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- Herausgeber: Thieme
- Kategorie: Fachliteratur
- Sprache: Englisch
The long and eagerly awaited third edition of this popular and compact textbook is here.
Often labelled an "exam bible" in its previous editions, Key Topics in Otorhinolaryngology provides a concise yet comprehensive overview that clinical students and trainees alike can use. It will serve as an ideal introduction to ENT and also prove to be a valuable revision aid for ENT examinations.
Conceived and edited by three very knowledgeable and highly respected ENT surgeonsfrom the UK with a wealth of examining experience and an in-depth understanding of the British, European, and International examination formats and contents.
Key Features:
- Contents organised alphabetically in manageable sized chapters, covering individual topics in a systematic style with great clarity.
- Liberally updated to reflect new developments in the field – with 21 new chapters, and inclusive coverage of all sub-specialties in the discipline.
- An ideal introduction to the specialty for medical students, and an accessible source of reference for general practitioners and junior doctors covering ENT.
- It is insightful and succinct, whilst providing sufficient detail to be used as a valuable revision aid for those studying for post-graduate examinations in Otolaryngology and Head & Neck Surgery.
Key Topics in Otolaryngology is certain to become a much-used reference for students, primary healtcare physicians and surgical trainees alike.
This book includes complimentary access to a digital copy on https://medone.thieme.com.
Das E-Book können Sie in Legimi-Apps oder einer beliebigen App lesen, die das folgende Format unterstützen:
Seitenzahl: 1352
Veröffentlichungsjahr: 2019
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Key Topics in Otolaryngology and Head & Neck Surgery
3rd Edition
Nick Roland, MBChB, MD, FRCS (ORL)
Consultant ENT/Head and Neck SurgeonUniversity Hospital AintreeLiverpool, UK;Southport and Ormskirk NHS TrustLancashire, UK
Duncan McRae, MD, FRCS (ORL)
Consultant ENT SurgeonColchester General HospitalColchester, UK
Andrew W. McCombe, MD, FRCS (ORL)
Consultant ENT SurgeonCity HospitalDubai Healthcare City;Adjunct Clinical Professor of SurgeryMohammed Bin Rashid University Medical SchoolDubai, UAE
58 illustrations
ThiemeStuttgart • New York • Delhi • Rio de Janeiro
Library of Congress Cataloging-in-Publication Data
Names: Roland, N. J., author. | McRae, R. D. R. (Robert Duncan Roderick), author. | McCombe, A. W. (Andrew Wightman), author.
Title: Key topics in otolaryngology/Nick Roland, Duncan McRae, Andrew W. McCombe.
Other titles: Key topics in otolaryngology and head and neck surgery
Description: Third edition. | Stuttgart; New York: Thieme, [2019] | Preceded by Key topics in otolaryngology and head and neck surgery/N. J. Roland, R. D. R. McRae, A. W. McCombe. Second edition. 2001. | Includes bibliographical references and index.
Identifiers: LCCN 2018052322 (print) | LCCN 2018053752 (ebook) | ISBN 9783132406872 (ebook) | ISBN 9783132404779 (softcover: alk. paper) | ISBN Subjects: | MESH: Otorhinolaryngologic Diseases | Handbooks
Classification: LCC RF56 (ebook) | LCC RF56 (print) | NLM WV 39 | DDC 617.5/1—dc23
LC record available at https://lccn.loc.gov/2018052322
© 2019 by Georg Thieme Verlag KG
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ISBN 978-3-13-240477-9
Also available as an e-book:
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Important Note: Medicine is an ever-changing science undergoing continual development. Research and clinical experience are continually expanding our knowledge, in particular our knowledge of proper treatment and drug therapy. Insofar as this book mentions any dosage or application, readers may rest assured that the authors, editors, and publishers have made every effort to ensure that such references are in accordance with the state of knowledge at the time of production of the book.
Nevertheless, this does not involve, imply, or express any guarantee or responsibility on the part of the publishers with respect to any dosage instructions and forms of application stated in the book. Every user is requested to examine carefully the manufacturer's leaflets accompanying each drug and to check, if necessary in consultation with a physician or specialist, whether the dosage schedules mentioned therein or the contraindications stated by the manufacturer differ from the statements made in the present book. Such examination is particularly important with drugs that are either rarely used or have been newly released on the market. Every dosage schedule or every form of application used is entirely at the user's risk and responsibility. The authors and publishers request every user to report to the publishers any discrepancies or inaccuracies noticed.
