recently been communicated presence of dysplasia at surgical margins is not considered to
following a national workshop attended by 80 clinicians be an indication for further excision or biopsy.
(40  ENT surgeons and 40 pathologists), held under the Management should be considered in the light of the
auspices of ENT-UK and the Royal College of Pathologists.5 patient’s age and other co-morbidities/risk factors, with the
This attempts to develop some local unified standard to patient fully informed and consented to the potential risks
histopathology reporting and clinical management in of permanent voice change and disease recurrence. Any
laryngeal dysplasia, so as to provide an evidence-based histological grading subsequently should not be used in
management approach and better report audit and research isolation to guide treatment and follow-up strategy; instead,
for comparing outcomes of management. within the MDT due consideration should be made for all

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 Dysplastic lesions of the larynx

other clinical information, as well as the locality, extent and cord stripping, as routinely practiced in certain parts of the
endoscopic accessibility of dysplasia changes and the potential world, is not recommended.
for lifestyle modification (smoking and drinking cessation). It is recommended that all patients should receive
The recommended modality of surgical treatment is cold counselling to reduce risk factors (smoking and drinking)
steel or CO2 laser resection, with radiotherapy offered only and patients with symptomatic laryngopharyngeal
with discretion in rare circumstances to a very small number reflux should also be counselled and offered appropriate
of patients (i.e. poor access for resection in a primary high- treatment. Follow-up and surveillance is recommended for
grade lesion, two or more recurrences, patient high risk all high-risk dysplastic lesions (severe dysplasia/CIS) in a
for general anaesthesia, persistent or recurrent widespread similar manner to T1 laryngeal SCC patients, although for
severe dysplasia, patient preference). CO2 laser ablation is low-risk lesions diverse opinions were expressed preventing
discouraged so that maximum specimen is presented to the consensus, some arguing that a 6-month follow-up is
pathologist for diagnosis and the risk of vocal cord damage sufficient and others recommending at least a 2-year follow-
and impact on voice is minimised. The  procedure of vocal up or much longer still.

Future horizons
Through rapidly emerging technological advances, which high grades of dysplasia and carcinoma, as well as facilitate
are allowing the development and clinical translation of real-time, intraoperative delineation of tumour-free surgical
novel optical imaging modalities, the means for more resection margins, making frozen tissue sections obsolete.
accurate, non-invasive, multimodal endoscopic optical The consequences are profound, resulting in reduced
diagnosis is emerging that overcomes the subjectivity and healthcare expenditure through targeted larynx screening
inter- and intra-observer limitations of histopathology. The and earlier, more resource efficient and precise intervention,
classification of dysplastic laryngeal lesions can be expected particularly in the high-risk patient groups. Not least, these
to evolve further still in coming years as these tools are developments will result in better survival and functional
validated against the present gold standard histopathology. outcomes for the patient and should be enthusiastically
This will facilitate targeted screening of laryngeal lesions for embraced.

Acknowledgements
The author would like to thank Dr Paul Tadrous and Dr also grateful to Dr Ramona Cernat (Applied Optics Group,
Ezra Nigar (Department of Cellular Pathology, Northwick University of Kent) and Mr Hugh Sparks (Department of
Park Hospital, London) for providing histopathology Photonics, Imperial College London) for their assistance
images, commentary and review of the manuscript. I am with the OCT and FLIM optical tools.

References
1 Pierce NH (1920) Leukoplakia laryngis. Ann Otol 5 Mehanna H, Paleri V, Robson A et al. (2010) Consensus
Rhinol Laryngol 24:301–308. statement by otolaryngologists and pathologists on the
2 Kleinsasser O (1963) Die Klassifikation und diagnosis and management of laryngeal dysplasia. Clin
Differentialdiagnose der Epithelhyperplasien der Otolaryngol 35:170–176.
Kehlkopfschleimhaut auf Grund Histomorphologischer 6 Barnes L, Eveson J, Reichart P et al. (2005) (eds.) World
Merkmale. Z Laryngol Rhinol Otol 42:339–362. Health Organisation Classification of Tumours. Pathology
3 McLaren KM, Burnett RA, Goodlad JR et al. (2000) and Genetics of Tumours of the Head and Neck. IARC
Consistency of histopathological reporting of laryngeal Press, Lyon.
dysplasia. The Scottish Pathology Consistency Group. 7 Gale N, Kambic V, Michaels L et al. (1999) Criteria
Histopathology 37:460–463. for grading in the Ljubljana classification of epithelial
4 Fleskens SA, Bergshoeff VE, Voogd AC et al. (2011) hyperplastic laryngeal lesions: a study by members
Interobserver variability of laryngeal mucosal of the Working Group on Epithelial Hyperplastic
premalignant lesions: a histopathological evaluation. Laryngeal Lesions of the European Society of
Modern Pathol 24:892–898. Pathology. Histopathology 34:226–233.

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 References

8 Bouquot J, Gnepp DR (1991) Laryngeal precancer: a 17 Pierce M, Javier, Richards-Kortum R (2008) Optical
review of the literature, commentary and comparison contrast agents and imaging systems for detection and
with oral leukoplakia. Head Neck 13:488–497. diagnosis of cancer. Int J Cancer 123:1979–1990.
9 Weller MD, Nankivell PC, McConkey C et al. (2010) 18 Cernat R, Tatla TS, Pang J-Y et al. (2012) Dual
The risk and interval to malignancy of patients with instrument for in vivo and ex vivo OCT imaging
laryngeal dysplasia: a systematic review of case series in an ENT department. Biomed Opt Express 3(12):
and meta-analysis. Clin Otolaryngol 35: 364–372. 3346–3356.
10 Ricci G, Molini E, Faralli M et al. (2003) Retrospective 19 Watanabe A,Taniguchi M,Tsujie H et al. (2009) The value
study on precancerous laryngeal lesions: long-term of narrow band imaging for early detection of laryngeal
follow-up. Acta Otorhinolaryngol Ital 23:362–367. cancer. Eur Arch Otorhinolaryngol 266:1017–1023.
11 Grasl MC, Neuwirth-Riedl K, Vutuc C et al. (1990) 20 Ni X-G, He S, Xu Z-G et al. (2011) Endoscopic diagnosis
Risk of vocal cord dysplasia in relation to smoking, of laryngeal cancer and precancerous lesions by narrow
alcohol intake and occupation. Eur J Epidemiol band imaging. J Laryngol Otol 125(3):288–296.
6(1):45–48. 21 Arens C, Dreyer T, Glanz H et al. (2004) Indirect
12 Sadri M, McMahon J, Parker A (2006) Laryngeal autofluorescence laryngoscopy in the diagnosis of
dysplasia: aetiology and molecular biology. J Laryngol laryngeal cancer and its precursor lesions. Eur Arch
Otol 120:170–177. Otorhinolaryngol 261:71–76.
13 Nankivell P, Weller M, McConkey C et al. (2011) 22 Hughes OR, Stone N, Kraft M et al. (2010) Optical
Biomarkers in laryngeal dysplasia: a systematic review. and molecular techniques to identify tumour margins
Head Neck 33(8):1170–1176. within the larynx. Head Neck 32(11):1544–1553.
14 Sarioglu S, Ozer E, Kirimca F et al. (2001) Matrix 23 Bergholt MS, Lin K, Zheng W et al. (2012) In vivo,
metalloproteinase-2 expression in laryngeal real-time, transnasal, image-guided Raman endoscopy:
preneoplastic and neoplastic lesions. Pathol Res Pract defining spectral properties in the nasopharynx and
197:483–486. larynx. J Biomed Opt 17(7):0770021–0770027.
15 Murnane MJ, Cai J, Sjuja S et al. (2011) Active matrix 24 McGinty J, Galletly NP, Dunsby C et al. (2010) Wide-
metalloproteinase-2 activity discriminates colonic field fluorescence lifetime imaging of cancer. Biomed
mucosa, adenomas with and without high-grade Opt Express 1(2):627–640.
dysplasia, and cancers. Hum Pathol 42:688–701. 25 Sadri M, McMahon J, Parker A (2006) Management of
16 Chen Y, Liang C-P, Liu Y et al. (2012) Review of laryngeal dysplasia: a review. Eur Arch Otorhinolaryngol
advanced imaging techniques. J Pathol Inform 3:22. 263:843–852.

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 CHAPTER 16

Paediatric laryngeal disorders

Richard J. D. Hewitt, Benjamin E. J. Hartley & Thushitha Kunanandam

Introduction
The majority of paediatric laryngeal pathology is benign in focusing on assessment of the airway, which is crucial. The
nature and may be either congenital or acquired in origin. initial discussion centres around elective clinical assessment,
Two of the main functions of the larynx are protection of including descriptions of common diagnostic procedures
the airway and speech, and so laryngeal pathology tends (e.g. fibreoptic nasendoscopy, microlaryngobronchoscopy).
to present with either disorders of breathing or of voice. Subsequent sections discuss airway management in the
The degree of severity of the underlying lesion dictates the acute scenario of an unwell child and the increasingly
duration of symptoms and subsequent presentation of the common scenario faced in the hospital setting concerning
patient for medical attention. children with intubation/extubation difficulties.
This chapter describes a practical guide for the
management of children with benign laryngeal pathology

Clinical assessment
Assessment should begin with history and examination. laryngomalacia whereas constant stridor is most likely due
The history should focus on the two main symptoms: to fixed, structural pathologies.
breathing difficulty and voice. Table 16.1 summarises the If there is a history of recurrent or prolonged croup,
presentation of common pathologies according to these consideration should be given to the need to diagnose an
symptoms. Other factors to consider include the neonatal underlying structural abnormality affecting the airway calibre
history and associated co-morbidities. or to eliminate the possibility of an inhaled foreign body.
Cough can be related to episodes of croup but can also be
Airway assessment related to choking or aspiration events either acutely due to
The point of presentation will correlate with the severity foreign bodies or more chronically related to feeds and the
of the airway symptoms, with more significant pathology presence of a laryngeal cleft or tracheoesophageal fistula. In
presenting in the emergency room setting and milder, fact, a feeding history and failure to thrive are often good
intermittent symptoms leading to presentation in the out- indicators of respiratory difficulty in infants, as they are
patient environment. Stridor is the most common airway obligate nasal breathers in the first 3 months of life. Cyanotic
symptom and sign. It is important to note the time of onset episodes certainly indicate severe respiratory difficulty and
and the duration of stridor alongside any progression of can be due to several causes, but they are often associated
symptoms. The character of the stridor itself can indicate with tracheal disease such as external compression due to the
the likely level of pathology; for example, biphasic stridor presence of a vascular ring.
indicates subglottic and distal pathology whereas inspiratory The neonatal history, particularly that pertaining to
stridor points to glottic or supraglottic abnormalities. neonatal intubation and ventilation, is a strong predictor of
Stridor that has been present since birth is most likely to the likelihood of airway pathology.
be associated with congenital pathologies such as laryngeal Examination of the child should clarify the nature of
webs or bilateral vocal cord paralysis. A more gradual any upper airway noise (e.g. stridor versus stertor) and
onset over days or weeks to months is more likely due to quantify the degree of respiratory distress. Inspection of
laryngomalacia, subglottic haemangiomas or cysts. If the the child alone will indicate the level of difficulty, taking
onset is acute, diagnoses such as foreign body aspiration or into account the respiratory rate and signs of accessory
inflammatory or infectious conditions should be considered muscle use (tracheal tug, sternal/intercostal recession).
and an appropriate history sought. The intermittent General inspection of the child should also be carried
nature of stridor can point to dynamic conditions such as out to look for scars (due to cardiac surgery), cutaneous

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 Paediatric laryngeal disorders

Table 16.1  Benign laryngeal pathologies and their presentation according to the two
main symptoms of voice and airway problems
Voice problems Airway problems Airway plus voice
Thin laryngeal web Thick laryngeal web Thick laryngeal web
Small volume RRP Large volume RRP Large volume RRP
Unilateral vocal fold palsy Bilateral vocal fold palsy Bilateral vocal fold palsy
Vocal fold nodules Laryngomalacia
Subglottic stenosis
Subglottic haemangioma
Laryngeal cleft
Tracheomalacia
Vascular anomalies
RRP = recurrent respiratory papillomatosis.

haemangiomas, any dysmorphic features, particularly of ventilation and topical anaesthesia is applied to the vocal
the craniofacial area, and also of the overall neuromuscular cords allowing instrumentation of the airway. Positioning
tone, which can have a major impact on the airway. of the patient is optimally achieved with both a shoulder
A growth chart can be a useful measure, providing an roll and head ring. Diagnostic laryngoscopy can be achieved
objective indicator of the burden of respiratory distress. with the anaesthetic laryngoscope and 4 mm zero-degree
endoscope to allow for full visualisation of the airway to
Fibreoptic laryngoscopy the main bronchi with minimal irritation. Ventilating
Fibreoptic laryngoscopy can be useful in diagnosis of the bronchoscopes can allow for further instrumentation
underlying pathology. This is most often the case when in the distal airway such as suctioning and retrieval of
the pathology is at or above the level of the vocal folds. foreign bodies. Suspension laryngoscopy also allows for
Fibreoptic laryngoscopy is also invaluable  for dynamic instrumentation and is more useful for more proximal
and functional assessment of the airway, showing clearly, airway instrumentation. Standard MLB should initially
for example, the supraglottic collapse that occurs in involve inspection of all subsites followed by palpation for
laryngomalacia, and also for detecting immobility of the cricoarytenoid fixation and laryngeal clefts, and finally
vocal folds. As this assessment is carried out in the awake by dynamic assessment of vocal cord movement and
patient, it is occasionally difficult to obtain satisfactory views supraglottic prolapse. Visual assessment of the airway in
of the larynx despite best efforts. Topical preparation of the this manner should be complemented by adequate photo
nose with local anaesthetic and decongestant is beneficial in documentation using image capture systems.
the older child but omitted in the infants.
Voice assessment
Microlaryngoscopy and bronchoscopy Benign laryngeal pathology also presents with vocal
Microlaryngoscopy and bronchoscopy (MLB) is the abnormalities and this is mostly a presenting feature in the
gold standard for most airway diagnosis. It allows for out-patient setting unless it is accompanied by significant
full visualisation of the upper airways but additionally airway symptoms. Depending on the age of the child,
allows for palpation and dynamic assessment. Any lesional vocal abnormalities may only present as abnormalities of
pathology is also amenable to biopsy with this technique, the cry rather than of speech, as in the infant population.
allowing histological confirmation of the diagnosis. Formal In the older child, dysphonia and hoarseness are the
endoscopy such as this can also be therapeutic as well as common symptoms. Isolated vocal symptoms can be
diagnostic. thoroughly assessed in a specific paediatric voice clinic
MLB assessment in children requires an anaesthetised where a full assessment of the voice quality itself can be
but spontaneously ventilating patient. This can be achieved made, including the impact on quality of life. Fibreoptic
with inhalational gas/air techniques, which has been the laryngoscopy can again be a useful diagnostic tool and
traditional approach, or via the modern approach involving additional stroboscopy can augment the examination
total intravenous anaesthesia. A nasal prong facilitates findings with this technique.

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 Intubation and extubation difficulties

MLB is still often required to assess the full extent of in children other than in pathologies such as respiratory
any pathology or to rule out additional pathologies, as in papillomatosis, where disease debulking will lead to voice
the case of glottis webs, which can be associated with a improvement in most cases.
subglottic stenosis (SGS). Phonosurgery is rarely performed

Emergency airway management

Management of the marginal airway requires clear and airway, providing a ‘holding measure’ while deploying
methodical assessment to aid prompt diagnosis and these teams to definitively manage the situation. These
treatment to optimise the airway. include oxygen, nebulised adrenaline, Heliox (79% helium
The history is again important but should focus on and 21% oxygen mix) and steroids.
the immediate history leading up to the current episode If an infective aetiology is suspected, a diagnostic MLB
of airway difficulty, and specific attempts should be made may not be necessary and in fact is often contraindicated
to identify established diagnoses such as SGS. Often the in severe cases such as acute epiglottitis. The aim should
acute presentation can be a deterioration from a chronic be to stabilise the airway with either medical treatment,
condition. The duration of symptoms together with which can include oxygenation, steroids and antibiotics,
associated features, such as coryzal symptoms or a chocking or to secure the airway with intubation, often by the
episode, may suggest a likely cause for the presentation. anaesthetists with an ENT surgeon merely on standby in
Examination of the child in this situation is often case of difficulty. Equipment such as the video Glidescope®
performed in parallel with the history taking, as rapid can improve the grade of view at laryngoscopy and are
assessment is required. The principle of assessment in often used by anaesthetists to secure the airway in difficult
this scenario is to establish the need for a secure and safe situations. Fibreoptic intubation is also more commonplace.
airway. The degree of respiratory effort made by the child Techniques for a difficult intubation favoured by ENT
should be carefully observed, looking for signs such as surgeons include the use of the ventilating bronchoscope or
an opisthotonic posture and severe chest wall recession. intubation with an endotracheal tube placed over a 2.7 mm
Pulse oximetry can be extremely useful in this situation Hopkins rod. If intubation is not possible, the option of a
but should not be relied upon, as decompensation can be surgical airway must be considered. The situation can still
rapid with reduced oxygen saturations being a late sign. be controlled if ventilation is possible via bag and mask
A  child that is quietening in terms of their respiratory technique or a laryngeal mask airway.
effort could be tiring and deteriorating rather than MLB can in these cases be deferred in order to investigate
improving. A  general assessment of signs of toxicity the possibility of underlying pathology in infective cases
should also be made and these include measurement of or to deal with structural abnormalities such as cysts and
temperature, heart rate and capillary refill. These signs granulation tissue, the latter situation requiring an earlier
can be determined by inspection of the patient alone intervention.
with minimal contact, therefore reducing the likelihood If the history is suggestive of an airway foreign body,
of distressing the child and exacerbating the airway. MLB is indicated at the time of presentation to relieve the
Further attempts at evaluating the child should occur in obstructing cause. Initial assessment should always be with
a relatively more controlled theatre environment with a the Hopkins rod, as this identifies a high/laryngeal foreign
senior anaesthetist and ENT surgeon present to assess and body, which can then be removed. More distal foreign
secure the airway as deemed appropriate. There are several bodies will require the use of the ventilating bronchoscope
measures that can be employed to manage an emergent and optical forceps.

Intubation and extubation difficulties

In children with infective aetiologies, treatment of lead to an irritation and worsening of the structural
the underlying condition often results in successful component such that extubation is challenging. There
extubation. This is not, however, always the case and the are also an increasing number of cases with difficulties
child who is difficult to extubate can be as challenging as in extubation correlating with the number of premature
an emergent airway. Some children requiring intubation, infants requiring prolonged periods of intubation and
but with an underlying structural abnormality, may ventilation. Unfortunately, difficulty with extubation
require surgical intervention, as often intubation can often leads to cases of multiple reintubations, which can

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 Paediatric laryngeal disorders

lead to further airway trauma, particularly to the very a recurrent problem, however, MLB should be performed
fragile neonatal subglottic mucosa. with a view to aiding extubation. MLB in these instances can
Successful extubation relies on optimal respiratory identify underlying airway pathology, which can be corrected
function. Lung function should always be optimised prior to facilitate extubation. For example, seal flipper granulations
to consideration of extubation, as any compromise may lead or subglottic cysts can be identified and removed to relieve
to failure. In the very premature, therefore, the preferential any airway obstruction. The calibre of the subglottis can
management may require the neonate to remain ventilated also be assessed and, most importantly, an early and evolving
for a prolonged period of time, allowing lung function to SGS can be treated. An early, soft stenosis can be managed
improve. As the neonate approaches their expected delivery endoscopically: this involves radial incision of the stenosis
date with a corresponding improvement in lung function, (‘Mercedes-Benz’ configuration) and balloon dilatation
extubation can be more successful. Prolonged intubation of the segment, which can be followed by topical steroid
may well have implications for the neonatal subglottis, but injection. Repeating this procedure every 2–3 weeks may
this can be investigated and treated once extubation has been prevent the formation of an established, more solid stenosis. If
achieved.1 A period of expectant intubation can also minimise the stenosis is not amenable to endoscopic treatment, airway
the problems that occur with repeated attempts at intubation reconstructive surgery will be required. This may be in the
following failed extubations. This period of ‘laryngeal rest’ form of cricoid splits, although more commonly in the form
is often overlooked as a management option. In these cases, of laryngotracheoplasty with (costal) cartilage grafts.
when extubation is finally planned, a 24–48-hour period of If there are continued difficulties with failed extubations
steroid cover is beneficial prior to the subsequent attempt. relating to ventilation issues or continued and significant
If a failed attempt at extubation is associated with stridor airway pathology, a tracheostomy may be required in this
requiring reintubation, this should suggest the likelihood of period. If a tracheostomy is performed, it is important to
airway pathology. It may not be necessary to investigate this monitor these children regularly so that any changes in
immediately if successful extubation can be achieved with the clinical situation can be monitored and the option of
the more conservative measures described above. If there is decannulation entertained.

Laryngomalacia
Aetiology/pathogenesis Diagnosis
Laryngomalacia is the most common congenital laryngeal Diagnosis can be made by flexible laryngoscopy in the
pathology. The term laryngomalacia was first used by ­out-patient clinic setting. A good view of the supraglottic
Jackson and Jackson in 19422 to describe the inward collapse collapse is seen; however, visualisation of the vocal folds may
of the larynx during inspiration. The underlying aetiology not be possible and the distal airway cannot be examined. In
of laryngomalacia is not fully understood and is thought children in whom there is significant associated respiratory
to relate to anatomical, histological and neurological distress, a  suspicion of a second pathology or failure to
factors. The epiglottis is tall, tubular and omega-shaped,
the aryepiglottic folds are shortened, tight and bulky and
the arytenoid mucosa is bulky with a tendency to prolapse
(Figure 16.1). Immaturity of the laryngeal and supraglottic
cartilages tends towards an inherent softness, which  also
contributes to laryngeal collapse during inspiration.
Neurological immaturity is thought to result in arytenoid
muscle incoordination and reduced laryngeal tone.

Clinical findings
Intermittent inspiratory stridor is the classical mode of
presentation for laryngomalacia typically at or within a
short period of time from birth. The stridor is exacerbated
by the exertion of feeding and crying and lying in the supine
position.  The stridor worsens up until the age of about
6 months and then gradually subsides with full resolution Figure 16.1 Laryngomalacia depicted by a tubular/omega-shaped
around the 2 years of age mark. epiglottis and arytenoid prolapse.