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Contents
Preface
Contributors
1 Adenoids
Nick Roland, Duncan McRae, Andrew W. McCombe
2 Age-Associated Hearing Loss
Nick Roland, Duncan McRae, Andrew W. McCombe
3 Anaesthesia—General
Peter Charters
4 Anaesthesia—Local
Peter Charters
5 Anaesthesia—Sedation
Seema Charters, Peter Charters
6 Audit, Quality Improvement and Clinical Governance
Linnea Cheung
7 Barotrauma
Nick Roland, Duncan McRae, Andrew W. McCombe
8 Caloric Tests
Andrew McCombe, Tony Kay
9 Cervical Lymphadenopathy
Nick Roland, Duncan McRae, Andrew W. McCombe
10 Cholesteatoma
Tristram Lesser
11 Clinical Assessment of Hearing
Nick Roland, Duncan McRae, Andrew W. McCombe
12 Cochlear Implants
Andrew C. Hall, Shakeel R. Saeed
13 Congenital Hearing Disorders
Soumit Dasgupta
14 Consent and Capacity
Kate McCombe
15 Cosmetic Surgery
Alwyn D'Souza, Kevin Kulendra
16 Cough
Andrew J. Kinshuck, Jarrod J. Homer
17 Day Case ENT Surgery
Nick Roland, Duncan McRae, Andrew W. McCombe
18 Drooling
Raymond W. Clarke
19 Epiglottitis
Nick Roland, Duncan McRae, Andrew W. McCombe
20 Epistaxis
Nick Roland, Duncan McRae, Andrew W. McCombe
21 Eponyms in ENT
Christopher Loh, Nick Roland
22 Evidence-Based Medicine
Martin J. Burton
23 Evoked Response Audiometry
Andrew W. McCombe, Tony Kay
24 Examination of the Ear
Nick Roland, Duncan McRae, Andrew W. McCombe
25 Examination of the Head and Neck
Nick Roland, Duncan McRae, Andrew W. McCombe
26 Examination of the Nose
Nick Roland, Duncan McRae, Andrew W. McCombe
27 Examinations in ENT
Andrew C. Swift
28 External Ear Conditions
Nick Roland, Duncan McRae, Andrew W. McCombe
29 Facial Nerve Palsy
Samuel C. Leong
30 Fistula
Nick Roland, Duncan McRae, Andrew W. McCombe
31 Foreign Bodies in ENT
Nick Roland, Duncan McRae, Andrew W. McCombe
32 Functional Endoscopic Sinus Surgery
Nick Roland, Duncan McRae, Andrew W. McCombe
33 Globus Pharyngeus
Jarrod J. Homer
34 Halitosis
Nick Roland, Duncan McRae, Andrew W. McCombe
35 Headache and Facial Pain
Nick Roland, Duncan McRae, Andrew W. McCombe
36 Hearing Aids
Angeles Espeso
37 Hearing Loss—Acquired
Simon Lloyd
38 HIV in Otolaryngology
Nick Roland, Duncan McRae, Andrew W. McCombe
39 Hypopharyngeal Carcinoma
Nick Roland, Duncan McRae, Andrew W. McCombe
40 Imaging in ENT
Rebecca Hanlon
41 Impedance Audiometry
Nick Roland, Duncan McRae, Andrew W. McCombe
42 Labyrinthitis
Nick Roland, Duncan McRae, Andrew W. McCombe
43 Laryngeal Carcinoma
Nick Roland, Duncan McRae, Andrew W. McCombe
44 Laryngectomy
Nick Roland, Duncan McRae, Andrew W. McCombe
45 Lasers in ENT
Mike Dilkes
46 Literature Review and Statistics
Vinidh Paleri
47 Mastoid Surgery
Tristram Lesser
48 Medicolegal Aspects of ENT
Nick Roland, Duncan McRae, Andrew W. McCombe
49 Ménière's Disease
Don McFerran
50 Nasal Reconstruction
Tim Woolford
51 Nasal Trauma
Nick Roland, Duncan McRae, Andrew W. McCombe
52 Nasopharyngeal Tumours
Nick Roland, Duncan McRae, Andrew W. McCombe
53 Neck Dissection
Nick Roland, Duncan McRae, Andrew W. McCombe
54 Neck Swellings
Nick Roland, Duncan McRae, Andrew W. McCombe
55 Neck Space Infection
Paul Pracy
56 Neck Trauma
Johannes Fagan
57 Noise-Induced Hearing Loss
Nick Roland, Duncan McRae, Andrew W. McCombe