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 Subglottic haemangioma

thrive, an MLB is necessary. Up to 20% of children with reduce the added insult to the larynx from reflux contents.3
laryngomalacia have been reported to have a second Surgical treatment is undertaken in patients with severe
pathology. laryngomalacia and failure to thrive. A supraglottoplasty
is the surgical procedure of choice.4 The mucosa and soft
Management tissue of the aryepiglottic folds are excised using cold steel
For the vast majority of children with isolated laryngomalacia instruments or, less commonly, CO2 laser, with the extent of
who are thriving, the treatment is conservative. Medical tissue removal dependent on local anatomy.
treatment for concomitant reflux and feed thickeners will

Congenital subglottic stenosis

Congenital SGS arises due to a narrowing of the subglottis
due to failure of full canalisation of the cricoid cartilage with
residual thickened cartilage or excess submucosal tissue.
Patients present with variable degrees of airway obstruction.
Symptoms are usually precipitated by the added insult of
oedema from an upper airway infection, commonly croup,
to an already compromised airway.
The Cotton–Myer grading system is used to classify SGS
by the degree of obstruction of the cross-sectional area of
the subglottis: Grade I: 0–50% obstruction; Grade II: 51–70%
obstruction; Grade III: 71–99% obstruction (Figure  16.2);
Grade IV: no detectable lumen.

Diagnosis
Diagnosis is made by MLB with inspection of the subglottis.
The airway is ‘sized’ using the age-appropriate endotracheal
tube with assessment of its ease of placement, position
relative to the airway circumference and the presence of
an air leak on ventilation. There are two distinct types of
cartilage anatomy associated with congenital SGS. The first
Figure 16.2 Grade III subglottic stenosis.
is a cricoid ring that is of normal dimensions in the anterior-
posterior direction and narrowed bilaterally. The second
morphology is a small cricoid cartilage with a thickened Endoscopic incision and dilatation may suffice for soft
anterior lamina and a small posterior airway. tissue stenosis5; however, it is not beneficial in cartilaginous
stenosis. These latter cases will require cricotracheal
Management resection with excision of the stenotic segment or
Surgical treatment is required for symptomatic patients. laryngotracheal reconstruction (LTR) with anterior and/or
In the emergency setting a tracheostomy may be required. posterior cartilage grafts.6

Subglottic haemangioma
Aetiology/pathogenesis Clinical findings
Subglottic haemangiomas are benign neoplasms of the Patients present with stridor several weeks after birth.
subglottic area of the larynx. These lesions undergo
a period of rapid growth during the first year of life Diagnosis
followed by a period of slow involution. In 50% of cases Diagnosis is made by MLB.   The classical finding is a
a cutaneous haemangioma is seen; however, only 2% of compressible red lesion in the subglottis (Figure 16.3),
cutaneous haemangiomas are associated with a subglottic more frequently located on the left than the right. However,
haemangioma. it may extend inferiorly into the trachea. The overlying

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 Paediatric laryngeal disorders

mucosa may have a normal appearance. Biopsy is not

usually required due to the constant physical findings on
examination, although in suspicious cases a biopsy (or
aspiration) is warranted.
Management
The mainstay of treatment is medical, using the beta blocker
propranolol.7 The exact mechanism of action of propranolol
is unclear but is reported to be related to the inhibition of
the release of pro-angiogenic factors, which are involved in
the endothelial cell proliferation seen in haemangiomas.
Other medical options for treatment are systemic steroids,
which can produce a rapid reduction in the size of large
haemangiomas. Surgical treatment avoids the complications
of pharmacotherapy. Submucosal excision for small isolated
lesions can be performed without significant risk of
bleeding. For severe cases a tracheostomy may be required
to secure the airway while further management is planned,
Figure 16.3 Red lesion in the (right) subglottic lesion typical of or a tracheostomy may be left in situ until the haemangioma
subglottic haemangioma. regresses with age.

Laryngeal webs
Aetiology/pathogenesis Diagnosis
Laryngeal webs occur due to a failure of complete Diagnosis of a laryngeal web requires MLB for visualisation
canalisation of the embryological larynx. Most webs occur and palpation. Flexible laryngoscopy, although useful for
at the level of the glottis; however, they may also occur in visualisation, is unable to establish the full extent of the web.
the subglottis. Laryngeal webs typically occur in the anterior
glottis with fusion of both vocal cords. Management
Cohen’s Classification system categorises laryngeal webs
Treatment of the web is directed by its extent. Type I webs
into four types:
may require incision and dilatation only. Type II webs,
●● Type I. An anterior web involving 35% of the glottis particularly those with thick webs, require incision along
or less. The vocal folds are visible through these thin the margin of one vocal fold and dilatation. This may need
webs. to be repeated. Type III webs will often require a covering
●● Type II. An anterior web involving 35–50% of the tracheostomy; the web is endoscopically incised along the
glottis, which may be thin or thick, with extension into free edge of one vocal fold and a keel inserted to prevent
the subglottis. The vocal folds are usually visible within recurrence. Type IV webs require a tracheostomy to secure
the web. the airway, and open surgery is preferable to avoid multiple
●● Type III. An anterior web involving 50–70% of the endoscopic procedures with poor outcomes.6 This is delayed
glottis, typically with a thick anterior portion and until the child is around 3 years or older when a laryngofissure
extension into the subglottis. and keel placement can be adequately performed. In Type IV
●● Type IV. 75–90% of the glottis is involved by a uniformly cases with cricoid cartilage deformity causing an SGS, LTR
thick web, which extends into the subglottic larynx.The with an anterior graft is required; this may be performed as
individual vocal folds are not identifiable and may be a single-stage procedure with endotracheal intubation for
fused together. There may be an associated abnormality 1 week postoperatively. In cases where a tracheostomy is
of the anterior cricoid cartilage. in place, the reconstruction can be delayed for a few years,
allowing for growth of both the child and the airway.
Clinical findings All types of web require voice therapy, which may be a
The common presenting features are airway obstruction, necessity for several years. However, despite long-term voice
usually inspiratory stridor, and voice changes, typically a therapy, children with Type IV webs may never achieve a
high-pitched voice. normal voice.

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 Laryngeal clefts

Laryngeal atresia
Laryngeal atresia may result in a complete glottic web If laryngeal atresia is diagnosed antenatally, an extra-
and is commonly associated with tracheal agenesis or uterine intrapartum procedure to insert a tracheostomy
tracheoesophageal fistula. This communication permits and secure the airway can be planned. Most cases are
ventilation of the lungs via a tube in the oesophagus. incompatible with life.

Laryngeal clefts
Aetiology/pathogenesis make a diagnosis, particularly of Type I and II clefts. The
arytenoids must be lateralised during endoscopy to permit full
Laryngeal clefts comprise laryngeal and
visualisation and palpation of the interarytenoid area,which
laryngotracheoesopheageal clefts. These clefts occur due
may be obscured by redundant mucosa filling the cleft.
to a failure of fusion of the posterior cricoid cartilage and
interarytenoid muscles and failure of formation of the dividing Management
septum between the trachea and the oesophagus. Laryngeal
Treatment is dependent on the type of cleft. Type I clefts
clefts can co-exist with a second pathology and approximately
may typically require no surgical intervention. In patients
25% of these patients will have a tracheoesophageal fistula.
who have mild symptoms, feed thickeners and anti-reflux
Tracheomalacia may also be  an  associated pathology
medication may suffice. However, for symptomatic and more
secondary to tracheal cartilage deformities associated
extensive clefts, surgery is required.8 Types I and II clefts are
with the cleft. Laryngeal clefts are associated with several
amenable to endoscopic two-layer closure. Type III clefts
syndromes including Opitz-Frias, Pallister-Hall syndrome,
require open surgery with laryngofissure and tracheostomy
VACTERL (Vertebral anomalies, Anal atresia, Cardiac
during recovery and healing. The suture line must be
anomalies, Tracheoesophageal fistulas, Ear anomalies, Renal
protected and therefore a gastrostomy for feeding is preferred
anomalies, Limb  anomalies) and CHARGE (Coloboma,
to a nasogastric tube. Type IV clefts may require either a
Heart anomalies, choanal Atresia, growth Retardation, Genital
neck incision or a lateral neck incision and a thoracotomy
anomalies and Ear anomalies) syndromes.
for extended clefts.9 Postoperative intubation for a period of
The Benjamin and Inglis Classification describes four
1 week is necessary as a tracheostomy must not be inserted in
types of laryngeal cleft:
a position that will compromise the surgical repair.
●● Type I. The cleft extends down to the level of the vocal
cord.
●● Type II. The cleft extends below the level of the vocal
cords into the cricoid cartilage.
●● Type III.The cleft extends down into the cervical trachea.
●● Type IV. The cleft extends to the thoracic trachea and
may reach the carina (Figure 16.4).

Clinical findings
Laryngeal cleft morphology covers a wide spectrum and
subsequent presentation also covers a range of symptoms
relating to aspiration and airway compromise.These include
coughing with feeding, recurrent chest infections, stridor
and cyanosis.

Diagnosis
Assessment of swallowing using a video swallow or functional
endoscopic evaluation of swallowing may demonstrate
aspiration; however, this may be missed in children who Figure 16.4 Laryngeal cleft (Type IV) giving rise to the double-
aspirate intermittently. MLB is the key method for accurate lumen appearance, with an anterior airway lumen and posterior
diagnosis. Careful inspection and palpation is required to oesophageal lumen.

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 Paediatric laryngeal disorders

Tracheomalacia
Aetiology/pathogenesis tracheomalacia tends to affect the lower third of the trachea
and may be associated with bronchomalacia.
Tracheomalacia is the abnormal collapse of the tracheal
wall due to reduced cartilage strength. It may be classified
Management
as primary or secondary. The former is seen in otherwise
normal babies or in premature babies with inherently soft Treatment for primary tracheomalacia is infrequently
cartilage tracheal rings. Secondary tracheomalacia occurs indicated, as with time the cartilage matures and the
in tandem with another pathology, particularly lesions that tracheal lumen adopts a more robust and consistent
compress the airway such as vascular anomalies and chest anatomy. In secondary tracheomalacia, removing the
wall deformities. Tracheomalacia is frequently identified in source of external compression permits the trachea to take
cases of tracheo-oesophageal fistula. up its normal shape and the ensuing cartilage maturation
takes place over time.10
Clinical findings
The symptoms associated with tracheomalacia depend on
the length of affected trachea and the degree of anterior-
posterior compression. Stridor is the main presenting
feature. This occurs in the first few weeks of life and is
exacerbated by exertion such as crying and feeding. In
cases of significant tracheomalacia there may be cyanotic
attacks, also known as death attacks. Intrathoracic
tracheomalacia typically causes wheeze and may be
mistaken for asthma.

Diagnosis
Diagnosis is made by MLB, with careful observation of the
movements of the tracheal wall. The posterior tracheal wall
is observed to collapse anteriorly (Figure 16.5). There is a
reduced cartilage to membranous trachea ratio.
In cases that are secondary to external compression, there
may be visible deformity of the cross-sectional shape of the
tracheal lumen into a triangular shape, suggesting localised Figure 16.5 Primary tracheomalacia characterised by collapse of
compression. In cases of tracheo-oesophageal fistula, the the posterior tracheal wall anteriorly.

Vascular anomalies
Congenital vascular anomalies arise during the of the sternum, is required for cases of life-threatening
development of the aortic arch and great vessels. These apnoeas.
vessels cause compression on the structures they encircle, A double aortic arch results in a vascular ring that
namely the oesophagus and trachea. Tracheal compression encircles both the trachea and oesophagus. The most
may present with stridor, wheeze, cough or apnoeic common type is an ascending aorta that splits around the
episodes.11,12 Aberrant innominate artery compression trachea and oesophagus and then re-joins the descending
of the trachea affects the right anterolateral area of the aorta. Other variants include a right aortic arch and a
trachea. On diagnostic MLB a characteristic endoscopic left ligamentum arteriosum. Symptoms commence at
appearance is seen. The pulsations of the vascular anomaly birth with predominantly airway problems, and stridor in
are visible and can be abolished by pressing the tip of these cases is usually exacerbated by feeding. Dysphagia is
the bronchoscope against the corresponding tracheal rare due to the predominantly liquid diet in this age group.
wall.  Treatment is usually conservative as improvement A  contrast swallow can clearly demonstrate the posterior
occurs as the child grows. Surgery, by way of innominate indentation of the oesophagus. CT  delineates the full
arteriopexy to suspend the artery to the posterior surface anatomy.

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 Vocal fold palsy

In the presence of a pulmonary artery sling, the progressive breathing difficulties. MLB demonstrates
normal left pulmonary artery is absent and an aberrant anterior compression of the trachea, which may be subtle.
vessel arising from the right pulmonary artery surrounds The right main bronchus is narrowed.The lower half of the
the right bronchus passing between the trachea and trachea is compressed from the right, laterally.
oesophagus. Presentation is usually with a history of

Juvenile-onset recurrent respiratory papillomatosis

(See also Chapters 4 and 13). Management
Aetiology/pathogenesis Treatment is undertaken to reduce the bulk of disease
from the larynx to restore an airway with minimal trauma
Recurrent respiratory papillomatosis (RRP) is caused by
to the vocal folds. The current recommended treatment
human papilloma virus (HPV) and results in benign epithelial
modality is the microdebrider, which permits removal of
proliferation. It is predominantly found at sites in the airway
papillomata and blood from the surgical field with minimal
where there is a transition from one type of epithelium to
soiling of the distal airway. Cold steel instrumentation,
another, commonly found on the vocal folds and anterior
including the microdebrider, also avoids thermal damage,
commissure of the larynx. Symptoms at presentation include
although haemostatic control can be less efficient with
hoarseness and varying degrees of respiratory distress.
these techniques. Laser ablation of papillomata is in
HPV is a DNA virus and types 6, 11, 16 and 18 are
widespread use and achieves papilloma removal with
associated with RRP. These are transmitted vertically from
little in the way of bleeding. However, scarring may be
mother to child. The virus is thought to enter epithelium
more of a problem with this technique and its popularity
through a breech in its surface and subsequently takes up
is reducing. Adjuvant medical therapies, such as the anti-
residence in the basal layer of the mucosa.
viral agent cidofovir13,14, are also used to supplement
Diagnosis surgical excision. This is most commonly employed when
Diagnosis can be made using fibreoptic laryngoscopy in the frequent and repeated surgical excision, for example on
out-patient clinic setting and confirmed on MLB, which a monthly basis, is required to gain control of the disease
will allow biopsy and histological confirmation. and symptoms.

Vocal fold palsy

Aetiology/pathogenesis vocal fold palsy may present with paradoxical movements of
the vocal folds as the vocal folds function as a one-way valve –
Vocal fold immobility is the accepted term that includes
drawing together during inspiration and passively opening
vocal fold palsies. Unilateral vocal fold palsies are largely
during expiration. It is important to rule out other causes of
congenital or of congenital central origin. Bilateral vocal
vocal fold immobility such as cricoarytenoid joint fixation by
fold palsy is usually secondary to a central cause such
palpating the larynx during the microlaryngoscopy. Once the
as myelomeningocele, Arnold–Chiari malformation or
diagnosis is established, further investigations are warranted
hydrocephalus. Unilateral vocal fold palsy may be congenital
to detect the underlying cause.
in origin, largely left-sided cardiovascular pathology, but is
chiefly due to acquired causes. Management
Treatment may include a period of watchful waiting as
Clinical findings vocal fold mobility may recover within a year; however, if
Bilateral vocal fold palsy may present with significant there are no signs of recovery by the second year, it is very
stridor and airway obstruction; unilateral palsies tend to unlikely to recover at all. A surgical tracheostomy may be
present less acutely with stridor, aspiration, an abnormal cry required for cases of bilateral vocal fold palsy that present
and dysphonia. in extremis. Airway expansion procedures such as posterior
cordotomy and arytenoidectomy may be of benefit.15 For
Diagnosis unilateral cases injection medialisation may be performed,
MLB in the very young or fibreoptic laryngoscopy permits a although often in the paediatric population, speech and
view of the larynx and assessment of the vocal folds. Bilateral language therapy input is the mainstay of treatment.

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 Paediatric laryngeal disorders

Vocal fold nodules

Aetiology/pathogenesis Diagnosis
Vocal fold nodules are benign bilateral swellings located at Diagnosis can be made in the out-patient setting with
the junction of the anterior third and posterior third of the fibreoptic laryngoscopy or stroboscopy. Speech therapy is the
vocal fold and arise due to inappropriate and excessive voice mainstay of treatment and surgery is very rarely indicated.
use.They initially start as small soft swellings but harden and
enlarge with continued vocal trauma.

Clinical findings
The most common presenting feature is dysphonia or
hoarseness.

References
1 Wei JL, Bond J (2011) Management and prevention of 9 Propst EJ, Ida JB, Rutter MJ (2013) Repair of long
endotracheal intubation injury in neonates. Curr Opin type IV posterior laryngeal cleft through a cervical
Otolaryngol Head Neck Surg 19(6):474–477. approach using cricotracheal separation. Laryngoscope
2 Jackson C, Jackson C (1942) Diseases and Injuries of the 123(3):801–804.
Larynx. Macmillan, New York, pp. 63–69. 10 Montgomery J, Sau C, Clement W et al. (2014)
3 Hartl TT, Chadha NK (2012) A systematic review of Treatment of tracheomalacia with aortopexy in
laryngomalacia and acid reflux. Otolaryngol Head Neck children in Glasgow. Eur J Pediatr Surg 24(5):389–93.
Surg 147(4):619–626. 11 Rogers DJ, Cunnane MB, Hartnick CJ (2013) Vascular
4 Preciado D, Zalzal G (2012) A systematic review of compression of the airway: establishing a functional
supraglottoplasty outcomes. Arch Otolaryngol Head diagnostic algorithm. JAMA Otolaryngol Head Neck
Neck Surg 138(8):718–721. Surg 139(6):586–591.
5 Lang M, Brietzke SE (2014) A systematic review 12 Kussman BD, Geva T, McGowan FX (2004)
and meta-analysis of endoscopic balloon dilation of Cardiovascular causes of airway compression. Paediatr
pediatric subglottic stenosis. Otolaryngol Head Neck Anaesth 14(1):60–74.
Surg 150(2):174–179. 13 Clamp PJ, Saunders MW (2013) Systematic review
6 Gallagher TQ, Hartnick CJ (2012) Laryngotracheal of intralesional cidofovir dosing regimens in the
reconstruction. Adv Otorhinolaryngol 73:31–38. treatment of recurrent respiratory papillomatosis. Int J
7 Bajaj Y, Kapoor K, Ifeacho S et al. (2013) Great Pediatr Otorhinolaryngol 77(3):323–328.
Ormond Street Hospital treatment guidelines for 14 Chadha NK, James A (2012) Adjuvant antiviral therapy
use  of propranolol in infantile isolated subglottic for recurrent respiratory papillomatosis. Cochrane
haemangioma. J Laryngol Otol 127(3):295–298. Database Syst Rev 12:CD005053.
8 Broomfield SJ, Bruce IA, Rothera MP (2011) Primary 15 Worley G, Bajaj Y, Cavalli L et al. (2007) Laser
endoscopic repair of intermediate laryngeal clefts. arytenoidectomy in children with bilateral vocal fold
J Laryngol Otol 125(5):513–516. immobility. J Laryngol Otol 121(1):25–27.

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 CHAPTER 17

In-clinic procedures
Nancy Solowski, Greg Postma & Paul Weinberger

Introduction
Clinic-based procedures and laryngology are a perfect diameter endoscopes while improving image quality and
match, and the average laryngologist’s practice involves magnification. Other advances such as fibre-based lasers and
a significant amount of in-clinic work. In fact, the field new injection materials have further advanced the range of
of laryngology developed historically as an out-patient in-clinic interventions that can be performed.
(clinic-based) discipline well over 100 years ago. This Clinic-based laryngology procedures are well tolerated
initial period where laryngology was practiced almost overall and are easily learned. Procedures done in the clinic
entirely outside of the operating room, over time offer many advantages, including the ability to monitor
transitioned to largely operating theatre-based procedures. voice throughout the procedure, improved patient safety
This was largely due to better equipment available and and cost-effectiveness. The use of topical anaesthesia in
improving general anaesthesia techniques. Most recently, particular is advantageous in that it allows patients to tolerate
with the rising costs of medical care and the advent of in-clinic procedures without general sedation. Patients are
newer technology, in-clinic laryngology procedures have often able to return to work following these procedures
again become commonplace. and do not require a caregiver to drive them to and from
Improved technology has greatly increased the the appointment. This is especially appealing when treating
laryngologist’s ability to diagnose and treat laryngological diseases that may require multiple rounds of intervention,
disorders in the clinic. The advent of distal chip such as recurrent respiratory papillomatosis (RRP).
technology has allowed development of ever-smaller

Equipment
While many otolaryngology practices are well equipped instrumentation to perform biopsies and other procedures.
to support a variety of in-clinic procedures, it is helpful to TNOs with add-on cameras have the camera at the proximal
develop a checklist of equipment needed if you are adding part of the scope, where the eyepiece is. TNO systems may
in-clinic procedures to your armamentarium. Specific also utilise single-use external wrappers (endosheaths)
equipment will be listed later in this chapter under each that often allow for passage of biopsy forceps or other
procedure, but most of the basic equipment is universal to instruments through the sheath. This makes cleaning of the
these in-clinic procedures. endoscope far easier, as it keeps body fluids and potentially
sharp instruments outside of the scope. The most common
Transnasal oesophagoscope length for a TNO is 60 cm, although the authors have
The transnasal oesophagoscope (TNO) is arguably the found a shorter endoscope quite valuable for bronchoscopy
single most important tool to support in-clinic procedures. and laryngeal biopsy, as the longer true TNO length can
While older-style TNOs with the camera at the proximal make working proximally more physically taxing to the
end (similar to traditional fibreoptic flexible laryngoscopes) endoscopist.
are still available, most laryngologists agree that the cost
difference to upgrade to modern distal chip-style TNOs are Other equipment
well worth the extra investment. A distal video-chip TNO A video monitor (usually incorporated into a video tower
provides improved visualisation coupled with decreased with a light source and recording system) is essential to
scope diameter, as the camera is located at the distal portion allow adequate visualisation and freedom of movement
of the endoscope. Most distal chip TNOs have a 2 mm for in-clinic procedures. Recording the examination is
working channel, which allows for irrigation and air- extremely beneficial, as it allows the physician to review
insufflation, as well as the ability to pass a wide variety of the examination at slower speeds. High-definition video

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 In-clinic procedures

and frame-by-frame playback further enhance the ability equipment (bayonet forceps and cotton pledgets), topical
to discriminate subtle findings. Other essential equipment decongestants and anaesthetics, examination chairs capable
items to enable in-clinic procedures are usually omnipresent of raising and lowering the patient position and medical
in otolaryngology clinics. These include nasal packing suction devices (either portable or in-wall).

Preparing the patient

Ideally, an in-clinic procedure will start with a calm and be unable to tolerate passage of the TNO. Additionally, for
relaxed patient who has been well informed regarding procedures requiring a single-use item, such as a potassium
the upcoming procedure. The informed consent process titanyl phospate (KTP) laser or a pulsed dye laser (PDL) fibre,
serves to satisfy ethical and legal requirements for ensuring the authors’ practice is to use a flexible laryngoscope just
patient autonomy and participation in their medical care. prior to the procedure to examine the larynx and confirm
It also has the benefit of mentally preparing the patient for previous findings and the need for the surgery.
the procedure. For instance, if the patient knows ahead of
time that during the oesophagoscopy they may experience Dietary restrictions
eructation, oesophageal gas and some gagging, they may Patients scheduled for some in-clinic procedures do
be better prepared to tolerate these admittedly unpleasant not have any pre-procedure dietary restrictions. Most
sensations with less drama. In the authors’ practice, the laryngologists agree that patients who undergo in-clinic
patient is informed about what to expect at the time of transnasal oesophagoscopy or bronchoscopy should not
booking the appointment for the procedure, and provided eat or drink for 3 hours before the procedure. There are
with a short one-page information sheet on what to expect. several reasons for this: (1) to allow for gastric emptying
The day of the procedure, a signed informed consent is to facilitate full visualisation of the lower oesophageal
obtained, the procedure is explained again and, finally, the sphincter on retroflexion; (2) to minimise regurgitation;
preparation for the procedure takes place. and (3) to minimise aspiration risk. It should be
noted, however, that a recent meal is not an absolute
Vital signs monitoring contraindication for a TNO examination.
Following informed consent, the patient is seated in the
otolaryngology examination chair in the sitting position. Anticoagulants
As routine, vital signs are obtained for patients undergoing In the vast majority of cases patients do not need to stop
in-clinic procedures. The authors, and others, have found anticoagulation; most surgeons agree that airway and
that continuous monitoring of vital signs throughout oesophageal examination and biopsy may be performed
the procedure is NOT necessary, although this may be without complication in patients on clopidogrel, aspirin
appropriate for elderly individuals with severe hypertension or warfarin, although patients should be warned of
or coronary artery disease. One helpful tip is that for new the slightly increased risk of bleeding and haematoma
patients, a trial passage of a (more abundant and easier to formation while on anticoagulation. In light of these data,
clean) flexible laryngoscope should always be attempted in- there is logically an increased risk to the patient if they are
clinic prior to using the TNO for examination or procedures. instructed to discontinue anticoagulants simply by rote, due
If significant nasal obstruction is present or the patient is to the increased risk of a thromboembolic event from the
poorly tolerant of flexible laryngoscopy, he or she will likely discontinuation.

Anaesthesia
In most practices, ‘clinic-based procedures’ are generally suite, specialised training in conscious sedation and
considered surgical procedures performed on an awake monitoring and increased risk compared with a simple
patient using topical or local anaesthesia, with no clinic examination. On the contrary, in-clinic unsedated
sedation. This is an important point to remember, both bronchoscopy is safe and requires no additional monitoring
in planning the feasibility of clinic-based procedures in a because patients are not sedated. Some physicians may have
specific practice setting and in the actual implementation. been tempted to stretch the boundaries of clinic-based
Some facilities may initially balk at adding clinic-based surgery by adding mild sedation for ‘patient comfort’.
procedures (for instance in-clinic bronchoscopy) because Unless performed in a more traditional procedure-room
traditionally this involves an expensive procedure type setting, this is to be discouraged as the vast majority

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 Anaesthesia

of data documenting the safety of these techniques are advanced transnasally and paused at the nasopharynx. The
based on procedures done without sedation. Certainly, washpipe can then be slightly advanced to clear the tip,
if a surgeon prefers to perform ‘in-clinic procedures’ in a while the endoscope is still straight. If instrumentation is
procedure room with additional equipment and staff, this advanced after turning caudally, there is an increased risk
is acceptable and indeed many otolaryngologists prefer the of damaging the working channel at the flexure point,
additional support available in this setting. Ultimately, the which can be an expensive misadventure.
underlying concepts are unchanged regardless of location. Topical lidocaine (4%) may be then be applied dropwise
through the washpipe. The authors’ usual practice is to
Topical anaesthesia begin with the tongue base in small aliquots (2–4 drops at a
The majority of laryngologists apply topical nasal time). After approximately 30 seconds, attention is focused
anaesthesia and decongestant for procedures including on the epiglottis in a similar fashion. At this point further
‘simple’ transnasal flexible laryngoscopy (TFL). Although anaesthesia is procedure- and anatomical site-specific.
some studies have indicated that topical anaesthesia does For laryngeal and tracheal procedures, the vocal folds and
not improve patient satisfaction, one crossover study laryngeal inlet must be completely anaesthetised. This is
showed improved tolerance of TFL with combined nasal accomplished by applying a bolus mist spray (1–2 ml) of
decongestant and anaesthesia. In the authors’ experience, anaesthetic over the glottis while the patient is phonating /
adequate nasal anaesthesia and decongestion are vital to ee/, which will usually anaesthetise the true and false vocal
patient comfort and tolerance and, therefore, to successful folds. A repeat ‘laryngeal gargle’ may be necessary to obtain
completion of the procedure. The patient is seated upright the desired level of anaesthesia. These same manoeuvres
in the examination chair, facing the endoscopist.The nose is may also be accomplished via an Abraham cannula passed
topically decongested first with a 1:1 mixture of aerosolised transorally combined with transnasal flexible endoscope
topical anaesthetic (4% lidocaine) and decongestant visualisation.
(0.05% oxymetazoline). Standard flexible laryngoscopes An alternative method to anaesthetise the
are generally 3–4 mm and often do not require additional laryngotracheal mucosa is to utilise nebulised lidocaine.
topical nasal preparation to pass the endoscope. In patients Two to four millilitres of 4% topical lidocaine may be
with ‘tight’ nasal anatomy or in patients who will have the placed in a standard albuterol nebuliser chamber and
larger TNO passed, additional topical nasal anaesthesia attached to room air. The patient is instructed to inhale
is usually given. The solution is vigorously sprayed onto a the aerosolised lidocaine via a facemask. It may take up to
cotton pledget and the pledget placed along the floor of the 10 minutes to complete nebulisation. This method may
nasal cavity for 10 minutes. Either surgical pledgets (more be used in conjunction with other methods of topical
expensive) or unwound cotton balls may be used. A spray of anaesthesia application as long as weight-based lidocaine
20% benzocaine may be administered to the oropharynx if toxicity thresholds are observed. This latter method
needed. (Note: When using benzocaine it would be wise to can be particularly effective for facilitating in-clinic
limit application to no more than two sprays, due to the risk bronchoscopy.
of methaemoglobinaemia.)
Application of topical anaesthesia directly to the surgical Local anaesthesia
site is then performed, most often using the TNO itself. Some procedures are best facilitated using a percutaneous
A substantively unchanged initial approach is required for local anaesthetic approach. This can be accomplished
procedures, whether involving the supraglottis, glottis, via the cricothyroid or thyrohyoid membranes.
oesophagus or trachea. The authors preferred method is Careful palpation of neck landmarks will reveal the
to passage a 1.8 mm  × 800  mm hollow plastic catheter applicable landmarks, including thyroid cartilage,
(‘washpipe’) into the working channel of the TNO. The hyoid bone, cricothyroid and thyrohyoid membranes.
catheter is advanced outside of the patient until the tip A small amount (1–2 ml) of lidocaine with epinephrine
is directly at the exit from the end of the scope but not (1%  lidocaine with 1:100,000 epinephrine) may
protruding; placing the washpipe (or other instrument for be  applied to the subcutaneous neck tissues overlying
that matter) before introduction of the scope into the patient the desired membrane. A 10 cm thin (25-gauge) needle
greatly facilitates procedure time, as there is no concern attached to a syringe filled with 3 ml of lidocaine
for going too quickly and causing injury. Attaching a can then be passed through the anaesthetised soft tissue,
syringe of lidocaine directly to the working channel of the through the cricothyroid or thyrohyoid membrane. If
endoscope is possible, but does not permit fine control and the needle is passed through the cricothyroid membrane,
will ‘waste’ anaesthesia. This can be problematic if larger aspiration of air will confirm intratracheal positioning
doses of lidocaine are necessary. The  endoscope is then prior to injection of anaesthetic. The lidocaine is then

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 In-clinic procedures

quickly injected, causing reflex coughing that will the hypopharynx becomes overly anaesthetised, secretions
distribute topical anaesthesia over the laryngotracheal tend to pool, leading to aspiration and subsequent
mucosa. Conversely, the needle position through the coughing during the procedure.This can be frustrating for
thyrohyoid membrane may also be confirmed by direct the patient and the surgeon.) Lidocaine toxicity may occur
visualisation using flexible endoscopy. The thyrohyoid when additional dosing is then applied in the mistaken
membrane approach will allow lidocaine to be directly belief that inadequate anaesthesia is to blame. While the
administered onto both the true and false vocal folds recommended dose limits for local injections of lidocaine
under direct visualisation. The level of anaesthesia may without epinephrine are 4.5 mg/kg, it should be noted
be tested by gently placing the tip of the endoscope that many manufacturers recommend a 3.0 mg/kg dose
along the appropriate tissue to see if stimulation is limit for topically applied lidocaine due to more rapid
noted. system absorption across mucous membranes. Thus for
The appropriate level of anaesthesia is obtained almost 4% topical lidocaine, this would be 5.25 ml for a 70 kg
immediately with these approaches and typically lasts for patient. Lower dosing may be needed for patients with
20–30 minutes. Repeat application of a small amount certain cardiac conditions or hepatic or renal compromise.
of anaesthetic may be necessary for longer procedures, Patients should always be questioned about prior reactions
although this generally is not required. (Note: More is to lidocaine and other topical anaesthetics before the
not always better; excess anaesthetic administration has the start of the procedure (although true lidocaine allergy is
potential to increase the difficulty of the procedure. When uncommon).

Complications related to in-clinic procedures

Overall, the incidence of complications associated with in- a vasovagal episode should be placed in a reclined position,
clinic procedures is quite low and serious complications preferably with the feet elevated above the head. Most
almost non-existent. In the thousands of patients reported cases resolve with no further intervention and no sequelae,
in the literature, only a single serious complication has but it would be wise to monitor vital signs until the
been reported. This case was an oesophageal perforation patient returns to full awareness and normal physiological
encountered during a prospective trial. To date, no other function. Patients who have pre-existing heart conditions
serious complications have been reported. or worrisome symptoms (e.g. radiating chest pain) should
Less serious complications do occur, but are uncommon. be referred to the emergency room for further evaluation,
The most common is epistaxis; obviously, passage of the although this has never been encountered in the authors’
endoscope through the nose may result in mucosal abrasion practices.
and epistaxis. Such bleeding is usually self-limited and only Vocal fold haemorrhage following in-clinic procedures
rarely requires intervention such as nasal packing or cautery. is also rare, but must be carefully managed. Patients
Patients with underlying uncontrolled hypertension or experiencing an unusual amount of dysphonia (or aphonia)
hypercoagulable states (especially anticoagulant medication following in-clinic surgery should undergo laryngoscopy to
such as warfarin) are at increased risk of epistaxis following rule out a vocal fold haemorrhage. If found, these patients
in-clinic procedures. It is important to note that these are should be placed on complete voice rest for 5–7 days. The
not contraindications for in-clinic procedure, and the vast reasoning behind voice rest is that vibration and movement
majority of patients even in this higher risk group do not of the vocal folds during phonation could cause dispersion
experience epistaxis or other complications. Intervention of the blood into the surrounding tissue, including the
for epistaxis follows standard recommendations and superficial lamina propria of the vocal fold. Blood in the
will vary based on practice location. In the US, for superficial lamina propria is thought by most experts to
example, first-line therapy is topical oxymetazoline nasal carry significant risk of subsequent inflammatory response
decongestant spray applied liberally to the nares and direct and scar tissue formation, which can lead to irreversible
pressure by applying external compression bilaterally over hoarseness.
the nasal ala to compress the sides of the nose against the Other even less common complications include
midline septum. lidocaine toxicity (discussed above in the anaesthesia
The second most common complication from an in- section) and vocal fold haematoma, which has been
clinic procedure is vasovagal episode. This is characterised reported following in-clinic injection or laser treatment
by a dramatic reduction in pulse rate, syncope or pre- but is extremely rare. As with epistaxis and vocal fold
syncope, and loss of circulatory tone. Patients experiencing haemorrhage, there is likely a slightly higher risk for

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 Post-procedure instructions

patients on anticoagulation and they should be counselled under each specific procedure heading. In general, however,
on this, but again it is not a contraindication. When patients who exhibit high levels of anxiety may not be
a haematoma is diagnosed, the patient should be followed good candidates for in-clinic procedures. This can usually
closely and placed on complete voice rest until the be assessed during the initial examination when flexible
haematoma subsides. laryngoscopy is performed. Patients who balk or react
The most serious complication of flexible (and poorly to the simple laryngoscopy are unlikely to cooperate
rigid oesophagoscopy) is oesophageal perforation. successfully with a more involved in-clinic procedure,
As  mentioned above, only one case of oesophageal especially since most of them also require a larger diameter
perforation has been reported when utilising a TNO and scope. Similarly, even cooperative patients who have
this was reported by a non-otolaryngologist. Owing to significant anatomical nasal obstruction often cannot be
the paucity of complications in transnasal oesophagoscopy, treated in the clinic; this again can usually be predicted with
knowledge is necessarily derived from experience with the flexible laryngoscope.
sedated oesophagoscopy. Most serious oesophagoscopy
complications occur when forcing the endoscope past a Vocal professionals
stricture or inadvertently mistaking the pyriform sinus A final category of patients deserves special mention,
for the oesophageal inlet and forcing the oesophagoscope the vocal professional or professional voice user. (Note:
through. General principles of endoscopy, such as ‘Professional voice user’ is not limited to opera or musical
avoiding undue force when advancing the endoscope theatre singers, but also includes patients with other
and never advancing blindly, should protect from such vocations that regularly place demands on the voice.
a misadventure in transnasal oesophagoscopy as well as These include people in careers such as radio personalities,
traditional oesophagoscopy. In transnasal oesophagoscopy, salespeople, company executives, telemarketers, teachers
the fact that the patient is awake and unsedated is thought and others.) When a procedure involves the vocal folds,
to be responsible for the increased safety. It is unlikely an these vocal professionals are usually treated by more
unsedated patient would allow a forced perforation of the traditional intraoperative procedures. This is due to the
pyriform sinus without offering vigorous protest, while higher level of magnification and precision afforded in
the same patient relaxed with propofol and midazolam in the operating theatre. A notable exception to this is that
the endoscopy suite undergoing traditional oesophagoscopy in-clinic laser using angiolytic wavelengths (such as KTP
may offer no complaint. laser or PDL) is quite safe and is often the procedure of
choice for such vocal professionals.
Contraindications
There are few absolute contraindications for in-clinic
procedures and more detailed discussions will be found

Post-procedure instructions
Following in-clinic procedures, most surgeons provide If a biopsy was performed or mucosa breached (such
the patient with standardised post-procedure instructions. as from injections, some laser interventions, etc.), patients
For procedures that required topical anaesthesia of the should be warned that they may notice some blood-tinged
laryngotracheal complex, patients are advised to wait sputum. Patients with larger amounts of bleeding should
2–3  hours before ingesting food or liquids to reduce call for medical assistance and go to the local emergency
the risk of aspiration. In the authors’ practice, time is room. Many authors recommend a period of vocal rest after
taken to ensure patients understand these instructions; a surgical procedures involving the true vocal folds. If voice
well-educated patient is far more likely to comply with rest is not prescribed, patients should be informed that minor
instructions. A picture or model of the pharynx and amounts of hoarseness and voice changes are expected
larynx is helpful to show the areas of anaesthesia and the immediately after vocal fold surgery. Markedly strained
proximity of the oesophageal inlet and the airway. Patients voicing or aphonia after completion of prescribed voice
are also advised to initially attempt a small sip of water rest should prompt an in-clinic laryngoscopic examination
after the waiting period has elapsed to determine if the to evaluate for possible vocal fold haemorrhage. If a vocal
anaesthetic has worn off sufficiently. Coughing should fold haemorrhage is noted, close follow-up and strict voice
herald an additional 30-minute wait before attempting rest are indicated to minimise the chance of permanent scar
another liquid challenge. tissue formation and dysphonia.

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 In-clinic procedures

Individual in-clinic procedures

Transnasal oesophagoscopy themselves and do not have to have a caretaker following
the procedure. This translates to improved convenience,
Overview and reduced work hours lost by both the patient and the
A major change in otolaryngological practice over the would-be driver/caregiver. One of the best evaluations
last decade is the refinement of in-clinic unsedated of patient preference for oesophagoscopy is a randomised
oesophagoscopy. Transoral passage of an endoscope (as crossover study by Jobe et al. (see Further reading). In
traditionally performed in an endoscopy suite) elicits an this study, patients undergoing screening for Barrett
intense gag reflex in most individuals as the endoscope metaplasia and dysplasia were examined by either transnasal
passages the base of the tongue, thereby mandating sedation oesophagoscopy or sedated flexible oesophagoscopy,
for the procedure.This transoral approach was mandated by and then crossed over to the opposite examination for
the fact that until recently, flexible oesophagoscopes with a subsequent surveillance oesophagoscopy. More than
a working channel were of too large a diameter to pass 70% of patients in the study reported a preference for the
through the nasal cavity. As flexible endoscope technology unsedated transnasal oesophagoscopy over conventional
has advanced, particularly through the development of endoscopy for future surveillance. Interestingly, in this study
distal chip imaging, endoscopes have become dramatically there was also no difference between the two modalities in
thinner. Current distal chip TNOs (Figure 17.1) retain terms of ability to detect Barrett metaplasia, although the
a true working channel, and can still easily be passaged use of transnasal oesophagoscopy following surveillance of
transnasally with only topical anaesthesia. Several Barrett’s oesophagus patients is controversial.
studies have demonstrated that patients prefer transnasal Initially, there was some fear that in-clinic procedures, such
oesophagoscopy to sedated oesophagoscopy, likely due as transnasal oesophagoscopy, would create opportunities
to avoidance of sedation or general anaesthesia. Patients for increased complications. This has been shown not
undergoing transnasal oesophagoscopy may transport to be the case, and it is generally accepted that transnasal
oesophagoscopy is well tolerated by patients and has a low
complication rate. In a large retrospective study of patients
undergoing transnasal oesophagoscopy for diagnostic
oesophagoscopy, Postma et al. (see Further reading) found
no major complications and a minor complication rate
of 1.1%. Complications in these 700 patients included six
cases of self-limited epistaxis and two vasovagal episodes.
Similarly, Dumortier et al. (see Further reading) reported
a very low incidence of complications in a series of 1,100
patients undergoing transnasal oesophagoscopy in France.
These studies provide evidence consistent with transnasal
oesophagoscopy being of equivalent safety to sedated
oesophagoscopy.   There are additionally several cogent
arguments suggesting transnasal oesophagoscopy may
indeed be safer than rigid or sedated flexible endoscopy.
Patients undergoing transnasal oesophagoscopy are
alert and more able to protect their airway in the event
of regurgitation. Similarly, in sedated flexible or rigid
oesophagoscopy the pyriform sinus can be perforated while
trying to advance the endoscope into the oesophageal
inlet; however, during transnasal oesophagoscopy, patients
are awake and may be able to alert the surgeon, as severe
discomfort would be experienced. Indeed, Tsao et al. (see
Further reading) recommended transnasal oesophagoscopy
over rigid oesophagoscopy during oesophageal screening in
Figure 17.1 Distal chip transnasal oesophagoscope (right) and head and neck cancer patients to reduce the complication
a fibreoptic laryngoscope (left). of oesophageal perforation.