58 Non-Healing Nasal Granulomata
Nick Roland, Duncan McRae, Andrew W. McCombe
59 Non-Organic Hearing Loss
Nick Roland, Duncan McRae, Andrew W. McCombe
60 Nutrition in Head and Neck Cancer
Bella Talwar, Rachel Donnelly, Rachel Skelly, Muriel Donaldson
61 Oral Cavity Carcinoma
Nick Roland, Duncan McRae, Andrew W. McCombe
62 Oral Lesions
Richard Shaw
63 Oropharyngeal Carcinoma
Nick Roland, Duncan McRae, Andrew W. McCombe
64 Otalgia
Nick Roland, Duncan McRae, Andrew W. McCombe
65 Otitis Externa
Nick Roland, Duncan McRae, Andrew W. McCombe
66 Otitis Media with Effusion
Nick Roland, Duncan McRae, Andrew W. McCombe
67 Otoacoustic Emissions
Nick Roland, Duncan McRae, Andrew W. McCombe
68 Otorrhoea
Nick Roland, Duncan McRae, Andrew W. McCombe
69 Otosclerosis
Nick Roland, Duncan McRae, Andrew W. McCombe
70 Ototoxicity
Nick Roland, Duncan McRae, Andrew W. McCombe
71 Paediatric Airway Problems
Raymond W. Clarke
72 Paediatric Endoscopy
Raymond W. Clarke
73 Paediatric Genetic Syndromes and Associations
Raymond W. Clarke
74 Paediatric Hearing Assessment
Soumit Dasgupta
75 Paediatric Nasal Obstruction
Raymond W. Clarke
76 Papilloma of the Larynx
Christopher Loh
77 Parathyroid Disease
M. Shahed Quraishi
78 Perilymph and Labyrinthine Fistula
Don McFerran
79 Pharyngeal Pouch
Christopher Loh
80 Pure-Tone Audiometry
Andrew W. McCombe, Tony Kay
81 Radiotherapy and Chemotherapy for Head and Neck Cancer
Christopher Nutting
82 Reconstructive Surgery
Nick Roland, Simon Rogers
83 Rhinitis—Allergic
Nick Roland, Duncan McRae, Andrew W. McCombe
84 Rhinitis—Non-Allergic
Nick Roland, Duncan McRae, Andrew W. McCombe
85 Rhinoplasty
Tim Woolford
86 Rhinosinusitis—Appropriate Terminology
Nick Roland, Duncan McRae, Andrew W. McCombe
87 Rhinosinusitis—Acute
Nick Roland, Duncan McRae, Andrew W. McCombe
88 Rhinosinusitis—Chronic without Nasal Polyps
Nick Roland, Duncan McRae, Andrew W. McCombe
89 Rhinosinusitis-Chronic (with Nasal Polyps)
Nick Roland, Duncan McRae, Andrew W. McCombe
90 Rhinosinusitis—Complications
Nick Roland, Duncan McRae, Andrew W. McCombe
91 Rhinosinusitis—Fungal
Nick Roland, Duncan McRae, Andrew W. McCombe
92 Robots in ENT/Head and Neck Surgery
Vinidh Paleri
93 Salivary Gland Diseases
Nick Roland, Duncan McRae, Andrew W. McCombe
94 Salivary Gland Neoplasms
Nick Roland, Duncan McRae, Andrew W. McCombe
95 Septal Perforation
Nick Roland, Duncan McRae, Andrew W. McCombe
96 Sinonasal Tumours
Andrew C. Swift
97 Skin Cancer—Melanoma
Nick Roland, Duncan McRae, Andrew W. McCombe
98 Skin Cancer—Non-Melanoma
Nick Roland, Duncan McRae, Andrew W. McCombe
99 Smell and Taste Disorders
Nick Roland, Duncan McRae, Andrew W. McCombe
100 Snoring and Sleep-Related Breathing Disorder
Nick Roland, Duncan McRae, Andrew W. McCombe
101 Speech and Swallow Rehabilitation Following Head and Neck Surgery
Camilla Dawson
102 Speech Audiometry
Andrew McCombe, Tony Kay
103 Speech and Language Therapy for Benign Voice Disorders
Julia Selby
104 Stertor and Stridor
Nick Roland, Duncan McRae, Andrew W. McCombe
105 Sudden Hearing Loss
Nick Roland, Duncan McRae, Andrew W. McCombe
106 Suppurative Otitis Media—Acute
Nick Roland, Duncan McRae, Andrew W. McCombe
107 Suppurative Otitis Media—Chronic
James Mitchell