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 Individual in-clinic procedures

Indications for transnasal oesophagoscopy may be of the examination. The newer version TNOs utilise distal
classified as diagnostic (oesophageal, extra-oesophageal) or video-chip technology.This involves placing a miniaturised
procedural. Oesophageal diagnostic indications for transnasal CCD video chip (the fundamental unit inside a video
oesophagoscopy include dysphagia, recurrent regurgitation, camera) at the distal end of the endoscope. This allows
odynophagia and complicated or refractory reflux disease. dramatically improved image quality, combined with a
Extra-oesophageal indications include globus pharyngeus, reduction in endoscope diameter, while maintaining the
chronic cough, dysphagia, screening for head and neck cancer 2 mm working channel.
and moderate to severe laryngopharyngeal reflux. Procedural Recording a transnasal oesophagoscopy examination is
indications include oesophageal biopsy, oesophageal important, as it allows the physician to review the endoscopic
dilatation, secondary tracheo-oesophageal puncture (TOP) findings at slower speeds. This can be accomplished with a
placement and percutaneous endoscopic gastrostomy tube variety of methods, ranging from simple and inexpensive to
placement. Some oesophageal foreign bodies are amenable digital units costing tens of thousands of pounds. A simple
to TNO removal, although most endoscopists prefer an solution when costs are a significant concern is to use a
operating theatre-based setting for foreign body removal in consumer-grade DVD recorder (such as used to record
case difficulties are encountered. live television). More robust capabilities are found in the
digital recording systems, which encode the video and save
Contraindications it onto a computer drive.These allow high-definition video
Absolute contraindications are primarily anatomical or and frame-by-frame playback capabilities that can further
patient-related inability to passage a flexible endoscope enhance the examination’s usefulness.
through the nasal cavity. Relative contraindications include A variety of flexible endoscopic instruments are available
meal <4 hours prior to procedure, hyperactive gag reflex and that are designed to be passaged through a 2.0 mm working
anatomical considerations (such as skull base defect or fresh channel. The washpipe for administering local anaesthetic
surgical repairs to the upper aerodigestive tract). It should has already been discussed. Other useful instruments for
also be noted that transnasal oesophagoscopy (like traditional the otolaryngologist include micro-cup biopsy forceps (see
sedated transoral flexible oesophagoscopy) offers limited Laryngeal or oesophageal biopsy), paediatric polypectomy
visualisation of the post-cricoid region. If necessary, this is best snares for foreign body retrieval and paediatric sclerotherapy
visualised by rigid endoscopy in the operating theatre. Distal needles for injections. If there is difficulty encountered in
gastrointestinal evaluations using transnasal oesophagoscopy obtaining these instruments, it would be wise to check
have not been evaluated.Therefore, evaluation of the pyloric with the traditional endoscopy suite at the local hospital.
sphincter and small intestine is not currently recommended These instruments are commonly used by paediatric
for transnasal oesophagoscopy and should be performed by gastroenterologists and may already be in stock at the hospital.
traditional transoral flexible oesophagoscopy.
Technique
Equipment The nose is sprayed with topical anaesthetic and
The typical TNO is 60 cm or longer to allow for adequate decongestant mixture and packed with cottonoids as
visualisation of the stomach and retroflexion. Diameters described above. It is wise to wait at least 5 minutes to
range from 3.1–5.1 mm (compared with 10–12 mm for the allow the topical medication to take effect. The TNO
conventional flexible  oesophagoscope). All TNOs should is lubricated with surgical lubricant jelly. (Note: Take
have a 2 mm working channel, which allows for irrigation care not to allow lubricant jelly to touch the tip of the
and air-insufflation, as well as the ability to perform biopsies endoscope where the camera lens is; it can be very difficult
and other procedures. Some TNOs utilise ultrathin single- to remove during the examination and will adversely affect
use endosheaths that fit around the outside of the endoscope. picture quality.) The TNO is then introduced into the
These sheaths can incorporate an extrinsic channel to allow naris and passed along the floor of the nose or between
for passage of biopsy forceps or other instruments instead the middle and inferior turbinates. Most patients report
of relying on an internal endoscope channel within the improved tolerability when the TNO is ‘cheated’ towards
endoscope itself. Outside of these differences, two types of the substance of the inferior turbinate, compared with the
TNO may be found.The older style TNOs utilise fibreoptic mucosa of the bony floor of the nose. Once the larynx is
light carriers to deliver illumination to the endoscope tip visualised, the physician prepares to enter the oesophageal
and a fibreoptic channel to return the image from the tip inlet (Figure 17.2). Many endoscopists choose to have
back to the eyepiece at the proximal end of the endoscope. the patients slightly flex their head toward the chest as the
An attachment then allows addition of a camera to the endoscope is passed toward the post-cricoid region. When
eyepiece, allowing visualisation on a monitor and recording the TNO is in position, the patient is asked to swallow

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 In-clinic procedures

Figure 17.2 The endoscopist visualises the larynx and prepares to enter the oesophageal inlet.

twice hard, and while the patient executes these, the TNO At this point excess air in the stomach should be suctioned
is gently advanced into the oesophagus while insufflating (while still retroflexed), which will provide a significant relief
air. The TNO is then advanced distally down the to the patient. Suctioning after coming out of retroflexion is
oesophagus. Once in the oesophagus, most physicians have possible, but will not evacuate as much air since the mucosa
the patient lean back in the examination chair and relax will collapse earlier onto the endoscope. The endoscope
(as much as possible); this does not affect the examination. can now be returned to the neutral position and carefully
Gentle periodic air insufflation is used as needed and the withdrawn through the GOJ. Once past the GOJ, careful
instrument is advanced only when the oesophageal lumen attention should be given to observing the GOJ and the
is visualised. Suctioning and/or water irrigation to clear squamocolumnar junction (SCJ). Close examination of
debris are also used periodically. The objective at this stage this area may detect oesophageal lesions such as Barrett’s
of the examination is not to visualise structures or screen oesophagus or adenocarcinoma and a comment on the
for mucosal lesions (although any that do become apparent GOJ/SCJ is considered an essential component of a full
should be noted). Instead, the goal of the endoscopist is to oesophagoscopy. Although not yet proven, narrow band
safely advance the TNO to the stomach. imaging (NBI) may be utilised theoretically to enhance the
Once the TNO is advanced into the stomach, retroflexion contrast between squamous and columnar mucosa based
is performed to turn the endoscope 180 degrees to view the on vascular supply. Initial evaluation indicates that NBI may
gastric cardia and gastric side of the gastro-oespophageal provide improved diagnostic sensitivity; however, additional
junction (GOJ). Retroflexion can be challenging when studies are certainly needed. The endoscopist should review
first learning flexible oesophagoscopy, but there is a quick several good reference articles on Barrett’s oesophagus and
learning curve. It is accomplished by simultaneously adenocarcinoma of the distal oesophagus to become familiar
rotating the TNO in towards the patient, while rotating the with the appearance of these lesions. Any suspicious lesion
tip control wheel towards the physician. One advantage of should be biopsied (see Laryngeal or oesophageal biopsy).
transnasal oesophagoscopy over sedated oesophagoscopy is The TNO is then withdrawn through the rest of the
that the oesophageal transit time can be directly observed – oesophagus, keeping the view centred in the lumen. It is far
have the patient swallow a single small sip of water and count easier to keep the lumen visualised on the way ‘back up’ as
the number of seconds it takes for the bolus to enter the opposed to the anterograde first portion of the examination.
stomach; it will be seen squirting through the GOJ. (Note: Again, if mucosal lesions or irregularities of concern are
There is no formal establishment of a normal oesophageal appreciated, biopsy forceps are passed through the working
transit time by direct observation, but it can assist with channel and multiple biopsies under direct vision are
establishing an overall clinical picture.) Most transnasal obtained. Biopsies, if necessary, should be performed after
oesophagoscopy experts agree that an oesophageal transit the entire oesophagus has been examined. New brush-based
time longer than 11 seconds in the upright position is biopsy methodologies may represent an improved technique
abnormal and should be further investigated. to increase diagnostic accuracy, but further trials are needed.

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 Individual in-clinic procedures

Laryngeal or oesophageal biopsy biopsy to the point where a sedated oesophagoscopy

becomes the better choice. Common sense also would
Overview advise against in-clinic biopsy of a potentially critical airway
An easy extension of transnasal oesophagoscopy is to mass such as a near-obstructive supraglottic or tracheal
utilise the 2.0 mm working channel of the TNO to take tumour. These are obviously much better managed in the
biopsies. These biopsies can be taken of lesions anywhere controlled environment of the operating room.
along the upper aerodigestive tract including laryngeal
lesions (even of the true vocal fold, provided adequate Equipment
topical anaesthetic is administered). Many surgeons use In addition to the usual transnasal oesophagoscopy
transnasal oesophagoscopy as a rapid screening tool for equipment mentioned above, a flexible cup biopsy forceps
panendoscopy/biopsy of patients with newly diagnosed (Figure 17.3) is required. Numerous brands and styles
head and neck squamous cell cancer. Due to the high are available that all work well. The authors recommend
incidence of synchronous primaries, an evaluation of the a 1.8 mm biopsy forceps to facilitate easy passage through
entire upper aerodigestive tract is mandatory for all such the endoscope, and this particular forceps has a short
newly diagnosed patients. Use of transnasal oesophagoscopy spear to facilitate tissue capture. (Note: While transnasal
to meet this need is far less costly, and can usually be oesophagoscopy can be done by the surgeon without
performed much more expediently than scheduling an assistance, endoscopic biopsy requires a surgeon to operate
operative panendoscopy under general anaesthesia. the endoscope plus an assistant to deliver the biopsy
It is important to note that the biopsy taken in transnasal forceps through the working channel and close the biopsy
oesophagoscopy biopsy is exceedingly small (remember, the jaws. Depending on the rules in your practice setting, the
entire instrument has to fit inside a 2.0 mm channel, so the assistant tasks can usually be performed by a competent
fragment of tissue is more on the order of 1.5–1.77 mm in nurse with appropriate training.)
diameter maximum). It is unlikely that such a biopsy will For the modified transoral technique, appropriate curved
encompass tumour and surrounding stroma to show the instruments must be available. There are several of these
depth of invasion. For this reason, early iterations of transnasal specifically made for the purpose, and many sinus instruments
oesophagoscopy biopsy were prone to the frustrating ‘at designed for reaching the frontal sinus may work depending
least carcinoma in situ’ pathological diagnosis obtained on where the lesion to be biopsied is located.
from a patient with a large, exophytic tumour. Therefore,
when first implementing transnasal oesophagoscopy biopsy Technique
of suspected cancer at an institution, it would be prudent As with transnasal oesophagoscopy, the true key to success
to meet with the pathologist first. Often, sufficient clinical lies with obtaining adequate topical anaesthesia of the nose,
information can be provided to accompany the biopsy and epiglottis and biopsy site. Additionally, for the transoral
enable the pathologist to make the proper call. Additionally, route adequate anaesthesia of the base of the tongue must
it is wise to take 2–3 biopsies of a given lesion, given the be ensured. Failure to provide excellent topical anaesthesia
small instrument size. will predispose the procedure to patient discomfort and
It should also be mentioned that laryngeal and pharyngeal
biopsies can also be obtained using a modification of
this technique where a visualisation endoscope without
a working channel is used and a curved ‘giraffe-style’
instrument in passaged transorally. This method is
somewhat more cumbersome in that care must be taken to
avoid stimulating the gag reflex as the instrument traverses
the base of tongue region, but has the advantage of not
requiring a channelled endoscope.

Contraindications
In addition to the contraindications for transnasal
oesophagoscopy, a relative contraindication for transnasal
oesophagoscopy biopsy is the patient with suspected
eosinophilic oesophagitis or Barrett’s oesophagus. In both
of these settings, the number of biopsies required degrades
the time and cost advantage of transnasal oesophagoscopy Figure 17.3 A cupped biopsy forceps.

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 In-clinic procedures

movement at the most inopportune times and will likely through the entry port, but in most cases this affords less
compromise the ability to obtain optimal biopsies. control than the ‘en-masse’ approach. Once the forceps are
buried in the lesion, the jaws are closed and the forceps
Transoral technique withdrawn completely through the channel. After this,
The flexible laryngoscope is passed through the nose until the specimen is removed from the jaws into a suitable
the base of the tongue comes into view. At this point, the fixative (usually neutral buffered 10% formalin). (Note: An
patient is asked to stick out their tongue and an assistant 18-gauge needle or wooden toothpick can be extremely
grasps it with a dry gauze (exactly the same technique useful for dislodging stubborn biopsy specimens from the
as transoral indirect mirror laryngoscopy). The curved forceps.) Remember that formalin is toxic; if the forceps
instrument is then carefully passed through the mouth come in contact with the formalin, a rinse in water is
and over the base of the tongue, avoiding direct contact mandatory. Rinsing the tip under running tap water for
with the posterior oropharyngeal wall or the tongue base 2–3 three seconds is sufficient, as the aerodigestive tract is
(both of which are richly enervated with mechanosensors not sterile. During this process (performed by the assistant),
triggering a gag reflex). Both operators then observe the endoscope is usually held at the nasopharynx by the
the final manoeuvring of the instrument on the video surgeon in preparation for re-advancing the endoscope
monitor. An alternative scenario not requiring an for additional biopsies. Occasionally, a larger than usual
assistant is possible, but is substantially more challenging. specimen will be obtained. If the tissue sample is too large
The patient grasps their own tongue and retracts it to easily pass through the working channel, the entire scope
forward. The surgeon passes a rigid endoscope with a and forceps may be removed while keeping the biopsy
70- or 90-degree lens transorally in their non-dominant forceps closed.
hand, while simultaneously passing the curved biopsy Following biopsy, quick endoscopic inspection is made
instrument over the base of the tongue with the dominant of the surgical site. A small amount of bleeding is normal
hand. Visualisation is obtained from the video monitor, and concerning bleeding is almost never encountered.
much as in endoscopic sinus surgery. Although feasible, In the event of a more significant bleeding episode, a
this approach is not recommended for those new to in- nasal vasoconstrictor such as oxymetazoline (or diluted
clinic surgery, but is mentioned here for completeness. epinephrine) can be administered via the working
A more useful technique is via the working channel channel. If the bleeding is in the vallecula, pyriform sinus
of the TNO and this will likely be the preferred method or oropharynx, it is also possible to use direct pressure.
for most surgeons. After obtaining topical anaesthesia as Epinephrine-soaked tonsil sponges are grasped in a McGill
described earlier, the washpipe must be exchanged for the forceps (used for supraglottic foreign body retrieval) and
biopsy instrument. Remember that if instrumentation is passed transorally to apply direct pressure to the biopsy
passed through the working channel while the endoscope site while maintaining visualisation endoscopically. This is
is flexed, expensive and sometimes irreparable damage a daring manoeuvre, as loss of control of the tonsil sponge
can occur to the endoscope channel. If transnasal passage could easily result in an emergent airway foreign body.
was easy, instrument exchange can be accomplished by
removing the endoscope from the patient. This takes extra Secondary tracheo-oesophageal puncture
time, however, as the endoscope must be reintroduced and other oesophageal procedures
and advanced to the biopsy site again. An alternative is to
withdraw the endoscope slightly to the nasopharynx and Overview
straighten the tip (so that it points straight along the floor of In the head and neck cancer patient, rigid oesophagoscopy
the nose toward the posterior wall of the nasopharynx).The is sometimes problematic secondary to post-treatment
washpipe is then removed and the biopsy forceps threaded fibrosis, trismus and pre-existing cervical spine osteophytes.
through the working channel. Once the forceps exit the While many surgeons perform primary TOP at the time
endoscope channel and are seen on the video monitor, of laryngectomy, occasionally a secondary TOP is necessary.
they should be withdrawn back until just visible (but not At the authors’ institution, such secondary TOPs are most
retracted all the way). This allows safe advancement and often performed in-clinic, using a TNO, rather than in the
flexing of the endoscope to regain the biopsy position. The operating room. Because of the easy visualisation afforded
biopsy forceps are then advanced, the jaws opened and a by the flexible endoscope, it allows TOP placement even
biopsy obtained. It is usually easier to extend the forceps a in the setting of a failed operative secondary TOP. Other
set distance from the endoscope tip and then advance the oesophageal procedures such as dilation of a stricture are also
endoscope and forceps forward into the lesion as a unit. possible in the clinic setting, although patient discomfort is
Alternatively, the forceps can be advanced by pushing them a significant limiting factor for the latter.

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Contraindications visualisation. Once distal placement of the red rubber

There are no additional contraindications beyond those for catheter is confirmed, the red rubber catheter is held firmly
transnasal oesophagoscopy. in place while pulling the two tabs of the Peel-Away®
introducer apart. This simultaneously splits the introducer in
half and withdraws it around the red rubber catheter until the
Equipment entire introducer has been removed and is now in two pieces;
This procedure requires a primary surgeon as well as a these are discarded.The red rubber catheter is secured with a
surgical assistant with a headlight. In addition to the standard suture and the procedure is terminated. In experienced hands,
transnasal oesophagoscopy equipment described earlier, the entire process usually takes between 7 and 15 minutes and
several other items are necessary for in-clinic secondary is easily tolerated by the patient. Subsequent replacement of
TOP. Injectable local anaesthetic with vasoconstrictor is the red rubber catheter with a transoesophageal prosthesis is
used, along with a 3 ml syringe and small gauge needle.The performed after the usual interval, with no difference from
authors prefer 1% lidocaine with 1:100,000 epinephrine, TOP under general anaesthesia.
but any of a number of combinations are sufficient.A curved Other oesophageal procedures can be similarly
haemostat, 11-blade scalpel, small gauge needle and trochar, performed, in both the laryngectomee and in other
standard Seldinger guidewire and red rubber catheter are patients. The most common of these is dilation of a simple
also needed. A secondary TOP kit, such as the one made oesophageal stricture. A standard transnasal oesophagoscopy
by Blom®, contains all of these items or the surgeon can procedure is performed including topical anaesthesia,
assemble the components separately. Additionally, a special with the addition of topical anaesthesia to both sides
Peel-away™ introducer is used to facilitate the advancement of the nose. The transnasal oesophagoscopy proceeds as
of the red rubber catheter. A suture to secure the red rubber per routine until the stricture is identified. The tip of the
catheter to the neck is also advised. TNO is then advanced well distal to the stricture (gastric
placement preferred). A standard soft-tipped oesophageal
Technique guidewire is then placed through the working port and the
Local anaesthetic is infiltrated into the posterior tracheal TNO withdrawn while advancing the guidewire to leave
party wall at the level of the stoma. Following topical nasal it in place. At this point, the patient has a guidewire passing
anaesthesia, the TNO is advanced through the oesophageal transnasally into the oesophageal inlet and into the stomach.
inlet and the room lights are  dimmed. The endoscope is While this may sound disconcerting at first, in actuality it is
advanced until maximal light can be seen through the party as well tolerated as a simple nasogastric tube, which traverses
wall and the endoscope is withdrawn slightly.Air is insufflated the same route. A standard oesophageal balloon dilator
through the TNO to distend the oesophageal lumen and (e.g.  Boston Scientific CRE™ system) is then advanced
a finder needle inserted by the assistant at the site of the over the guidewire into the nose, while the TNO is
planned TOP placement. If the needle is not immediately advanced through the opposite nostril. The TNO provides
visible, it should be removed and the procedure repeated visual guidance and both are advanced simultaneously until
to avoid inadvertent damage to the TNO. Once the needle the stricture is reached. Once the balloon is confirmed to
is identified, the 11-blade scalpel is inserted adjacent to the straddle the stricture, the patient is warned of the discomfort
finder needle until the tip is observed within the oesophagus, and the balloon is inflated per usual.After balloon takedown,
and then both are removed. The trochar is then inserted the endoscope provides visual feedback as to the extent of
through this tract and the guidewire advanced into the distal dilation and any complications.The procedure is terminated
oesophagus. Occasionally, the guidewire will curl and attempt and the patient returned to out-patient ambulatory status.
to advance proximally. The trochar should be angled cranial Most surgeons place these patients on a soft diet for
to caudal to facilitate distal passage; alternatively, the TNO 24–48 hours, and in-patient admission is not required.
can be used to push the guidewire tip in the appropriate
direction. At this point, the trochar is withdrawn and the Laser procedures
mosquito forceps used to gently dilate the tract. The Peel-
Away® introducer is then advanced over the guidewire and Overview
advanced several centimetres distally. The guidewire is then The in-clinic use of lasers remains one of the most useful
removed leaving the introducer in place. The red rubber tools in the laryngologist’s armamentarium.This is especially
catheter (be sure to tie off or cap the proximal end) is then true as new technology opens the door for additional
lubricated with sterile surgical lubricant and advanced into wavelengths to be delivered by flexible fibre. Complete
the introducer completely, leaving 4–5 cm external. During discussion of medical lasers is obviously beyond the scope
this entire process, the first surgeon maintains endoscopic of this chapter, but a brief overview is provided. As  most

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 In-clinic procedures

surgeons are aware, the laser wavelength is the primary Equipment

determinant of tissue effect.This is due to the varying energy
The standard TNO equipment is necessary. Most
absorption characteristics of the target tissue to different
endoscopes with distal chip cameras are tolerant of reflected
wavelengths.The molecule absorbing laser energy is called a
laser energy encountered during these procedures, but one
chromophore, with water and haemoglobin being the most
should check with the manufacturer to be certain. Most
important. The most common medical laser is the CO2
older-style endoscopes with fibreoptic image delivery to
laser. Until recently, the CO2 laser, required line of sight or
a camera head may require a wavelength-specific filter to
mirror-based delivery systems, precluding its use via flexible
protect the CCD camera chip from damage. A medical
endoscopes. It emits light at 10,600 nm, where this energy
laser and fibre delivery system is of course needed. Most
is primarily absorbed by water. Since light from the CO2
fibre-based lasers have an integral delivery sheath (such
laser is within the infrared spectrum, it is invisible and must
as the  KTP laser), but if it does not, a separate sheath is
be coupled with a helium-neon aiming laser to be seen. In
mandatory to prevent endoscope damage as the fibre tips
recent years, several companies have developed fibre-based
are often quite sharp. An easy ‘work-around’ is to cut the
CO2 laser delivery systems, which allows their deployment
needle and deployment handle off a pediatric snare or
as in-clinic lasers through flexible endoscopes. The two
sclerotherapy needle and discard the inner workings. The
most commonly used lasers with fibre-based delivery
surrounding plastic sheath that remains is ideal for passage
options are the PDL, which emits light at 585 nm, and the
of a laser fibre, and is designed to fit through a 2.0 mm
KTP laser, which emits light at 532 nm. Both of these laser
working channel.
wavelengths are highly absorbed by oxyhaemoglobin and
Finally, although the laser energy is being delivered
have negligible absorption by water. At moderate power
entirely within the body, prudence dictates that standard
settings, this results in intravascular coagulation and lysis of
laser precautions for medical procedures be followed.These
subepithelial microcirculation; such lasers are commonly
include proper training updated annually, laser testing
termed ‘angiolytic’. Higher power settings can be used to
before the patient enters the room, warning signs on the
vaporise tissue, similar to the CO2 laser. The ‘gold’ laser is a
door and wavelength-specific eye goggles for all personnel
relative newcomer for medical applications but may prove
in the room including the patient.
quite useful. It uses a wavelength of 980 nm, is fibre based
and has an extremely small spot size of 0.1 mm. It may also
be used in both contact mode (for tissue vaporisation and Technique
cutting) and non-contact ‘free-beam’ mode to coagulate Following topical anaesthesia as described previously, the
small vessels without rupture. laser is passed through the working channel of the endoscope.
Patient tolerance of in-clinic procedures performed with (Note: Because of the sharp tip of the laser fibre, this is best
angiolytic wavelength lasers is high, and the vast majority accomplished with the endoscope outside the patient.) The
of patients do not require post-treatment pain medication. laser fibre should be kept inside the sheath and the sheath
(Note: This only applies to angiolytic lasers, and in the advanced just to the tip of the endoscope. The endoscope
authors’ practice it has been noted that the gold and CO2 is then advanced to the site of the lesion and the sheath
lasers both result in significantly more discomfort both advanced 4–5 mm. The laser fibre can then be advanced out
during and post procedure, which limits their usefulness.) of the sheath for delivery. At this point, the laser can be safely
The most common laryngological application for in- energised. For angiolytic treatments, the goal is to ablate the
clinic laser is the angiolytic treatment of laryngeal RRP feeding blood vessels while minimising tissue trauma. In
(see Chapter 19, Recurrent respiratory papillomatosis). In this case, the beam is kept diffuse and tissue treated until a
addition to being well tolerated, there is reduced risk of visible blanching or faint whitening (‘frosting’) is observed.
vocal fold scar and it is therefore the procedure of choice Note that PDLs do not have an aiming beam, so the angle
for treating papilloma involving the anterior commissure. of the laser fibre must be judged and mentally adjusted as
Additional uses include treatment of vocal polyps, Reinke’s tissue effect is observed. As with other laser procedures, the
oedema, glottic granulomas not responding to conservative power applied is a function of multiple factors that can all
measures and other glottic lesions. be adjusted. These include pulse width and duration, and
beam intensity (watts). Additionally, the laser energy can
Contraindications be concentrated on a small spot or diffused across a wide
In addition to the usual transnasal oesophagoscopy area by changing the distance between the laser tip and
contraindications, patients with pharmacological the tissue. With angiolytic lasers, caution should be taken
photosensitivity may not be well suited to in-clinic laser to avoid tissue trauma or aggressive or concentrated laser
procedures. energy to microscopic feeding vessels, as vessel rupture