108 Suppurative Otitis Media—Complications
Nick Roland, Duncan McRae, Andrew W. McCombe
109 Temporal Bone Cancer
Jarrod J. Homer
110 Temporal Bone Fractures
Simon Freeman
111 Thyroid Disease—Benign
Ricard Simo
112 Thyroid Disease—Malignant
Ricard Simo
113 Tinnitus
Nick Roland, Duncan McRae, Andrew W. McCombe
114 Tonsil Disease
Nick Roland, Duncan McRae, Andrew W. McCombe
115 Tonsillectomy
Nick Roland, Duncan McRae, Andrew W. McCombe
116 Tracheostomy
Nick Roland, Lesley Dempsey
117 Tympanoplasty
Tristram Lesser
118 Tympanosclerosis
James Mitchell
119 Vertigo
Nick Roland, Duncan McRae, Andrew W. McCombe
120 Vestibular Function Tests
Andrew W. McCombe, Tony Kay
121 Vestibular Schwannoma
Shakeel R. Saeed, Andrew C. Hall
122 Vocal Fold Paralysis
Nick Roland, Declan Costello
123 Voice Disorders
Declan Costello
Index
Preface
Otolaryngology is a rapidly changing discipline that encompasses a broad range of sub-specialties. Many weighty texts exist, which give exhaustive coverage of the subject, but they risk hiding the wood from the trees. Common problems occur commonly, and this is as true for post-graduate examinations as it is for clinical practice. Certain ‘key’ topics tend to present themselves far more frequently than others. The aim of this book has always been to give a succinct overview of the key topics in otolaryngology and head and neck surgery in a comprehensible, easy-to-read style. This is the third edition of this very successful format and aims to refresh and update on previous editions.
Basic information is contained in some topics (e.g. examination of the ear, nose and throat), and a symptom-orientated approach is used in others (e.g. epistaxis, foreign bodies, otalgia, otorrhoea). The breadth and simple style should make the book an ideal introduction to the specialty for medical students, and an accessible source of reference for general practitioners and junior doctors cross-covering ENT Surgery.
The text is up-to-date and provides sufficient detail to be used as a valuable revision aid for those studying for post-graduate examinations in otolaryngology and head and neck surgery. Scrutiny of past papers and discussion with candidates reveal that there are certain key areas which tend to be repeated. We have endeavoured to cover these areas using a common framework for each topic. It is hoped that this will engender an approach which will be of use to the candidate considering questions that are not discussed in this book.
A text of this size cannot pretend to be all-inclusive and this one does not set out to be so. Anatomy is only described in the context of a particular clinical topic and the principles of surgical techniques are covered only when deemed appropriate. Clarity and brevity have been our aim. We suggest the book be used early in the revision process before turning to more major texts. The reader is encouraged to refer to the articles and texts which are recommended for further reading at the end of each topic. We are confident, following feedback from past readers and candidates, that Key Topics in Otolaryngology will be of particular value in those overwhelming days just before examination, for which we wish you every success!