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 Individual in-clinic procedures

may occur. While not a problem in terms of blood loss, the experiencing abnormal (counterproductive) vocal fold
blood will preferentially absorb any subsequent laser energy, movement either during phonated speech (abductor SD)
and thus termination of the procedure is usually indicated. or non-phonated speech (adductor SD). Mixed forms
For laser procedures involving the true vocal folds, post- and combinations with tremor or other neurological
treatment instructions usually include a short period of disorders are also possible. SD is a relatively rare condition,
voice rest. Most patients do not require pain medicine, and and management of these patients can be complex. The
no antibiotics or other interventions are needed. optimal location of injection varies according to the type
of SD present, and these patients are best treated by high-
Vocal fold injections: vocal fold medialisation volume, sub-specialty trained laryngologists. Therefore,
and other injections BTX injection is mentioned for completeness, but will not
be covered specifically.
Overview
As an alternative to operative laryngoplasty, in-clinic Contraindications
injection vocal fold augmentation is a viable option for There are no additional contraindications beyond those for
many patients. There are several injection techniques standard transnasal oesophagoscopy.
available depending on physician preference and patient
anatomy. Multiple substances are suitable for in-clinic
Equipment
laryngoplasty, and for all the procedure is essentially
identical: a bulking agent is injected into the paraglottic The standard transnasal oesophagoscopy equipment
space (deep to the thyroarytenoid muscle), pushing the previously described is needed. Similar to other procedures,
entire tri-layered vocal fold complex medially. Available an assistant is required. Many injectable materials for
materials vary according to durability, tissue reaction use in injection laryngoplasty come packaged with an
and source of components. The shortest duration is injection syringe and needle, but these are optimised for a
carboxymethylcellulose (a common food additive), which line-of-sight operative technique and poorly suited to in-
is very short lasting and often used to allow a patient to clinic injection. The transoral approach requires a curved
trial the effect of injection laryngoplasty on their voice. injection syringe and needle, whereas the transcervical
It is resorbed in 4–12 weeks and is often used in cases approach requires local anaesthetic with syringe and needle
of unilateral vocal fold immobility when the status of and a 3–4-inch long, small gauge needle for delivery of the
the recurrent laryngeal nerve is unknown. Micronised material.
acellular dermis is a common surgical tissue filler and may
be used for intermediate effect, but some patients dislike Technique
the concept of receiving even highly processed allografts. The transoral approach may be accomplished with either
Calcium hydroxylapatite (CAHA) is commonly utilised a flexible laryngoscope or, less commonly, a rigid transoral
in patients desiring longer lasting effects. Patients with 70-degree endoscope providing visualisation. The curved
presbylarynges, vocal fold atrophy or permanent unilateral injection cannula with a small calibre needle is attached
vocal fold paralysis (UVFP) are good candidates for to the syringe of injectable material and primed to ensure
CAHA injection, which has been reported to last a mean smooth flow of material. Topical anaesthesia should
of 18.6  months. Autologous fat injection in the clinic be performed as described previously. It is especially
setting is not commonly performed, and is much better important to apply topical anaesthesia to the tongue base
suited for the operating room. Indications for in-clinic when using the transoral approach. It is usually beneficial
medialisation are the same as those for traditional operative for the surgeon to be seated in front of the patient, while
injection augmentation. They include presbylarynges, the assistant stands and holds the endoscope so as not to
vocal fold atrophy, UVFP or paresis and sulcus vocalis. obstruct the surgeon’s view. A headlight is worn by the
Steroid injections to posterior glottic granulomas or surgeon to help guide the injection cannula through the
vocal fold scar may also be performed in the clinic. Steroid oral cavity and over the tongue. Typically, the surgeon’s
preparations such as triamcinolone are to be avoided; dominant hand holds the injection syringe and pushes
rather a sterile ophthalmic preparation of 10 mg/ml of the plunger to inject, while the non-dominant forefinger
dexamethasone is recommended when injecting into the and thumb gently grasps the mid portion of the injection
vocal fold to prevent particulate deposition in the fold. cannula for guidance. Once the injection cannula passes
A final laryngeal injectable is botulinum toxin (BTX), the palate and overlies the supraglottis, it may be visualised
usually in the setting of spasmodic dysphonia (SD). This is by the endoscope. At this point, the surgeon uses the
a true task-specific neurological dystonia, with patients monitor for visualisation.

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 In-clinic procedures

The injection cannula is manoeuvred to the injection site. syringe angle. In these patients, the cricothyroid membrane
For injection augmentation, this is ideally at the junction of technique can often be used. In this approach, the injection
the posterior one-third and anterior two-thirds of the true needle is inserted 2–3 millimetres lateral to the midline,
vocal fold, injected through the superior surface as far lateral just below the inferior border of the thyroid cartilage.
to the vocal process as possible. Having the patient breathe As for the other techniques, endoscopic visualisation is
quietly will reduce the amount of vocal fold movement. provided by laryngoscopy. The needle passes through the
One advantage of the transoral approach is that more than cricothyroid membrane and is directed superiorly and
one injection site may be easily accessed if the vocal fold laterally into the paraglottic space. The challenge for the
needs additional augmentation at a different site. cricothyroid approach is that direct visualisation of the
Transcervical injection may be approached via the needle is not possible since it is entering the vocal fold
thyrohyoid or cricothyroid membrane (or, less often, directly from below. Instead, the needle is passed submucosally,
through the thyroid cartilage itself). While the patient is with the needle position inferred by corresponding vocal
seated, the neck landmarks – thyroid notch, thyrohyoid or fold movement when the needle is gently manipulated. An
cricothyroid membrane – should be palpated and noted. alternative approach can be used in difficult circumstances,
Topical lidocaine (1 or 2%) with epinephrine (1:100,000) is where the needle is inserted into the subglottic lumen
often injected subcutaneously over the desired site of needle and the flexible endoscope advanced to the vocal folds
entry. Injection via the thyrohyoid membrane is the most to provide visualisation. The needle can then be directed
common transcervical approach. Flexible or rigid laryngoscopy superolateral under direct visualisation.This latter technique
is performed by an assistant, and the work is carried out while obviously requires profound laryngeal anaesthesia, excellent
watching on the video monitor.The midline neck is swabbed endoscopy skills and patient cooperation.
with alcohol preparation.A 3.8 cm (1.5 inch) 23- or 25-gauge The transthyroid cartilage approach to the vocal folds is
needle is attached to the syringe filled with the injectable best suited to younger patients in whom the thyroid cartilage
material and passed superiorly over the thyroid notch in is completely unossified. It is unlikely to be successful in
the midline plane. The needle passes through anterior neck older patients. After prepping the midline neck skin and
tissue, the pre-epiglottic space and the petiole of the epiglottis obtaining endoscopic visualisation as described above, the
before entering the supraglottic airway. It is important to needle is passed lateral to midline and several millimetres
angle the needle inferiorly and slightly laterally. The needle is superior to the inferior border of the thyroid cartilage. The
then visualised on the monitor and can be manoeuvred into needle is angled to move through the cartilage towards
the appropriate position for injection. Note that unlike the the midline. As with the cricothyroid approach, the needle
transoral approach, accessing multiple injection sites can position is inferred from vocal fold movement transmitted
require significant manoeuvring to reposition the needle. from needle manipulation. If the needle becomes obstructed
The most important limitation of the thyrohyoid with cartilage, it is possible to apply gentle pressure in an
approach is that sometimes patient anatomy can render it all attempt to push out the cartilage plug and inject the vocal
but impossible. Obese patients can present with too much fold. Extreme care must be taken during this manoeuvre
neck tissue to traverse, and in patients with a short neck to prevent excessive material from being injected into the
the mandible often interferes with attaining a steep enough vocal fold.

Further reading
Amin MR, Postma GN, Setzen M et al. (2008) Transnasal Belafsky PC, Postma GN, Koufman JA (2001) Replacement
esophagoscopy: a position statement from the American of a failed tracheoesophageal puncture (TEP) under
Bronchoesophagological Association (ABEA). direct vision. Ear Nose Throat J 80:862.
Otolaryngol Head Neck Surg 138:411–414. Carroll TL, Rosen CA (2011) Long-term results of calcium
Amin MR (2006) Thyrohyoid approach for vocal hydroxylapatite for vocal fold augmentation. Laryngoscope
fold  augmentation. Ann Otol Rhinol Laryngol 115: 121:313–319.
699–702. Chow TL, Lee DTY, Choi CY (2009) Prediction of
Andrus JG, Dolan RW, Anderson TD (2005) Transnasal simultaneous esophageal lesions in head and neck
esophagoscopy: a high yield diagnostic tool. Laryngoscope squamous cell carcinoma. Arch Otolaryngol Head Neck
115:993–996. Surg 135(9):882–885.
Bastian R, Delsupehe K (1996) Indirect larynx and Clyne SB, Halum SL, Koufman JA et al. (2005) Pulsed dye
pharynx surgery: a replacement for direct laryngoscopy. laser treatment of laryngeal granulomas. Ann Otol Rhinol
Laryngoscope 106:1280–1286. Laryngol 114:198–201.

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 Further reading

Dumortior J, Napoleon B, Hedelius F et al. (2003) Unsedated Orban NT, Ogawa T, Atun R et al. (2009) Trans-nasal
transnasal EGD in daily practice: results with 1100 oesphagoscopy: cost implications for a change in
consecutive patients. Gastrointest Endosc 57(2):198–204. practice: how we do it. Clin Otol 34:380–385.
Falcone MT, Garrett CG, Slaughter JC et al. (2009) Postma GN, Bach KK, Belafsky PC et al. (2002) The role
Transnasal esophagoscopy findings: interspecialty of transnasal esophagoscopy in head and neck oncology.
comparison. Otolaryngol Head Neck Surg 140:812–815. Laryngoscope 112:2242–2243.
Farwell DG, Rees CJ, Mouadeb DA et al. (2010) Esophageal Postma GN, Cohen JT, Belafsky PC et al. (2005) Transnasal
pathology in patients after treatment for head and neck esophagoscopy: revisited (over 700 consecutive cases).
cancer. Otolaryngol Head Neck Surg 143:375–378. Laryngoscope 115:321–323.
Ford CN, Bless DM, Lowery JC (1990) Indirect Rees CJ, Halum SL, Wijewickrama BA et al. (2006) Patient
laryngoscopic approach for injection of botulinum tolerance of in-office pulsed dye laser treatments to the
toxin in spasmodic dysphonia. Otolaryngol Head Neck upper aerodigestive tract. Otolaryngol Head Neck Surg
Surg 103(5):752–758. 14:1023–1027.
Garcia RT, Cello JP, Nguyen MH et al. (2003) Unsedated Rosen CA,Amin MR, Sulica L et al. (2009) Advance in office-
ultrathin EGD is well accepted when compared with based diagnosis and treatment in laryngology. Laryngoscope
conventional sedated EGD: a multicenter randomized 119:S185–214.
trial. Gastroenterology 125(6):1606–1612. Schmidt H, Stasche N, Keller A et al. (2010)
Hogikyan ND (1999) Transnasal endoscopic examination Tracheobronchoscopy and esophagoscopy in
of the subglottis and trachea using topical anesthesia in current ear-nose-throat practice: an update. Eur Arch
the otolaryngology clinic. Laryngoscope 109(7, pt 1): Otorhinolaryngol 267:311–316.
1170–1173. Thota PN, Zuccaro G Jr., Vargo JJ 2nd et al. (2005)
Ivey CM, Woo P, Altman KW et al. (2008) Office pulsed A  randomized prospective trial comparing unsedated
dye laser treatment for benign laryngeal vascular polyps: esophagoscopy via transnasal and transoral routes using
a preliminary study. Ann Otol Rhinol Laryngol 117: a 4 mm video endoscope with conventional endoscopy
353–358. with sedation. Endoscopy 37:559–565.
Jobe BA, Hunter JG, Chang EY et al. (2006) Office- Tsao GJ, Damrose EJ (2010) Complications of esophagscopy
based unsedated small-caliber endoscopy is equivalent in an academic training program. Otolaryngol Head Neck
to conventional sedated endoscopy in screening and Surg 142:500–504.
surveillance for Barrett’s esophagus: a randomized and Woo P (2006) Office-based laryngeal procedures.
blinded comparison. Am J Gastro 101:2693–2703. Otolaryngol Clin N Am 39:111–133.
Koufman JA, Rees CJ, Frazier WD et al. (2007) Office-based Yung KC, Courey MS (2010) The effect of office-based
laryngeal laser surgery: a review of 443 cases using three flexible endoscopic surgery on hemodynamic stability.
wavelengths. Otolaryngol Head Neck Surg 137:146–151. Laryngoscope 120(11):2231–2236.
Morrison M, O’Rourke A, Dion GR et al. (2012) Zeitels SM,Akst LM, Bums JA et al. (2006) Pulsed angiolytic
Hemodynamic changes during otolaryngological laser treatment of ectasias and varices in singers. Ann
office-based flexible endoscopic procedures. Ann Otol Otol Rhinol Laryngol 115:571–580.
Rhinol Laryngol 121(11):714–718. Zeitels SM, Akst LM, Burns JA et al. (2006) Office-
Mouadeb DA, Belafsky PC (2007) In-office laryngeal based 532-nm pulsed KTP laser treatment of glottal
surgery with the 585nm pulsed dye laser (PDL). papillomatosis and dysplasia. Ann Otol Rhinol Laryngol
Otolaryngol Head Neck Surg 137:477–481. 115:679–685.

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 CHAPTER 18

Anaesthetic considerations in laryngology

Anil Patel

Introduction
Anaesthesia for operations on the airway are unique in ●● No coughing, bucking, breath holding or larynospasm
that both the surgeon and anaesthetist are working in the on emergence.
same area. At its most basic, anaesthesia involves provision ●● Conclude with a pain-free, comfortable, alert patient.
of amnesia and analgesia, maintenance of oxygenation
Unfortunately, the ideal anaesthetic technique does not exist.
and removal of carbon dioxide. The amnesia and analgesia
Anaesthetic techniques can be broadly classified into
component is usually accomplished by the administration of
two  groups. ‘Closed’ systems in which a cuffed tracheal
volatile anaesthetic gases or intravenous anaesthetic agents
tube is employed with protection of the lower airway but
and oxygenation and carbon dioxide removal through a
the potential for laser-related problems. In ‘open’ systems,
tracheal tube or laryngeal mask airway.
where  no tube is used, ventilation is achieved through
This system works well in most types of surgery where
spontaneous breathing or jet ventilation techniques. This
the presence of a tracheal tube or laryngeal mask airway has
leaves the airway ‘open’, allowing complete access for the
no influence on the surgery itself. During operations on the
surgeon but with the risk of lower airway soiling.
airway the presence of a tracheal tube or laryngeal mask
The decision to use a ‘closed’ or ‘open’ technique will be
airway in the same anatomical field as the proposed surgery
dependent on (1) the patient’s general condition, (2) the size
may make that surgery more difficult or impossible.
of the lesion, (3) the mobility of the lesion, (4) the location
The characteristics of an ‘ideal’ anaesthetic technique for
of the lesion, (5) requirement for surgical access, (6) surgical
laryngology are listed below:
experience and preference, (7) anaesthetic experience and
●● Simple to use. preference, (8) equipment available and (9) the requirement
●● Provide complete control of the airway. to use a laser.
●● No risk of aspiration. The technique chosen for any given procedure is not
●● Provide smooth induction of anaesthesia. absolute and may have to change as surgical and anaesthetic
●● Control ventilation with adequate oxygenation. requirements change. For example, an open system utilising
●● Control ventilation with adequate carbon dioxide removal. jet ventilation on a lesion thought to be relatively avascular
●● Provide smooth maintenance of anaesthesia. may change to a closed system employing a cuffed tracheal
●● Provide a clear motionless surgical field, free of secretions. tube if the lesion is bleeding, with the risk of soiling of the
●● No time restrictions for surgeon. tracheobronchial tree. Conversely, a system employing a
●● No risk of airway fire. cuffed tracheal tube may have to change during surgery to
●● No cardiovascular instability. an open system if the tracheal tube overlies a lesion, making
●● Allow smooth, safe emergence from anaesthesia. surgery very difficult or impossible.1

General anaesthetic considerations

Preoperative assessment Standard airway assessments to predict the ease of
ventilation, visualisation of the laryngeal inlet and tracheal
The preoperative assessment attempts to identify the extent
intubation should be performed. An assessment of airway
of the airway pathology, and the impact this will have on
pathology and its impact on airway management should
airway management after the induction of anaesthesia,
be made. Some patients are young, fit and healthy with no
and identify factors that may cause difficulty during the
airway compromise, and at the other end of the spectrum
perioperative course. An appreciation of the size, mobility
some patients have significant tobacco and alcohol intake,
and location of the lesion will help determine which
cardiovascular and respiratory dysfunction, and large
anaesthetic techniques are appropriate.
obstructing tumours of the airway.

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 Anaesthetic considerations in laryngology

Size of lesion uncommon. Obstruction is worse during anaesthesia with

spontaneous ventilation because of the loss of supporting
The size of the lesion gives an indication of potential airflow
tone in the oropharynx and laryngohypopharynx
obstruction and, depending on severity, will influence which
collapsing the airway.
technique is appropriate. Generally, as an obstructing lesion
increases in size, the placement of a tracheal tube becomes
more difficult and eventually will not be possible. Stridor Location of lesion
indicates a significantly narrowed airway with critical The location of lesions provides useful information as
airway obstruction of over 50% and in adults an airway to how the airway will respond following induction of
diameter of less than 4–5 mm. Stridor on exertion suggests anaesthesia. Supraglottic lesions, if mobile, can partially
airway obstruction is becoming critical and stridor at rest obstruct the airway or make visualisation of the laryngeal
suggests critical airway obstruction is present. The absence inlet difficult. Subglottic lesions may allow a good view of
of stridor is generally reassuring, but in exhausted adults and the laryngeal inlet but cause difficulty during the passage of
children there is limited chest movement and insufficient a tracheal tube.
airflow to generate enough turbulent flow for stridor. The recognition of a compromised or anatomically
These circumstances suggest life-threatening compromise. distorted upper airway is paramount in the preoperative
assessment of these patients. For elective procedures a
Mobility of lesion detailed history, examination and investigations should be
Very mobile lesions, such as multiple large vocal cord undertaken, but for more urgent procedures with severe
polyps or significant papillomatous lesions, may cause airway compromise investigations may not be possible.
partial airway obstruction following induction of The patient’s old anaesthetic records should be available for
anaesthesia, but total airway obstruction is extremely history of prior intubations.2

Induction of anaesthesia
When airway compromise is not an issue, most procedures leading to further airway collapse and a  reduction in
are routine and uneventful with an intravenous induction functional residual capacity. All of this ultimately impairs
technique and administration of neuromuscular blockade inspiratory airflow.
suitable for the majority of benign and malignant glottic, The deterioration in the airway following inhalational
subglottic and tracheal lesions. induction of anaesthesia and subsequent inability to
When airway compromise is an issue, traditional maintain spontaneous ventilation is described in the
teaching suggests that any technique that uses inhalational National Audit Project 4.5 This audit demonstrates that
induction and maintains spontaneous ventilation is safest. in many situations, as spontaneous ventilation became
This has been challenged1,3,4 and attempts at maintaining impossible and the airway was lost, there was reluctance to
spontaneous ventilation in obstructed airways have been use (or even an active decision to avoid) muscle relaxants
questioned. Inhalational induction for advanced laryngeal and controlled ventilation despite respiratory distress, airway
tumours with airway obstruction is slow, difficult and obstruction, hypoxia and a peri-arrest state. It was clear in
challenging, with apnoeic periods and episodes of total these cases that patients do not ‘rapidly awaken.’Therefore, it
obstruction. Physiological problems include reduction in seems that actively taking over ventilation for the patient –
airflow, reduction in respiratory drive as anaesthetic depth with intravenous induction, muscle relaxation and positive
is increased, increased collapsibility of the airway, increased pressure ventilation – is a safer, more efficient and more
work of breathing, critical instability at points of narrowing rapid means of ensuring anaesthesia and oxygenation.

Open systems for anaesthetic management

Open systems for anaesthetic management include jet material within the airway. However, they require specialist
ventilation techniques, intermittent apnoea techniques and equipment, knowledge and experience and all expose
spontaneous ventilation techniques. All of these techniques the lower airway to potential contamination from blood,
allow complete laryngeal visualisation for the surgeon and secretions and surgical debris because there is no protection
improved laser safety because of the absence of any foreign from a cuff.6

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 Open systems for anaesthetic management

Jet ventilation techniques surgery extremely difficult if not impossible. With the
absence of any foreign material in the airway there is no risk
Jet ventilation techniques are suitable for ventilation
of a laser airway fire and no obstruction to the placement
during surgery of most adult vocal cord and tracheal
of bougies to dilate the airway. In practice, ventilation is
lesions including benign laryngeal lesions, airway stenosis,
stopped during dilatation of the airway and this introduces
placement of airway stents, rigid bronchoscopy, tracheal
a time limit for the surgeon before oxygen desaturation
resection and dysplastic airway lesions. The main limitation
occurs and jet ventilation needs to be restarted.
for their use is the experience of the anaesthetist and the
absence of suitable equipment. Jet ventilation involves
the intermittent administration of high-pressure sourced Limitation of supraglottic jet techniques
oxygen, air or oxygen/air mixtures, which entrain room Supraglottic jet ventilation techniques can maintain
air and lower the delivered pressures. The risk of life- oxygenation in patients with significant stridor and
threatening barotrauma is the most serious complication severe airway stenosis. The main limitation is in obese
and occurs when entrainment of room air is absent. This patients, particularly in a neutral or head down position.
results in the delivery of continuous gas with no ability of In this difficult population (obesity and advanced airway
the delivered gas to escape, leading to pneumomediastinum, stenosis) a head up position, maximal driving pressure,
pneumothorax and surgical emphysema. Since 1967, when maximal oxygen concentration and optimisation of rate
Sanders first described the technique, modifications to the and inspiratory:expiratory ratio may still not be enough to
frequency of ventilation (low-frequency, high-frequency prevent oxygen desaturation. Under these circumstances a
or superimposed-frequency jet ventilation) and the site at number of options are available. A microlaryngoscopy tube
which the jet emerges in the airway (supraglottic, subglottic may need to be placed and the patient ventilated by hand to
or transtracheal) have been made. re-recruit collapsed basal lung units to improve ventilation–
High-frequency jet ventilation techniques typically perfusion mismatch and oxygen saturation readings.
use rates around 100–150/min. This allows a continuous Alternatively, disconnect the high-frequency jet ventilator
expiratory flow of air, enhancing the removal of fragments (HFJV) and use a manual Sanders Jet Injector. The shorter
of blood and debris from the airway, and reduces peak and tubing of the manual device (typically <1 metre) will result
mean airway pressure with improved cardiovascular stability. in a lower drop in the distal pressure compared to the
Enhanced diffusion and interregional mixing (compared automated HFJV (typically >2 metre). The increased distal
with low frequency) within the lungs result in more efficient pressure and flow of oxygen with a lower frequency may be
ventilation with better oxygenation and removal of carbon enough to re-recruit collapsed basal lung units.
dioxide. These advantages are of particular importance in Other limitations of supraglottic techniques relate to:
patients with significant lung disease and obesity. (1) misalignment of the suspension laryngoscope to the
High frequencies are achieved by automated high- glottic inlet, which results in poor ventilation and the risk of
frequency jet ventilators, which have alarms and automatic gastric distension with entrained air; (2) blood, smoke and
interruption of jet flow when preset pause pressure debris being blown into the distal trachea; (3) considerable
limits have been reached (i.e. blockage of entrainment or vibration and movement of the vocal folds, which may
exhalation has occurred). require ventilation to be stopped while undergoing
phonosurgical procedures; (4) inability to monitor end-
Supraglottic jet ventilation tidal carbon dioxide concentration; and (5) potential risk of
barotrauma with pneumomediastinum, pneumothorax and
This technique delivers a jet of gas into the supraglottis by subcutaneous emphysema.
attachment of a jetting needle to the rigid surgical suspension
laryngoscope. High- or low-frequency ventilation can be
used. Supraglottic jet ventilation techniques allow a clear, Subglottic jet ventilation
unobstructed view for the surgeon with no risk of a laser Subglottic jet ventilation is a more efficient form of jet
airway fire. However, if the surgeon places surgical swabs ventilation because the gas is delivered directly into the
into the operating field, there is a risk of an airway fire with trachea. The technique involves placing a small catheter or
the swab acting as a ‘fuel’ source. specifically designed tube through the vocal folds and into
Supraglottic jet ventilation techniques are probably the the trachea. Care must be taken when placing the catheter
most commonly employed of all jet ventilation techniques not to traumatise any glottic pathology and to ensure the
and are particularly useful for glottic, subglottic and tracheal catheter tip is positioned in the mid-tracheal region. Once
stenotic lesions where the presence of a tracheal tube makes the catheter has been placed, subglottic jet ventilation can

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 Anaesthetic considerations in laryngology

be commenced and, unlike supraglottic techniques, there is for laser use, and transtracheal jet ventilation techniques
no time constraint for the surgeon in the placement of the for endoscopic laser surgery of the larynx require a careful
suspension laryngoscope. This means that for an expected evaluation of the potential risks and benefits. In most
difficult suspension laryngoscopy or training laryngoscopy, institutions, because the technique is invasive and has the
subglottic ventilation and oxygenation can be started potential for barotrauma, it is not used for benign laryngeal
and are independent of laryngoscope alignment to the airway surgery where other non-invasive jet techniques
laryngotracheal axis. The delivery of gas directly into the are preferred. The technique should be reserved for use
trachea results in reduced driving pressures, typically half in patients with advanced airway pathology, usually of a
that required in supraglottic techniques. Surgically, one of malignant nature with a severely compromised airway,
the main advantages of the technique is the near absence where the catheter is placed electively with the patient
of vocal fold movement, allowing complex phonosurgical awake, allowing ventilation should airway difficulties arise.9
procedures on a still field with continuous ventilation.With
this technique there is a continuous flow of gas outwards Spontaneous ventilation technique
around the periphery of the airway, which results in a Spontaneous ventilation and insufflation techniques
continuous stream tending to remove smoke and secretions are useful in the removal of foreign bodies, evaluation of
outwards and keeping the lower airway clear. The marked airway dynamics (tracheomalacia) and paediatric airways.
difference between supraglottic and subglottic techniques The technique involves the preservation of spontaneous
on vocal fold movement makes subglottic jet ventilation the ventilation with the patient anaesthetised with either
ideal choice for phonosurgical procedures.7,8 volatile anaesthetic agents or intravenous infusion of agents.
The presence of a catheter in the airway means a Because the patient is breathing spontaneously there is no
potential fuel source is now present and care must be need for any instrumentation of the airway and there is
taken during laser airway surgery. Many of the subglottic complete laryngeal visualisation in a laser-safe environment.
catheters that are commercially available have some laser- The disadvantage of this technique is the lack of control over
resistant properties, but if their tolerance is exceeded, the ventilation, with loss of protective airway reflexes and the
catheters can degrade and fracture. This can be potentially potential for airway soiling. Movements of the vocal cords
serious if, following a fracture of the catheter, jet ventilation are minimal or absent despite a spontaneously breathing
is resumed and the distal fragment is forced into the distal technique provided an adequate level of anaesthesia is
airways. Some catheters have metal wires within the catheter maintained. For satisfactory spontaneously breathing/
to reduce the chances of distal fragmentation. The presence insufflation techniques an adequate depth of anaesthesia is
of a catheter within the airway results in a greater risk of vital before any instrumentation of the airway takes place.
barotrauma than supraglottic jet techniques, because any If the depth of anaesthesia is too light, the vocal cords may
airway obstruction proximal to the gas exit port will cease move, the patient may cough or laryngospasm occur. If the
entrainment but continue the delivery of gas with no ability depth of anaesthesia is too great, the patient may become
to escape, leading to pneumomediastinum, pneumothorax apnoeic with cardiovascular instability.
and surgical emphysema. An automated jet ventilator will
prevent this. Intermittent apnoea techniques
Intermittent apnoea techniques have been described in
Transtracheal jet ventilation infants and children for the laser resection of juvenile
Transtracheal placement of a small catheter is generally laryngeal papillomatosis when the presence of a tracheal
used electively for clinical scenarios including obstructive tube obstructs surgery. Following induction of general
supraglottic and/or glottic pathology and when attempts anaesthesia, muscle relaxants are administered followed by
at obtaining an airway via an intraoral approach are likely tracheal intubation. The patient is hyperventilated with a
to lead to bleeding and further airway compromise. volatile anaesthetic agent in 100% oxygen.The tracheal tube
Transtracheal jet techniques carry the greatest risks of is then removed, leaving the surgeon a clear, unobstructed,
barotrauma as well as blockage, kinking, infection, bleeding immobile surgical field. After an apnoeic period of typically
and failure to site the catheter. None of the commercially 2–3 minutes, surgery is stopped, the tracheal tube is
available transtracheal catheters are specifically designed reinserted and the patient hyperventilated once more.

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 References

Closed systems for anaesthetic management

Closed systems have no leak into the outside environment The only exception is stainless steel. Non-laser tubes are
or entrainment of air into the system and employ a tracheal therefore unsuitable for laser airway procedures. Dedicated
tube with an inflatable cuff. For laryngeal procedures this laser protective tubes should always be used during
includes microlaryngoscopy tubes and laser tubes. laser airway surgery with closed systems. It is important
This technique is routine for all anaesthetists and allows to recognise that all commercially available laser tubes
control of ventilation and protection of the lower airway. have laser-resistant properties, but with energy strikes of
However, the presence of a tracheal tube limits laryngeal sufficient magnitude, the tubes may ignite and produce an
visualisation and surgical access and risks a laser airway fire. airway fire. All commercially available laser tubes include
product literature provided by the manufacturer, which
Laser airway fire describes the types of laser the tube has protection from
When the three components of the ‘fire triangle’ – fuel and the limits of the power settings for different lasers. Both
source, oxidant source and ignition source – combine, surgeon and anaesthesiologist should be aware of this. Laser
a catastrophic airway fire including life-threatening resistant implies some laser-resistant properties, but with
blowtorch airway fires can result. The fuel source can sustained strikes outside of protective limits, an airway fire
include any flammable material such as tracheal tubes, can still occur.10,11 Laser proof implies that irrespective of
gauze, sponges, drapes, masks, nasal cannulae, suction the oxidant environment and laser settings, an airway fire
catheters, gloves, gowns, endoscopes or any material that cannot occur. No commercially available laser tube is laser
may burn in the presence of an oxidant-rich atmosphere. proof.

References
1 Patel A, Pearce A (2011) Progress in the management of the UK: a national survey of the use of high-pressure
the obstructed airway. Anaesthesia 66(S2):1–8. source ventilation. Brit J Anaesth 101:266–272.
2 Mitchell V, Patel A (2011) Tracheal tubes. In: Core 7 Rubin JS, Patel A, Lennox P (2005) Subglottic jet
Topics in Airway Management, 2nd edn. (eds. I Calder, ventilation for suspension microlaryngoscopy. J  Voice
A Pearce) Cambridge University Press, Cambridge, 19:146–150.
pp. 91–104. 8 Hunsaker DH (1994) Anesthesia for microlaryngeal
3 Patel A (2011) ENT surgery. In: Core Topics in Airway surgery: the case for subglottic jet ventilation.
Management, 2nd edn. (eds. I Calder, A Pearce) Laryngoscope 104(Suppl 65):1–30.
Cambridge University Press, Cambridge, pp. 227–244. 9 Ross-Anderson DJ, Ferguson C, Patel A (2011)
4 Nouraei SA, Giussani DA, Howard DJ et al. (2008) Transtracheal jet ventilation in 50 patients with
Physiological comparison of spontaneous and positive- severe airway compromise and stridor. Brit J Anaesth
pressure ventilation in laryngotracheal stenosis. Brit J 106:140–144.
Anaesth 101:419–423. 10 Caplan RA, Barker SJ, Connis RT et al. (2008)
5 Patel A, Pearce, Pracy P (2011) Head and neck Practice advisory for the prevention and management
pathology. In: 4th National Audit Project of the Royal of operating room fires. A report for the American
College of Anaesthetists and the Difficult Airway Society. Society of Anesthesiologists Task Force on Operating
Major Complications of Airway Management in the United Room Fires. Anesthesiology 108:786–801.
Kingdom. (eds. T Cook, N Woodall, C Frerk) Royal 11 Patel A (2013) Anaesthesia for laser airway surgery.
College of Anaesthetists, London, pp. 143–154. In: Benumof and Hagberg’s Airway Management, 3rd edn.
6 Cook TM, Alexander R (2008) Major complications (ed. CA Hagberg) Elsevier Saunders, Philadelphia,
during anasethesia for elective laryngeal surgery in pp. 824–858.

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 CHAPTER 19

Gender dysphoria and the larynx

Christella Antoni & Guri Sandhu

Introduction
Transgender is now the preferred umbrella term for gender the preferred sex through surgery and hormone
variance and is more widely used than the term ‘transsexual’. treatment.
Transgender individuals suffer ‘gender dysphoria’ and believe ●● The transsexual identity has been present persistently for
they have been born into the wrong body and prefer to at least two years.
live as a member of the opposite sex. The Royal College ●● The disorder is not a symptom of another mental
of Psychiatrists in England has issued a ‘Good Practice disorder or chromosomal abnormality.
Guidelines for the Assessment and Treatment of Adults with
In the UK these patients are managed by a multidisciplinary
Gender Dysphoria’1, stating that ‘Gender variance knows no
team (MDT) in Specialist Centres. The disciplines involved
social, ethnic, religious or socioeconomic boundaries but is
in the MDT are psychiatry, endocrinology, psychology,
likely to be more hidden in some cultures than in others.’
urological surgery, ENT surgery, speech therapy and
The prevalence is estimated as at 1 in 54,000 with
specialist nursing. In the UK the diagnosis must be made
three-quarters being male to female transgender.2 The
by two medical practitioners, one of whom should be a
International Classification of Diseases (ICD-10) lists three
psychiatrist or clinical psychologist working in the field.
diagnostic criteria for ‘transsexualism’:3
The first step to transition is hormone therapy. The patient
●● The desire to live and be accepted as a member of also has to live in their preferred gender identity for up
the opposite sex, usually accompanied by the wish to to 2  years, a period of real life experience (RLE), before
make his or her body as congruent as possible with gender reassignment surgery is considered.

Laryngeal development
There has to be an appreciation of laryngeal development effect on muscle bulk and laryngeal growth is slight, such
when considering potential treatments in this group of that the breaking of the voice is much less marked.
patients. The primordium of the larynx and respiratory There is a process of calcification of the laryngeal
system (trachea, bronchi and lungs) appears as an outgrowth cartilages that begins in the 3rd decade of life and starts in
from the ventral wall of the foregut when the embryo is the thyroid cartilage. Calcification is more marked in men
4 weeks old. Growth and maturity continues until birth. and by the 5th decade of life the thyroid cartilage consists
The infant larynx differs markedly from the adult larynx. largely of bone and may even possess a bone marrow.
It is smaller in absolute and relative terms and lies higher The angle between the two laminae of the thyroid
in the neck. During the first 3 years of life the child’s cartilage is 90° in men and 120° in women. This sharper
larynx descends to an adult position, lower in the neck. angle in men and the relatively greater anterior to posterior
Until puberty the larynx grows proportionately to crown- dimension leads to the more obvious laryngeal prominence
heel length. At puberty the female larynx grows slightly (‘Adam’s apple’).
whereas the male larynx enlarges in all directions. The The vocal cord comprises the vocal process of the
effects of androgens are irreversible and lead to vocal cord arytenoid (cartilaginous vocal cord) and the vocal fold
lengthening, increased muscle bulk and the production of (membranous vocal cord). It is only the vocal fold that
more viscous mucus. This leads to ‘breaking’ of the voice vibrates during speech. The length of the vocal fold is the
and lowered vocal pitch. In  females, the oestrogen surge same in both males and females until the age of 10 years
at puberty also causes thickening of mucus but there is no (6–8 mm). By the end of puberty the male vocal fold has

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 Gender dysphoria and the larynx

doubled in length (16–18 mm) whereas the female vocal from the fundamental frequency, the other differences
fold has increased by one-third (8.5–12 mm). between male and female communication are intonation,
The fundamental frequencies for male habitual voice may inflexion, gesturing and body language. Although a male-
vary from 90–130 Hertz (Hz) whereas the female range is to-female transgender may appear female, a masculine
from 170–260 Hz. It is widely accepted that a fundamental voice and a prominent Adam’s apple may still be a source of
frequency above 155 Hz is perceived as female.4 Apart embarrassment.

Transgender voice and the role of speech therapy

Speech and language therapists (SLTs) working in the field seek the services of a SLT. Furthermore, female transsexuals
of gender dysphoria work in a highly specialist, challenging who are professional voice users or who have high vocal
and small field within the remit of speech and language demands may require voice therapy as well as counselling
therapy as a whole. SLTs may treat gender dysphoric regarding some of the possible vocal restrictions.
individuals as part of their general voice caseload or, more The bulk of the voice therapist’s involvement nevertheless
unusually, have a specific interest in the field. A review of falls within the male-to-female caseload. Certainly, the
the literature by McNeill5 found that ‘speech and language therapy intervention with the latter client group is longer in
therapy is successful at creating an acceptable fundamental duration and generally covers a far wider number of speech
frequency in transgender patients’. In the UK, the SLT and vocal aspects, as well as related issues such as general
forms part of the MDT managing gender dysphoria. In female presentation. This chapter will therefore seek to
addition to an understanding of gender dysphoria, the SLT provide an overview of the SLT’s involvement with male-
needs to be conversant with the medical model of treatment to-female clients from the point of referral to the stage of
for transgender clients, for both male and female individuals. discharge. SLT intervention includes assessment, treatment
Psychiatric and medical elements (hormonal and and, with the ENT surgeon, making a decision with respect
surgical treatment) and various non-medical associated to the need for pitch elevation surgery.
aspects of transition, (hair removal, legal change of name) The overall aim of treatment is to help the client produce
are likely to be current issues in a patient’s life at the time a functional female voice. Aspects of female voicing and
of SLT intervention. As well as these medical and practical communication are first taught to the client, along with
aspects of gender transition, awareness is required of the general aspects of voice production and voice care. The
psychological and emotional aspects that frequently feature therapy room provides a safe environment for the client
in transsexualism. to experiment with her voice and to try out the exercises
There is a far greater number of male-to-female patients with the SLT prior to practising the exercises at home and
referred to speech and language therapy than female-to- in public. An  additional goal is for the client to develop
male. This corresponds to the greater incidence of male- a confident manner in speech and voicing. Inherent in
to-female transsexualism within the general population. In these  goals are emotional and psychological aspects of
addition, oestrogen hormone treatment given to male-to- voicing. These require the therapist to work beyond the
female patients has no effect on the cartilaginous framework remit of perceptual voice. Counselling therefore forms a
of the larynx or the vocal cords.6 Thus, oestrogen has no large part of the voice therapy.
effect on the pitch (fundamental frequency) of the voice. The timing of referral to speech and language therapy
For this reason, male-to-female patients need to learn to for male-to-female clients can vary widely and range from
produce a higher pitched voice and a more characteristically a referral while an individual is still living in male role
female voice, despite the constraints of a biological male to a referral only when the patient has undergone vocal
larynx, vocal folds (vocal cords) and vocal tract, the latter of pitch raising surgery. However, the majority of referrals
which is both longer and wider than a natal female larynx. are for patients with no previous experience of speech
In the female-to-male client group, androgen treatment and language therapy and in most cases, clients will have
leads to an increase in the mass of the vocal folds. The commenced their RLE or will be close to it. The authors
thickened vocal folds result in a lower pitched voice. believe best practice is to offer vocal surgery only after a
Although female transsexuals are therefore at a distinct course of voice therapy has been completed and when a
advantage in acquiring their desired voice, some speech and patient is well established on their RLE. However, some
language therapy intervention may still be indicated. Some patients access voice surgery without having any previous
female-to-male patients therefore may remain dissatisfied speech and language therapy. While research regarding
with their male voice, despite testosterone treatment and outcomes in these cases is lacking, our clinical experience

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 Initial assessment

suggests that surgery, without any speech and language in speech and language therapy. The speech and voice
therapy, generally leads to less effective outcomes and an work becomes more relevant for them and forms part of
increased incidences of dysphonia. In addition, patients their endeavour to present as a female.
already embarked on their RLE tend to progress quicker

Initial assessment
As with any voice client, a thorough initial assessment is ●● Voice history. This includes vocal abuse and misuse
crucial to the planning of treatment and therefore requires (i.e. factors such as smoking), previous voice difficulty,
a substantial time allocation. Approximately 75–90 minutes level of voice use and whether there are any laryngeal
is recommended. This may be the longest appointment symptoms.
time a client has experienced with a professional and ●● Voice presentation. An auditory judgement should
clients are often nervous and unsure of what to expect. It be made by the SLT and the client’s own perception of
is worthwhile outlining the session briefly to the client to voice should be noted. It is useful for the therapist to ask
help dispel anxieties. Chaloner and Cavalli wrote: “The the client how their voice serves them both in face-to-face
speech and language therapy consultation provides some contact with others in everyday life and when visual cues
transsexuals with the first safe, accepting and relaxed setting are absent, most commonly when using the telephone.
to ‘be themselves’”.7 As well as a detailed case history, the ●● Perceptual assessment. This includes vocal
aim is to impart the necessary information regarding what characteristics and any dysphonia. The latter can be
can be offered by speech and language therapy and to obtain graded according to the GRBAS perceptual assessment.8
recordings of the patient’s voice if possible. An audio recording should, if possible, be made of
With gender dysphoric clients, the voicing difficulties do a client reading a standard voice text, such as ‘The
not fit specifically into the category of a disorder.After all, in the Rainbow Passage’9, as well as a sample of free  speech,
majority of patients the voice is physically healthy and intact. such as ‘what I did at the weekend’.
The issue for the client is that their voice requires modification ●● Objective assessment, using instrumentation such as
and does not fit with their perception of self.There are several Visipitch or the electrolaryngograph to obtain a reading
similarities between a standard voice case history form and of the client’s habitual vocal pitch.
an initial assessment form used with a transsexual client, in ●● ENT history. This includes whether the patient is
that each will include sections on the client’s vocal habits and considering a reduction of the laryngeal prominence
level of voice use. In addition, an initial assessment form for a (thyroid chondroplasty), pitch elevation surgery, or both.
gender dysphoric client should include sections that pertain ●● Indications/suitability for treatment, particularly
specifically to gender reassignment. A speech and language the client’s level of motivation, degree of voice concern,
therapy department offering a service to gender dysphoric ability to commit to therapy, as well as the client’s
clients will most likely adapt their standard voice assessment expectations of treatment and any factors that may
form.The following headings are recommended: impede or aid progress.
●● SLT management. Following assessment, there may
●● Summary of status in the gender reassignment be many indications, including delaying treatment until
process. This includes medical information, relevant a more appropriate time or referral to an alternative
facts such as whether a client is receiving hormone service local to the patient. In most cases, a full treatment
treatment and details regarding a client’s RLE. block is offered, which may at some point lead to a
●● Medical history. This includes physical and mental referral for ENT surgery. It is recommended that all
health status or factors and current medications taken. suitable patients undergo individual therapy sessions
●● Social history. This includes employment, marital with an SLT prior to any voice surgery. In addition,
status and current level of support from family and some patients may be invited to attend a voice and
friends and other social networks. communication skills practice group.
●● Presentation of the client. This includes an outline
of the patient’s physical presentation made by the SLT In addition to the above, the SLT outlines the expectations
as well as the client’s perception of self and concerns of the client, which will include regular attendance at
regarding their overall presentation. Observations should sessions and a commitment to practising communication
also be made with respect to the client’s social skills and and voice exercises. There is a mutual decision about
competence as a communicator. whether a client should begin treatment. Occasionally,

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 Gender dysphoria and the larynx

a client attends the SLT assessment simply out of curiosity seeking confirmation of this by ‘an expert’ or is seeking
and has no overt concerns regarding voice. Although the some additional tips to ensure they are using their best
SLT may feel a patient’s voice is not convincingly feminine, voice possible. Others present with a perceptually close to
it is unwise to treat clients who are not highly motivated, feminine sounding voice or with an easily adaptable voice
as this usually wastes scarce treatment sessions. and will therefore require a short speech and language
Voice therapy covers many aspects and can be a long therapy intervention. The majority of clients, however,
and challenging experience. Some individuals present present with unmistakably masculine voices. For these
at initial assessment with a good female voice and overall individuals, a full course of speech and language therapy
presentation. In these cases, the client is usually merely intervention is required.