Nick Roland, MBChB, MD, FRCS (ORL)Duncan McRae, MD, FRCS (ORL)Andrew W. McCombe, MD, FRCS (ORL)
Contributors
Martin J. Burton, MA, DM, FRCS
Professor of OtolaryngologyNuffield Department of SurgeryUniversity of OxfordOxford, UK
Peter Charters, FRCA
Consultant AnaesthetistDepartment of AnaesthesiaUniversity Hospital AintreeLiverpool, UK
Seema Charters, FRCA
Consultant AnaesthetistWarrington and Halton Hospitals NHS TrustWarrington, UK
Linnea Cheung, MBChB, MRCS-DOHNS
ENT Specialty RegistrarDepartment of ENTGloucestershire Royal Hospitals NHS TrustGloucester, UK
Raymond W. Clarke, DCH, FRCS (ORL)
Consultant Paediatric OtolaryngologistRoyal Liverpool Children's HospitalLiverpool, UK
Declan Costello, MA, MBBS, FRCS (ORL-HNS)
Consultant Ear, Nose and Throat Surgeon(Voice Disorders)ENT DepartmentWexham Park HospitalSlough, UK
Soumit Dasgupta, MS, FRCS
Consultant Audiovestibular Physician/Neurotologist and Clinical LeadDepartment of Paediatric AudiologyAlder Hey Children's NHS Foundation TrustLiverpool, UK;Honorary LecturerManchester Centre for Audiology and DeafnessUniversity of ManchesterManchester, UK
Camilla Dawson, DClinP
Clinical Lead Speech and Language TherapistTherapy ServicesUniversity Hospitals Birmingham NHSFoundation TrustBirmingham, UK
Lesley Dempsey
Clinical Nurse Specialist in Head andNeck CancerUniversity Hospital AintreeLiverpool, UK
Mike Dilkes, MS, FRCS (ORL-HNS)
Consultant ENT SurgeonHealthHubLondon, UK
Muriel Donaldson, MSc, RD
Head and Neck Clinical Specialist DietitianDepartment of Dietetics and NutritionQMC Campus NottinghamUniversity Hospitals NHS TrustNottingham, UK
Rachel Donnelly, MSc
Head of Nutrition and DieteticsDepartment of Nutrition and DieteticsGuy's and St Thomas’ NHS Foundation TrustLondon, UK
Alwyn D'Souza, FRCS
Consultant ENT/Facial Plastic SurgeonDepartment of ENTUniversity Hospital LewishamLondon, UK
Angeles Espeso, FRCS (ORL-HNS), DONHS, MRCS GLAS, AFRCSI
Otology and Paediatric ENTConsultant SurgeonDepartment of ENTEast Suffolk and North Essex NHS FoundationTrust (ESNEFT)Essex, UK
Johannes Fagan, MBChB, MMed, FCS (ORL)
ChairmanDivision of OtolaryngologyUniversity of Cape TownCape Town, South Africa
Simon Freeman, MBChB, MPhil, FRCS (ORL-HNS)
Consultant Otolaryngologist andSkull Base SurgeonDepartment of OtolaryngologySalford Royal NHS Foundation TrustSalford, UK
Andrew C. Hall, MD
Specialist RegistrarDepartment of Otology and Auditory ImplantationRoyal National Throat, Nose and Ear HospitalLondon, UK
Rebecca Hanlon, FRCR
Consultant RadiologistDepartment of RadiologyUniversity Hospital AintreeLiverpool, UK
Jarrod J. Homer, MD, FRCS
Professor of Otolaryngology-Head and NeckSurgery and Consultant SurgeonDepartment of Otolaryngology-Head andNeck SurgeryManchester Head and Neck CentreManchester University NHS Foundation TrustManchester, UK
Tony Kay, registered with RCCP, MSHAA
AudiologistHead of Audiology ServicesAudiology DepartmentAintree University Hospital NHS Foundation TrustLiverpool, UK
Andrew J. Kinschuk, MBChB, DOHNS, FRCS (ORL-HNS)
Consultant of OtorhinolaryngologyDepartment of Otolaryngology and Head andNeck SurgeryUniversity Hospital AintreeLiverpool, UK
Kevin Kulendra, DOHNS, FRCS (ORL-HNS)
Consultant ENT SurgeonENT DepartmentChelsea and Westminster Hospital NHSFoundation TrustWest Middlesex University HospitalLondon, UK
Samuel C. Leong, MPhil, FRCSEd (ORL-HNS)
Rhinologist and Anterior Skull Base SurgeonDepartment of Otorhinolaryngology-Head andNeck SurgeryAintree University Hospital NHS Foundation TrustLiverpool, UK
Tristram Lesser, FRCSEd, FHKCORL, MS (Lon)
Consultant ENT SurgeonORL-HNS Ltd.Renacres Hospital NHS Treatment CentreLancashire, UK
Simon Lloyd, MPhil (Cantab), FRCS (ORL-HNS)
Professor of OtolaryngologyManchester Royal Infirmary andSalford Royal HospitalManchester, UK