Speech and language therapy treatment

Almost all voice therapy begins with a treatment session Aspects in this area include hair removal, which nearly all
that will include advice and information regarding vocal male clients require. Both electrolysis and laser removal are
hygiene, voice care, voice production and voice education. costly, lengthy and often painful. Clients undergo treatment
The latter is a logical starting point with gender dysphoric not only for removal of facial hair but also to eliminate body,
individuals, but the information needs to be expanded to and sometimes genital, hair prior to gender reassignment
include issues related to the differences between male and surgery. It is common for clients to  attend voice sessions
female voices. Aspects of treatment, both direct and indirect, with blotchy red faces, or expressing physical discomfort
are outlined below. relating to hair removal. The SLT merely needs to be aware
of this lengthy commitment for the client and the practical
Indirect therapy implications.
Indirect treatment and therapy centres around increasing a
client’s awareness of all aspects of female presentation and Communication and social skills
on providing background information on speech and voice Work in this area is another departure from the traditional
in general, rather than direct therapy exercises. form of voice therapy. The aim is to aid the individual to
‘have a convincing image within the framework of the
Voice education client’s personality and ability’.7 Socially challenged or
isolated individuals, or those who have concomitant
Voice education includes information about how voice is mental health issues, will generally benefit from assistance
produced, voice care advice and information regarding the in this area providing that that they are cognitively intact.
different ways male and female vocal tracts shape sound and Perhaps through a long-standing sense of ‘being different’,
how pitch and resonance are modified. or because of negative reactions or a lack of social
contacts, clients with gender dysphoria may lack general
Physical presentation communication, interpersonal and social skills and come
Advice regarding a client’s general female and physical across as being particularly self-referential. Clients may
presentation, although crucial, is rarely provided by the conversely present as being so lacking in confidence and
NHS. It generally falls to clients themselves to work on their experience with others that they find it very difficult to
overall look. Clients are advantaged or disadvantaged in talk about themselves. There may be a paucity of personal
this respect by their build, their perception and their social interests, social contacts or employment and therefore the
circumstances. Thus, while many clients have an excellent range of conversational subjects can be limited.
presentation, others struggle to look convincing or even It is also not unusual for clients to perseverate on
appropriate in the female role, particularly those who are certain topics, frequently about their physical presentation,
socially isolated or who have limited financial means. It viewing this as the major obstacle to their successful life as
may thus form part of the SLT’s role to offer advice and a woman.
suggestions in areas that are not directly related to speech As well as general communication skills, specific
and voice but are directly related to the client’s success in communication features pertaining more specifically
presenting as female. This supports the voice therapy and to women may need addressing, including posture, the
should, if possible, be client led. It is useful for the SLT to increased use of gesture, eye contact and facial expression.
have a list of resources to offer clients if they are seeking Again, a variety of presentations are seen amongst this
services regarding their physical presentation. client population. Some individuals’ body language and

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 Speech and language therapy treatment

non-verbal communication present them very naturally increases in pitch are associated with older males, as the
as women. Others have overt masculine presentations, vocal folds decrease in mass with age. The opposite is true
sometimes compounded by a large stature and strong for females where the vocal cords tend to thicken slightly
masculine physical characteristics. The majority of with ageing.Wolfe et al.4 report that the mean fundamental
patients referred to speech and language therapy will frequency of their transsexual subjects ranged from 93 Hz
wish to present as successfully as possible and tend to to 202 Hz, clearly overlapping the range of male and female
welcome suggestions in this area. It is worthwhile noting speakers.
how a client walks down a corridor or sits in a chair for It is useful to experiment with the pitch early on
example. Legs kept wide apart (sometimes despite the in therapy in order to gain a sense of the client’s natural
wearing of tights and a knee length skirt) and a masculine vocal ability in this area. Much of the client’s success will
gait is frequently one of the most telling aspects of be determined by whether they have an ‘ear’ for pitch.
presentation, one that the client is often unaware of, Without it, altering pitch will prove very difficult.The main
especially if, in other ways, there is a reasonable female aim of therapy is to encourage a slightly higher pitch to
presentation. begin, which is easily achievable by the client. A further
increase in pitch may be possible over time with increased
Direct therapy experimentation and confidence. Clients who attempt to
self-modify their voices generally aim too high regarding
Direct therapy with male-to-female clients centres on pitch and present with a hyperfunctional voice that may be
the speech and voice parameters of pitch, resonance, characterised by strain, breathiness, roughness or hoarseness.
intonation, articulation, prosody, intensity, language use, At worst, they will habitually employ a falsetto voice
communicative style and manner of voicing. The aim is quality (also known as loft register), which will result in
to modify the client’s voice so that it presents as female. an unnatural sounding voice akin to that of a pantomime
At best, this means that listeners will identify the voice as dame.
female, both in face-to-face exchanges and in exchanges While many clients will be focussed on their pitch as
where visual cues are absent, usually a telephone the essential marker for vocal femininity, in reality, ‘high
conversation, which can serve as the decisive test. pitch is not necessarily the result of high frequency but
Although formal data is lacking, there is more success may be caused by the acoustic characteristics imparted
achieving an adequate voice for face-to-face situations and to the voice by the supraglottic vocal tract’.10 Longer,
general voicing. This is because visual cues aid the listener’s wider vocal tracts are likely to impede the production
perceptions. A client who presents convincingly as female, of higher pitch in transsexuals. Spencer’s study11 found
perhaps due to small stature, attention to grooming and that transsexuals who were perceived as female were of a
confident social and speaking manner, will be accepted as small build (170 cm or below). He stated that since shorter
female despite a rather idiosyncratic voice or lower pitch. individuals are likely to have shorter vocal tracts, small
Feminising a voice is challenging. It is easier for a client to stature is likely to be an advantage for transsexual voice
feminise some aspects of voicing, rather than all aspects. when combined with high fundamental frequency.
However, every little bit helps the overall perception. An essential part of speech and language therapy
A gender neutral-type voice can often be achieved, which therefore often lies in teaching the client ways of gaining
may not be distinctly female but nevertheless serves the differentiated control of varying parts of the vocal tract,
individual well. The three most salient aspects that are such as altering tongue and lip positions and raising
likely to distinguish male and female voices are pitch, the  larynx. This type of work lends itself better to
intonation and resonance.4 professional voice users, actors or performers rather than
to the lay  public who, in the main, have a low insight
Pitch and limited experience regarding the workings and
Pitch is the most researched aspect of male transsexual potential of the human voice. However, breakdown of
voice. Many studies have sought to determine the speaking tasks and modelling sounds and vocal tract positions help
fundamental frequency that separates male and female the patient to grasp  what is intended by the exercises.
voices.The dividing line is around a fundamental frequency Alteration of vocal tract parameters allows for alterations
of 155–160 Hz.4 Greene and Mathieson10 record the in intonation, resonance and formant frequencies
average speaking fundamental frequency to be 128 Hz of vowels, all of which play an important role in the
in males and 225 Hz in females. Pitch varies according feminisation of a male voice.
to the individual and the circumstances. Emotional status Voice quality can be altered in a variety of ways.
influences pitch as does the age of the speaker. Mild Raising the back of the tongue raises the larynx. This,

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 Gender dysphoria and the larynx

in turn, shortens the length of the vocal tract, which can the various resonance chambers of the body.The resonating
help a client develop or sustain higher pitch. In addition, system of the voice is made up of the structures and air-
developing the ability to use thinner vocal folds will also filled cavities above and below the larynx, such as the nose,
lead to a higher pitched voice. The voice quality ‘twang’12 sinuses and pharyngeal spaces, which can be manipulated to
lends itself very well to voice feminisation. The quality produce specific harmonics. Indeed, ‘the laryngeal note is
can be adapted successfully for use with transgender clients insignificant without its system of resonators’.10
to develop higher pitched, brighter voices. Twang results The overall aim of treatment in this area is for the client
in a larynx free from constriction; its main features are a to develop skill in using oral, pharyngeal and sinonasal
high larynx setting, a high and forward placed tongue and resonance when voicing and aiming for a physically higher
aryepiglottic sphincter narrowing. Twang also allows for ‘placement’ of speech, which usually involves increased focus
safe voice projection, if taught correctly, another reason on articulation. In the majority of cases, patients are helped
why it is especially useful for working with transgender by learning to soften the contacts with the articulators for
voice, as one of the key worries of clients is that they are consonant sounds and by using more precise diction. The
unable to use raised volume in their ‘female’ voice. This is latter has been identified as being a more common feature
especially true if they have favoured the use of a breathy of female speech rather than male speech.14 In addition,
voice quality. increased or altered oral shaping for vowels can be a crucial
element of successful female voice.
Intonation
Intonation work is a crucial aspect of successful voice Psychosocial considerations
outcomes for transgender clients. The authors believe that It is also worth drawing the client’s attention to some of the
overall tone and the tonal range of a patient’s voice can basic differences suggested for the ways men and women
prove to be the single most discerning factor regarding communicate, such as the female conversational tendencies
female identification by a listener. Practising different to use more descriptors, more facial animation and to give
tones of voice to convey different emotions is one way more listener feedback than do males. Working on these
of developing this skill. Above all, the voice must be as far aspects as well as the sound of an individual’s voice could
away from a monotone as possible and display a variety of help their overall presentation. Many clients comment that
intonation shifts, even with relatively short length speech they fear sounding unnatural. Reassurance should be given
utterances, as the latter is more characteristic of female that the aim is to modify their voice and speech, not to
speech. adopt a totally alien sound.
Gelfer and Schofield13 defined an intonation shift as: A further psychosocial consideration is the patient’s need
“A change in frequency, with or without interruption of emotionally to adjust to the modified voice. This aspect is
phonation, of at least two semitones”. Further, the male- rarely given attention to in the literature or by clinicians or
to-female transsexuals in their study who were perceived as patients themselves. In many cases, patients wish to move
female used a greater number of upward intonation shifts quickly with their voice and speech feminisation, but cease
and a greater range (in semitones) of downward intonation to make progress or plateau early on in treatment because of
shifts. a reluctance, conscious or unconscious, to adopt the ‘new’
Regional accents can sometimes be a useful feature of voice. They fear sounding unnatural, or ‘too high’ and
a client’s voice and can be built on. The natural lilt and experience embarrassment, especially when trying to use
peaking of a Welsh accent lends itself very well to uprising a more feminine voice in front of family members, friends
tone and tone variation. Conversely, some London accents, or work colleagues. A common finding is that patients have
especially when coupled with a low pitch, can prove very more success using their feminised voice with strangers than
resistant to increases in tone variation. with people who are well known to them. Family members
in particular can have difficulty accepting any or every level
Resonance of a relative’s gender transition, including voice. Patients who
Resonance work is an important component of most have supportive families and friends, or who are determined
voice therapy. It is vital for male-to-female patients to and confident in nature, obviously tend to progress more
grasp that reduced chest resonance is a characteristic successfully and adopt the changes more permanently than
of female voice quality. Chest and oral resonance can those who struggle with their own resistance to transition,
easily be contrasted and the patient is encouraged to feel or the resistance of others. It is worth pointing out to clients
vibrations both on the upper part of the chest and on the that it takes time to learn new voice skills and time to adapt
face, to gain an understanding of how sound is altered in to having, and using, a different voice.

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 Vocal surgery

Vocal surgery
SLTs working in this field need to have an understanding In most cases, the patient is known to the SLT and
of the pitch raising surgeries offered, most commonly, the therefore baseline measurements of the individual’s voice
cricothyroid approximation (CTA) surgery. In addition, will already exist. Pre-surgically, an audio recording and
therapists should be very familiar with the chondroplasty a pitch measurement should be made if possible. The
procedure carried out for reducing the thyroid cartilage. therapist should also provide post-surgical voice care advice,
A prominent Adam’s apple is frequently cited by patients as which includes limiting all voice use for the first 72 hours
being of great concern to them. Even patients who present after surgery and conservative voice use for approximately
with a relatively small laryngeal prominence may show 2 weeks following surgery.
concern that it is a ‘tell-tale’ sign of masculinity. Post surgery, the patient should be followed up with a
Limited data exist regarding the formal outcomes of vocal view to assessing the outcome of surgery and to help the
surgery with transsexuals. However, empirical observation patient establish a comfortable voicing manner if there are
suggests that patients who successfully modify parameters signs of vocal strain. Audio and objective recordings should
of voice and speech other than pitch, for example, prosody, be taken if possible for comparison with pre-surgical voice.
intonation or manner of voicing, tend to have a more Follow-up speech and language therapy may also be required
successful surgical voice outcome than those patients who to address any dysphonia that may result from the surgery.
seek surgery without previous speech and language therapy. Kanagalingam et al.16 carried out an evaluation of medium
This is a logical conclusion as the surgery only addresses the term outcome for 21 transsexuals who had a cricothyroid
aspect of pitch. Postoperatively, a patient may still sound male, and subluxation procedure. Their conclusion was that CTA
albeit high pitched, without attention to other speech and effectively raised pitch in male-to-female transsexuals.
voice features. In the Spencer study11, the transsexuals related There was a concomitant rise in voice irregularities, which
that they “alter more than pitch”, citing in particular more is effectively addressed by speech therapy.16 A full evaluation
precise consonant production and the use of a “softer tone”. of the published data regarding these patients is difficult as
Pitch surgery can therefore support and extend the the speech and language therapy input they received had
progress made in speech and language therapy but is rarely been variable. Matai et al.15 agree that it is difficult to judge
a total substitute for it, much to the disappointment of many the relative contribution of the two methods: probably
patients who are hoping for a quicker ‘fix’ to the problem of both surgery and speech therapy work in conjunction and
their voice. This should be made clear to patients. Of course, increase the likelihood of a good result.
some patients (with or without speech and language therapy),
manage to make reasonable modifications to their voice and Surgery for pitch elevation
communication style, but find sustaining pitch consistently Through appropriate speech and language therapy, the
the single most problematic factor regarding feminising their majority of transsexuals will achieve a satisfactory female
voice adequately. For these individuals, phonosurgery can voice and manner. In the authors’ series, less than one-fifth
yield a satisfactory to excellent outcome. Psychologically, of patients request or are referred for pitch elevation surgery.
too, there may be a boost for patients who often report that An appreciation of the function of two intrinsic laryngeal
they experience less fear post surgically that their voice will muscles allows for a better understanding of how surgery
‘suddenly drop’ when they are in mid-conversation.Activities for elevating vocal pitch has evolved:
such as coughing or laughing or emotional states such as
anger or sadness are also potential trouble areas for sustaining ●● The cricothyroid muscle takes its origin from the
pitch consistently.Vocal surgery may also increase emotional anterior surface of the arch of the cricoid and inserts
security concerning these areas, which in turn can lead to a into the antero-lateral surface of the thyroid cartilage.
more confident communicator overall. Its action is to lengthen and exert tension on the vocal
Matai et al.15 conducted a survey on patients who had cord. By elevating the arch of the cricoid the distance
received CTA surgery and/or thyroid chondroplasty. Of between the angle of the thyroid cartilage and the vocal
the 42 completed questionnaires, 33 patients had the CTA process of the arytenoids is increased (Figure 19.1).
procedure, 79% of whom indicated an improvement in ●● The thyroarytenoid muscle passes from the base
their voice. Comments by patients included: “It has given and anterior surface of the arytenoid cartilage to the
me the confidence to face the world”, and “It’s the best inner surface of the thyroid cartilage in the midline.
thing I’ve ever had done!” Nine patients (21%) indicated The thyroarytenoid muscle shortens the vocal fold and
that they “were not pleased with surgery”. adjusts the tension within it during phonation.

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 Gender dysphoria and the larynx

Figure 19.1 Saggital section through the larynx (viewed from

the right side) demonstrating the action of the cricothyroid
muscle (not shown), increasing the distance between the anterior
commissure and the arytenoid; the vocal fold is thus stretched and Figure 19.2 The dot represents the internal attachment of the
the pitch rises. vocal folds. By advancing the anterior commissure the vocal folds
are tensioned. The final position is secured by a mini-plate.

The following is a well known equation describing the

relationship between frequency (f), length of a vibrating
cord (L), tension (T) and its mass per unit length (μ).

1 T
f =
2L µ

In principle it should be possible to raise vocal pitch

by shortening the vocal cords or reducing their mass.
Alternatively, increasing the tension in the vocal cords a
should achieve the same result.

Surgery options for elevating vocal pitch

Advancing the vocal cord attachment
The tension in the vocal cords can be increased by exposing
the larynx and advancing the anterior commissure, which
is then held forward by a mini-plate (Figure 19.2).
The disadvantage of this technique is that the laryngeal
prominence becomes more exaggerated and cannot be
reduced.

Cricothyroid approximation
b
CTA is carried out through a transverse skin incision over
the larynx. Permanent mattress sutures are placed between Figures 19.3a, b Horizontal matress sutures, using a braided
the thyroid and cricoid cartilages (Figures 19.3a, b). This monofilament suture, are used to approximate the thyroid and
cricoid cartilages (a). The surgical picture (b) demonstrates closure
has the effect of increasing the tension in the vocal cords,
of the cricothyroid gap.
much like the action of the cricothyroid muscle. A review
of this procedure16 showed that 80% of patients were
satisfied with the results and objectively 71% had gains in In patients aged over 50 years, allowance has to be made
vocal frequency (Fo) in free speech, reading and singing for vocal fold laxity related to the ageing voice and maximal
maintained at 41 months follow up. There was, however, CTA may not be enough to achieve adequate pitch
a narrowing of the vocal range following surgery. The elevation.17 In these patients it is frequently necessary to
reported success is attributed to both the surgery and post- drill 3–5 mm off the lower border of the thyroid cartilage to
surgical speech therapy. increase the cricothyroid gap prior to approximation.

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 Vocal surgery

Figure 19.4 Stripping the mucosa of the anterior third of the vocal folds, and suturing them together, will create a web and effectively
reduce the working length of the vocal fold.

Vocal cord shortening procedures

The authors’ initial surgical attempts at pitch elevation
surgery were directed at vocal fold shortening by way of a
vertical midline split of the larynx (laryngofissure approach).
Patients were appreciative of their new voice because of
increased ‘breathiness’; however, objective analysis did not
reveal an increase in fundamental frequency.
Surgically stripping the mucosa over the anterior ends of
the vocal folds and suturing them together can reduce their
effective working length by creating a web at the anterior
laryngeal commissure. This can be carried out through a
laryngofissure approach or endoscopically (Figure 19.4).The
anterior one-third of the vocal folds needs to be webbed to
duplicate the female working length. Unfortunately, a large
web may compromise the airway at the glottis. Although high
success rates have been published for this operation18, other
authorities have not been able to reproduce these. Figure 19.5 Vocal folds after a ‘blind’ reduction of the laryngeal
prominence. The anterior commissure has been detached, leading
Thyroid chondroplasty to a ‘U’-shaped glottis deformity and a weak breathy voice.
Thyroid chondroplasty (or ‘laryngeal shave’) is the surgical
reduction of the laryngeal prominence (‘Adam’s apple’) tethering to deeper structures. Unless there is a history of
to give the neck a feminine contour. Two techniques are hypertrophic or keloid scar formation, the incision is not
widely used. The first technique uses a small incision high easily visible after a few months.
in the midline neck. Scissors are passed through a soft tissue
tunnel and the laryngeal prominence is removed without Surgery to reduce vocal pitch
direct visualisation. The advantage of this technique is that It is very rare that a person transitioning from female to
the scar is hidden under the chin. However, the resection male requires surgery to reduce vocal pitch. A combination
often leaves an unnatural ‘open book’ appearance to the of treatment with androgens and sometimes speech therapy
larynx and the patient is likely to develop adhesions between is usually adequate. However, in the rare circumstances that
the skin and larynx such that there is ‘puckering’ of the skin this request is made the easiest approach is to increase the
on swallowing. There is also a small risk of detaching the mass of the vocal folds with a suitable injection material. The
vocal cords anteriorly, with an associated risk to voice and authors’ preference is to use autologous fat harvested using
airway (Figure 19.5). the technique described by Coleman.19 Fat has the advantage
The alternative is to place the small incision in a suitable that it survives for reasonable periods following injection, but
skin crease directly over the larynx. If a CTA (for pitch ‘top-up’ injections are often required. It also does not interfere
elevation) is also planned, then the same incision can be with the vocal fold mucosal wave. If vocal fold injections prove
used. This approach allows for the dimensions of the larynx inadequate, then surgical division of both cricothyroid muscles
to be measured accurately for maximal and safe removal may be considered.This does not produce a monotone voice,
of the laryngeal prominence (Figures 19.6a, b). The soft as other cord-tensioning muscles are intact, but it does allow
tissues are closed in layers so that there is little risk of skin the person to more easily maintain a lower pitch.