Christopher Loh, FRCS (ORL-HNS)
Consultant ENT SurgeonDepartment of OtolaryngologyAintree University Hospital NHS Foundation TrustLiverpool, UK
Kate McCombe, MRCP, FRCA, MA
Consultant AnaesthetistMediclinic City Hospital;Adjunct Assistant ProfessorMohammed Bin Rashid University of Medicineand Healthcare SciencesDubai, UAE
Andrew W. McCombe, MD, FRCS (ORL)
Consultant ENT SurgeonCity HospitalDubai Healthcare City;Adjunct Clinical Professor of SurgeryMohammed Bin Rashid University Medical SchoolDubai, UAE
Don McFerran, MA, FRCS
Consultant ENT SurgeonENT DepartmentEast Suffolk and North Essex NHSFoundation TrustColchester, UK
Duncan McRae, MD, FRCS (ORL)
Consultant ENT SurgeonColchester General HospitalColchester, UK
James Mitchell, FRCS (ORL-HNS)
Consultant ENT SurgeonENT DepartmentFrimley Park HospitalSurrey, UK
Christopher Nutting, MD, PhD, FRCP, FRCR
Professor of Clinical OncologyHead and Neck UnitRoyal Marsden HospitalLondon, UK
Vinidh Paleri, MS, FRCS (ORL-HNS)
ConsultantHead and Neck and Thyroid SurgeonThe Royal Marsden HospitalLondon, UK
Paul Pracy, MBBS, FRCS (ORL-HNS)
ConsultantDepartment of Otolaryngology, Head and NeckSurgeryUniversity Hospital BirminghamBirmingham, UK
M. Shahed Quraishi, OBE, FRCS
Consultant ENT SurgeonDepartment of Head and Neck SurgeryDoncaster Royal InfirmaryDoncaster, UK
Simon Rogers, MD
Consultant Maxillofacial SurgeonUniversity Hospital AintreeLiverpool, UK;ProfessorEdge Hilll UniversityOrmskirk, UK
Nick Roland, MBChB, MD, FRCS (ORL)
Consultant ENT/Head and Neck SurgeonUniversity Hospital AintreeLiverpool, UK;Southport and Ormskirk NHS TrustLancashire, UK
Shakeel R. Saeed, MD, FRCS (ORL)
Professor of Otology/Neuro-otologyUniversity College London Ear InstituteLondon, UK
Julia Selby, PhD
Consultant Speech and Language TherapistVoice, ENT and Respiratory ServicesThe Royal BromptonHospitalLondon, UK
Richard Shaw, MD, FDS, FRCS (OMFS)
ProfessorDepartment of Molecular and ClinicalCancer MedicineUniversity of Liverpool Cancer Research CentreLiverpool, UK
Ricard Simo, FRCS (ORL-HNS), PhD
Consultant Otorhinolaryngologist Head,Neck and Thyroid SurgeonHonorary Senior Lecturer KCLDepartment of Otorhinolaryngology,Head and Neck SurgeryGuy's and St Thomas’ Hospital NHSFoundation TrustLondon, UK
Rachel Skelly, BSc (Hons)
Advanced Head and Neck Oncology DietitianDepartment of Nutrition and DieteticsUniversity Hospital AintreeLiverpool, UK
Andrew C. Swift, ChM, MB, ChB, FRCS, FRCSEd
Consultant Rhinologist and ENT SurgeonHonorary Consultant,Alder Hey Children's Hospital and theWalton Centre for NeurosciencesDepartment of Otorhinolaryngology,Head and Neck and Thyroid SurgeryUniversity Hospital AintreeLiverpool, UK
Bella Talwar, RD, DADP
Clinical Lead DietitianHead and Neck CentreUniversity College London Hospital NHSFoundation TrustLondon, UK
Tim Woolford, MD, FRCS (ORL-HNS)
Consultant Ear, Nose and Throat SurgeonDepartment of Otolaryngology, Head andNeck SurgeryManchester Royal InfirmaryManchester, UK;Honorary Clinical ProfessorEdge Hill UniversityOrmskirk, UK
1 Adenoids
The adenoids are a mass of lymphoid tissue found at the junction of the roof and posterior wall of the nasopharynx. They are a normal structure and part of Waldeyer's ring which includes the palatine and lingual tonsils. Their function includes the production of antibodies and activated white blood cells in response to perceived infectious or other inflammatory threats. The size of the adenoids varies, but in general, they attain their maximum size between the ages of 2 and 7 years, as part of the widespread process of lymphoid hyperplasia that occurs in this age group, and then usually regress in size to become almost negligible by the age of 13 years.