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 Gender dysphoria and the larynx

Figure 19.7 Drawings demonstrating the Isshiki type III thyroplasty

to shorten and reduce tension on the vocal folds. Vertical slips of
cartilage are removed either side of the midline from the thyroid
cartilage.

certainly needs to be better reporting of outcomes with

b objective assessment tools. One of the difficulties of being
Figures 19.6a, b Resection of the thyroid laryngeal prominence a specialist centre is that patients travel great distances to
after marking the midpoint (b). attend and it is usually patients with successful surgical
outcomes who are most reluctant to return for voice
analysis. It  is fortunate that most transgender patients
Isshiki20 described the type III (vocal fold shortening) achieve appropriate voices through their own efforts or
thyroplasty (Figure 19.7) to reduce vocal fold tension, but assisted by the speech therapist. Surgery for pitch elevation
the authors have never had to use this procedure for gender is currently not perfected. The ideal surgical procedure
patients. would shorten and reduce the bulk of the male vocal cords,
with appropriate pitch elevation, maintained permanently.
Discussion It would also be carried out endoscopically to avoid scars.
Unfortunately, there are no studies looking at the long- Further surgical advances need to be made in the field of
term results of these various surgical approaches. There laryngology before this is possible.

References
1 The Royal College of Psychiatrists (2013) Good Practice 4 Wolfe V, Ratusnik D, Smith F (1990) Intonation and
Guidelines for the Assessment and Treatment of Adults fundamental frequency in male-to-female transsexuals.
with Gender Dysphoria. Royal College of Psychiatrists, J Speech Hear Disord 55:43–50.
London. 5 McNeill E (2006) Management of the transgender
2 Landen M,Walinder J, Lundstrom B (1996) Prevalence, voice. J Laryngol Otol 120:521–523.
incidence and sex ratio of transsexualism. Act Psychiatr 6 Money J, Walker P (1977) Counselling the transexual.
Scand 93:221–223. In: Handbook of Sexology. (ed. M Money) Elsevier,
3 World Health Organisation (1992) The ICD-10 Amsterdam, pp. 1289–1301.
Classification of Mental and Behavioural Disorders: Clinical 7 Cavalli L, Chaloner L (2001) Gender identity disorders.
Descriptions and Diagnostic Guidelines. WHO, Geneva. In: Communication and Mental Illness: Theoretical and

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 References

Practical Approaches. (eds. J France, S Kramer) Jessica 14 Glass L (1992) He Says, She Says. Judy Piatkus Ltd.,
Kingsley, London. London.
8 Hirano M (1981) Clinical Examination of Voice. Springer, 15 Matai V, Cheesman A, Clark P (2003) Cricothyoid
London. approximation and thyroid chondroplasty: a  patient
9 Fairbanks G (1960) (The Rainbow Passage) Voice and survey. Otolaryngol Head Neck Surg 128:841–847.
Articulation Drillbook, 2nd edn. Harper, New York. 16 Kanagalingam J, Georgalas C, Wood GR et al. (2005)
10 Mathieson L (2001) Greene & Mathieson’s The Voice and Cricothyroid approximation and subluxation in
Its Disorders, 6 edn. Whurr Publishing, London. 21 male-to-female transsexuals. Laryngoscope 115:
11 Spencer L (1988) Speech characteristics of male-to- 611–618.
female transsexuals: a perceptual and acoustic study. 17 Baken R (2005) The aged voice: a new hypothesis.
Folia Phoniatr 40:31–42. J Voice 19(3):317–325.
12 Colton R, Estill J (1981) Elements of voice quality: 18 Gross M (1999) Pitch raising surgery in male-to-
perceptual, acoustic physiologic aspects. In: Speech and female transsexuals. J Voice 13:246–250.
Language: Advances in Basic Research and Practice. 19 Coleman S (1997) Facial recontouring with
(ed. N Lass) Academic Press, New York. liposuction. Clin Plast Surgery 24:347–367.
13 Gelfer M, Schofield K (2000) Comparison of acoustic 20 Isshiki N, Morita H, Okamura H et al. (1974)
and perceptual measures of voice in male-to female Thyroplasty as a new phonosurgical technique.
transsexuals perceived as female versus those perceived Acta Otolaryngol 78:451–457.
as male. J Voice 14(1):22–33.

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 CHAPTER 20

New horizons in laryngology

Nick Hamilton & Martin Birchall

Introduction
Laryngology has recently been described as going through place, resulting in greater use of intensive care units, which
a golden age.1 Improved understanding of pathophysiology in turn will increase iatrogenic airway pathology.3 The on-
combined with new therapeutic and investigative tools have going presence of life style factors such as smoking and acid
allowed for major advances in the management of laryngeal promoting dietary habits will also continue to propagate
disease in the past 20 years. Despite this there still remain a laryngeal disease.4 Further advances within laryngology are
number of conditions that pose significant diagnostic and therefore essential to address unmet clinical need and keep
treatment challenges.The burden of laryngeal disease is also pace with the ever evolving laryngeal disease spectrum. In
likely to increase in the future. An ageing population and this chapter we aim to look to the future to describe new
reliance on telecommunication will expand the prevalence treatments and techniques that over the next 25 years are
of voice disorders.2 New techniques in surgery and critical likely to have the biggest impact in furthering the field of
care are allowing for more complex  procedures to take laryngology.

Voice
Most causes of dysphonia can be successfully treated by a transnasal route, which is better tolerated and provides a
conventional therapies, although in a subset of patients more physiological representation of phonation. However,
treatment fails, leading to permanent vocal dysfunction. the image is still two-dimensional, phased with a strobe and
The commonest cause of untreatable dysphonia is a severe does not provide an objective measurement of vocal fold
scarring of the vocal fold mucosa with fibrosis within the movement. The development of stereoscopic imaging has
lamina propria that reduces pliability of the vibratory edge the potential to provide a three-dimensional image of vocal
and, in turn, propagation of the mucosal wave.5 Surgical fold movement. Combining this with advances in high-
intervention in this setting often leads to further scarring speed digital video recording and miniaturised two-point
and subsequent deterioration in vocal function. New laser measuring devices promises to overcome the current
treatments currently under development aim to address shortcomings of conventional stroboscopy by delivering
this through the use of injectable biomaterials that attempt quantitative three-dimensional assessment of vocal fold
to direct extracellular remodelling towards restoration of a movement at over 10,000 frames per second.10–12 This will
normal mucosa while promoting little to no scarring on greatly improve the diagnostic detail of complex phonatory
application. Biomaterials such as chemically modified disorders and allow for a better understanding of the effect
hyaluronic acid gelatin hydrogel have been trialled in of phonosurgery on the larynx.
a number of animal models with improved vocal fold Intraoperative assessment of vocal fold pathology during
biomechanics and reduced scar tissue formation following phonosurgery still largely relies on the use of an operating
injury.6–8 Further modifications, such as the ability of microscope and palpating instruments. This form of
hydrogels to crosslink in  situ and thus better conform assessment lacks objectivity and has inherent limitations
to the anatomical arrangement of the vocal fold, and the in the assessment of complex mucosal disease. Advances in
introduction of cells such as vocal fold fibroblasts to direct technologies such as miniaturised ultrasonographic probes13
extracellular membrane formation, are likely to lead to even and the use of hand-held devices that can measure vocal fold
greater efficacy in the future.9 biomechanical properties intraoperatively14 should allow
The most significant evolution in videoendoscopy in for a more extensive evaluation of disease and  treatment
the past 10 years has been the introduction of the chip on during surgery in the future.
the tip flexible endoscope. This allows for high frame-rate Advancements in voice analysis software15,16 and the use
mucosal wave assessment, including using stroboscopy, via of portable internet linked devices such as OperaVOXTM17

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 New horizons in laryngology

will soon allow patients to routinely perform vocal training pathologist will also be possible remotely, preventing the
exercises with automated feedback within their own home. need for patients to travel long distances to regional centres
Further analysis and feedback from the patient’s speech for speech therapy.

Bilateral vocal fold impairment

Impairment of both laryngeal nerves results in the vocal laryngeal pacing. Pacing delivers a time-phased electronic
folds lying in the paramedian position, which narrows signal that is synced with the respiratory cycle to the
the glottic airway, leading to respiratory distress. Current posterior cricoarytenoid (PCA) muscle to stimulate
management involves glottic expansion in the form of either abduction during inspiration. This technology is not a new
laser arytenoidectomy or cordectomy/cordotomy or a concept, with early examples involving open exposure
suture lateralisation procedure. All of these treatments impair of the PCA muscle and direct implantation of pacing
glottic closure to some degree, leading to reduced power electrodes being trialled in animal studies in the 1980s25 and
and occasionally to aspiration. An improved understanding in a human trial involving seven patients in the 1990s.26
of the pathophysiology behind laryngeal nerve impairment While two of the seven human subjects were shown to
has led to a shift in the way this condition is viewed and exhibit laryngeal reanimation for greater than four years,
provides hope for more effective treatments in the future. the study was not continued following problems with
Electromyographic studies of the larynx indicate that there electrode design and the lack of a sensor to pace abduction
is persistent innervation of both the adbuctor and adductor with inspiration.27 This approach also involved open
muscles following laryngeal nerve injury, but there is insertion of the electrodes, which risked further damage to
discoordination of the neuromuscular action, leading to the recurrent laryngeal nerve and/or fibrosis of the exposed
a laryngeal synkinesis in place of vocal fold movement.18 muscles, further restricting vocal fold motion.28 With
The preservation of innervation to these muscles prevents improved electrode design, an alternative approach has been
atrophy and in doing so, makes it feasible for the muscles to tested in mini-pigs that places electrodes via a minimally
function again given the correct neuromuscular signal. This invasive transcricoid approach into neuromuscular hotspots
has led to attempts to ‘functionally’ reinnervate the abductor within the PCA muscle identified through an atraumatic
muscles, for example with one root of a phrenic nerve by testing needle.29 A number of hurdles exist before this
means of an interposition free nerve graft and the adductor technology can be adopted as routine practice in humans.
muscles with thyrohyoid branches of the hypoglossal nerve.19 A reliable method to overcome the pacing signal during
Following reinnervation in both animal and human studies, phonation and swallowing is needed and evidence that the
abduction can be seen in response to inspiratory effort pacing signal will not initiate neuropathic pain should be
and the maintenance of adductor innervation preserves established.The lack of any sensory feedback to synchronise
adductor muscle bulk.20 In addition, the use of ultrasound21 pacing with inspiration is also problematic and early clinical
or magnetic field22 devices to potentiate neural regeneration trials will likely involve an exercise-related on-demand
could further enhance this technique, as may the use of system in those with dyspnoea during exercise and an
neurotrophic agents, such as growth factors23 and FK506.24 adequate glottic airway at rest.28 Recent developments in
An alternative treatment, which tries to restore materials science and robotics may supplement or supplant
coordinated laryngeal muscle movement, is the use of these technologies in due course.30

Airway
The development of computerised airflow simulators from detailed analysis of airflow in a range of respiratory conditions
the aeronautical and motor industry and advances in three- (Figure 20.1). This will greatly improve understanding of
dimensional CT will hopefully provide new insight into the how different forms of laryngotracheal stenosis, for example,
pattern of airflow within the diseased upper airway.31 This impact on airflow and allow for an objective assessment of
technology has already been used to assess normal airway the effects of mechanical airway disturbance on patients’
physiology32, the delivery of inhaled medication33 and the respiratory function and symptoms. This would allow for
response of treatments for obstructive sleep apnoea34, and in treatments to be personalised to fit a patient’s disease and
the future should be available within hospitals to provide a would provide outcome data following interventions.

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 Airway

Figure 20.1 Computational fluid dynamic analysis of a normal airway. The coloured areas demonstrate spatial differences in airflow velocity
within the subglottis.

The application of the operating microscope and CO2

laser and developments in balloon dilatation devices have
allowed for the majority of airway stenosis patients to be
treated effectively via a transoral endoscopic approach with
a series of day case procedures.35–37 For extensive disease
or in those who do not respond to endoscopic treatment,
laryngotracheal reconstruction or tracheal resection remain
effective. Long segment tracheal stenosis involving greater
than 6 cm of trachea is, however, not amenable to resection
due to a lack of tracheal mobility preventing primary
anastomosis. A subset of patients also develop treatment-
resistant re-stenosis following reconstruction or resection.
This leaves a group that conventional therapies are unable to
address, resulting in severe disability and reliance on either a
tracheostomy or indwelling tracheal stent, which are in turn
associated with considerable co-morbidity. Developments
in tissue engineering technology have provided a potential
Figure 20.2 Decellularised trachea and bronchi seeded with
solution for these cases. In 2008, surgeons and scientists
mesenchymal stromal cells externally and respiratory epithelial
performed the world’s first stem cell-based organ transplant cells on the luminal side.
to replace a segment of stenosed left main bronchus and part
of the carina in a 30-year-old lady who was suffering from
post-tuberculosis stricture.38 A cadaveric donor trachea was complications with granulation of the mucosa, infection,
decellularised to prevent an adverse immune response from retained secretions and malacia, although both are functioning
the recipient and seeded with the patient’s own respiratory well at three and two years, respectively. Formal clinical trials
epithelium on the luminal side and mesenchymal stem cell- of this technology are funded and will demonstrate the true
derived chondrocytes externally (Figure 20.2). Following potential for tissue-engineered airway replacements.
implantation, lung function normalised, the mucosal lining An alternative approach has been to pre-implant
fully regenerated within 1 month and the patient has cadaveric trachea within the forearm of the recipient
remained airway prosthesis free. Later attempts at replacing under immunosuppression.41 Over the course of 6 months
the trachea in a child using a similar technique39 and in an the trachea is revascularised, lined with autologous buccal
adult utilising a synthetic scaffold40 experienced significant mucosa and then implanted to replace the damaged trachea as

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 New horizons in laryngology

part of a radial forearm free flap. Immunosuppression is then

withdrawn once the new trachea has remucosalised. While
the reported outcomes from this approach are promising,
the need for immunosuppression and the requirement of
fortnightly toileting of the implant embedded within the
forearm and anastomotic stenosis may limit the application
of this technique in certain patient groups.
These examples show that it is possible to apply tissue
engineering and transplantation to replace damaged trachea,
although a number of hurdles exist before the technology
can be expanded beyond a handful of end-stage airway
sufferers each year. Research into improved scaffold design is
already under way with the aim of producing an intelligent Figure 20.3 Compressed collagen scaffold embedded with
synthetic scaffold that contains all of the appropriate fluorescent chitosan nanoparticles containing vascular endothelial
extracellular structural cues to promote rapid epithelisation. growth factor (VEGF). Such scaffolds have been shown to promote
The use of synthetic material also avoids the need to source rapid revascularisation of the seeded epithelial layer.
and decellularise a cadaveric trachea and can be custom
designed to conform to the patient’s anatomy. Attempts at
improving vascularisation of the transplant will also yield the patient remains tracheostomy dependent, she has a
improved mucosal integrity following transplantation by restored nasal and oral airway allowing for vocalisation, smell
providing oxygenation to the transplanted cells from the and taste for the first time in 11 years. Following attempted
point of implantation. Such attempts may involve a two- reinnervation of the left donor recurrent laryngeal nerve
stage approach initially, with the first stage being focused to the recipient left phrenic nerve, there is also evidence
on vascularising the graft through pre-implantation. With of limited abduction of the left vocal fold on inspiration.
further developments in tissue engineering technologies, This procedure demonstrates the feasibility of laryngeal
such as three-dimensional bio-printing, it may be possible transplantation in restoring function in severe laryngeal
to arrange cell lines in a pre-determined three-dimensional stenosis, but was only possible as the patient was already
pattern to regenerate dedicated vascular channels that can receiving immunosuppression. An alternative approach
be microanastomosed to the recipient’s circulation.42 would be to use tissue engineering to regenerate a larynx
For laryngeal and tracheal functionality, epithelial cells that did not initiate an immune response, although this
delivered within the grafts need to be fully differentiated provides a range of technical challenges centering on the
with functioning cilia and mucus secreting goblet cells. dynamic nature of the larynx in respiration, phonation and
With advances in our understanding of respiratory swallowing.Advances in neural and muscle engineering may,
epithelial homeostasis43, coupled with new techniques such in the future, allow for the delivery of engineered muscle that
as non-viral gene therapy to promote ciliation44 or the use can be integrated into a synthetic larynx. This could then
of differentiation promoting growth factors embedded in be reinnervated through anastomosis to the patients existing
modified release nanoparticles (Figure 20.3)45, this goal nervous system to restore motor and sensory function.
might be feasible within the next decade. Another alternative approach could be the use of shape
In 2012 the world’s second laryngeal transplant was memory alloys that deform and reform to a specific shape
performed on a 51-year-old female prior kidney transplant in response to an electrical stimulus30 or the use of laryngeal
recipient with complete laryngeal stenosis.46 Even though pacing electrodes to trigger a coordinated muscular response.

Recurrent respiratory papillomatosis

Recurrent respiratory papillomatosis (RRP) affects system responds to human papilloma virus (HPV) infection
approximately 1–4 per 100,000 people in western countries has led to the use of immunotherapy as a new treatment to
and currently has no effective cure.47 Patients typically endure control this virus. Immunotherapy encompasses a range of
regular surgical procedures and chronic dysphonia and in treatments that enhances the immune system against diseases
children there is an estimated 11% chance of requiring a in which the immune system plays an important role.48
tracheostomy and a 3% mortality rate over a 10-year period.47 An example of its use in HPV can be seen in the successful
An increased understanding of how the human immune treatment of HPV-induced high-grade lesions of the vulva

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 Conclusion

using topical imiquimod to stimulate type I interferon from the patient and then conditionally reprogrammed
signalling and infiltration of T1 lymphocytes.49,50 Other using murine fibroblasts and Rho-kinase inhibitor to
examples include the selection of CD14+ monocytes from expand indefinitely in vitro.51 Chemosensitivity testing was
peripheral blood, which are then expanded in vitro to produce then performed on the mass of cultured cells and identified
a population of immature dendritic cells. HPV antigens are vorinostat (Zolinza™) as the most sensitive therapeutic
then added and taken up by the dendritic cells, which in turn agent.This in turn yielded a reduction in papilloma tumour
mature and present HPV-specific antigens through major size with stabilisation of growth at 15 month follow-up.This
histocompatibility molecule surface molecules. These can pioneering work is an example of personalised medicine
then be used to expand a T-cell population targeted against whereby treatments are customised to the individual patient.
RRP.47 It is likely that these strategies, combined with other The development of more accurate lasers, more portable
forms of immunotherapy, will provide an armory of new delivery systems and improved and finer flexible endoscopes
treatments that can be used in conjunction with surgery to with side ports has allowed for the treatment of RRP to
possibly provide a cure against RRP at some point in the move out of the operating room and into the clinic in a
next two decades. number of centres across the world. As these technologies
A ground-breaking case study used a new technique become cheaper and more widely accessible, clinic-based
termed conditional reprogramming to successfully treat a treatment of RRP is likely to become commonplace by
24-year-old patient with RRP extending from the larynx 20205, which will in turn reduce patient risk, inconvenience
to the lung parenchyma. Papilloma specimens were taken and cost by avoiding the need for a general anaesthetic.

Dysphagia
New technology, such as the transnasal oesophagoscope that have already been trialled in animals and two human
and wireless transoesophageal pH probes, make it easier cases.58 These examples, however, lack the neuromuscular
for the laryngologist to make a more complete assessment activity of the native oesophagus and are not suitable
of swallowing disorders within the clinic.52,53 This, as well at present to replace the entire oesophageal length. It is
as new surgical treatments for dysphagia, such as manual hoped that developments in muscle tissue engineering,
control devices for the upper oesophageal sphincter54 and the subsequent control of such muscle, might allow
and transnasal dilatation of the oesophagus under local for future constructs to include a functioning muscular
anaesthesia55, are already expanding the role of the layer. The integration of nickel-titanium shape memory
laryngologist in dysphagia diagnosis and management. alloys might also help to regenerate oesophageal peristalsis,
Further developments in areas such as transcranial direct for example. This alloy was integrated into a Gore-Tex
current stimulation and other similar neuromodulator scaffold in a helical arrangement and implanted to replace
techniques are likely to greatly improve our ability to an oesophageal segment in a goat. On direct stimulation,
successfully treat all forms of dysphagia.56 a contractile wave was found to propagate along the
Long-gap oesophageal atresia, large cancer resections oesophagus thus replicating peristaltic movement.59
and long segment strictures are managed with either Advances in epithelial engineering, scaffold manufacturing
gastric transposition or colonic interposition. These and bioreactor design will also yield larger oesophageal
procedures severely impair quality of life and are associated grafts with a more similar cellular architecture to the
with donor site morbidity.57 The use of tissue engineering native oesophagus. These advances will hopefully allow
to generate a neo-oesophagus has been suggested as a for the introduction of tissue engineered oesophageal
potential alternative, and a recent systematic review on the transplantation at some point in the future.
subject detailed a number of different scaffolds and cells

Conclusion
Recent advances in medical science offer great hope for of managing problematic laryngeal disease in the future.
the future of laryngology. This chapter has highlighted Mahatma Gandhi once stated “the future depends on what
how developments in the fields of regenerative medicine, you do today”60 and in order to ensure these new horizons
digitised medicine, physiology and immunotherapy could are arrived at, a determined effort in continuing research
possibly enhance existing treatments and deliver new ways and development is essential.

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 New horizons in laryngology

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 COSTELLO • SANDHU
Medicine

Practical Laryngology
Practical Laryngology is an invaluable guide to laryngol-
ogy. It covers all the relevant areas in the field, from basic
science to disorders and diseases to in-clinic procedures

PRACTICAL LARYNGOLOGY
and the future of laryngology.

In an easy-to-read format, the book discusses a wide vari-

ety of topics including neurological diseases of the larynx,
swallowing disorders, laryngeal trauma, stenosis, reflux,
acute infections, inflammatory disorders, paediatrics,
benign vocal cord lesions, and dysplastic lesions.

Colour drawings, clinical photographs, and imaging sup-

port the text throughout, making it an excellent reference
to help the clinician find information quickly and easily.
Essential information is presented in a succinct and read-
able style, making it vital for higher trainees preparing for
their final exit examinations and for consultants both in gen-
eral ENT and in the subspecialty of laryngology.

Practical
This book is the ultimate guide for those wanting to learn
more about the larynx, its disorders, therapeutic interven-
tions, and other challenges that may impact patients and
their families.

K17273
Laryngology
ISBN 978-1-4441-8366-5
90000 Edited by
9 781444 183665
Declan Costello • Guri Sandhu