1.1 Pathology
Inflammation, most commonly due to acute viral and bacterial infections, and also allergy and other inflammatory conditions, results in hyperplasia with enlargement and multiplication of the lymphoid follicles. Most of the pathological effects attributed to the adenoids are due to this increase in size. The symptoms caused by hypertrophy result from the obstruction of the nasopharynx and eustachian tube orifices. Persistent bacterial colonisation and biofilms are also contributory factors.
1.2 Clinical Features
1.Nasal obstruction leads to mouth breathing, snoring and hyponasal speech. Infants may have difficulty in feeding because they must stop sucking intermittently to take a breath. Nasal discharge, often mucopurulent, and post-nasal drip may develop because of secondary chronic rhinitis and sinusitis. Besides snoring, some children may suffer from episodes of sleep apnoea. The child with the characteristic adenoid facies appearance (an open lip posture, prominent upper incisors, a short upper lip, a thin nose, and a hypoplastic maxilla with a high-arched palate) is rarely seen nowadays because parents and GPs are better informed about the management of obstructive symptoms.
2.Eustachian tube obstruction may result in otalgia and deafness due to recurrent bouts of acute otitis media and otitis media with effusion (glue ear).
When there is mild-to-moderate obstruction, the clinical features of adenoid hypertrophy are not always clear-cut. Adenoidal hyperplasia may be incorrectly diagnosed when allergy and rhinitis may be the cause. In most children, examination of the nasopharynx with a paediatric nasopharyngoscope will identify large adenoids.
1.3 Investigations
A rarely required investigation is a lateral soft tissue radiograph. This will give a measure of the absolute size of the adenoids and an assessment of their proportion in relation to the size of the airway.
The most reliable means of assessing the size of the adenoids is examination under general anaesthetic at the time of the surgical procedure. If enlarged adenoids are identified then, with appropriate consent, they can be removed.
1.4 Indications for Adenoidectomy
Adenoidectomy is only indicated if troublesome symptoms can be attributed to abnormal adenoid hypertrophy. The indications for adenoidectomy are as follows:
• Nasal obstruction—especially if associated with significant and persistent mucopurulent rhinorrhoea, suggesting chronic nasal cavity infection.
• Otitis media with effusion (glue ear).
• Recurrent acute otitis media.
• Sleep apnoea—often an adenoidectomy is performed in association with a tonsillectomy. Traditionally, the procedure has been performed by curettage, but suction diathermy and coblation are popular alternative techniques.
1.5 Contraindications for Adenoidectomy
• Recent upper or lower respiratory tract infection.
• An uncontrolled bleeding disorder.
• Cleft palate—either overt or sub-mucosal. The adenoids assist in closure of the nasopharynx from the oropharynx during speech and deglutition, and velopharyngeal insufficiency is a rare complication. They should never be removed in a child who has had a cleft palate repair or a congenitally short palate. All children who have a bifid uvula should have a sub-mucous cleft excluded before proceeding with an adenoidectomy.
1.6 Complications
1. Immediate:
• Anaesthetic complications.
• Soft palate damage.
• Persistent haemorrhage.
• Sub-luxation of the atlanto-axial joint, or other damage to the cervical spine.
2. Intermediate:
• Secondary haemorrhage.
• Sub-luxation of the atlanto-occipital joint (secondary to infection).
3. Late:
• Eustachian tube stenosis.
• Nasal escape and regurgitation and hyper-nasal speech (rhinolalia aperta). Hypernasal speech can be a troublesome complication in some children. It often improves with time and speech therapy but may be sufficiently severe to require a pharyngoplasty to correct the problem. It is less likely to occur if children with palatal abnormalities are excluded from operation. Some surgeons advocate removal of the upper part of the adenoid mass leaving a lower ridge of adenoid tissue against which the defective palate may continue to make contact.
• Persistence of symptoms.
1.7 Haemorrhage
The most serious complication is reactionary haemorrhage. This is treated in the same manner as post-tonsillectomy haemorrhage. The child should be returned to theatre and an attempt made to localise and diathermy the bleeding point with suction diathermy. A post-nasal pack is rarely required because the adenoid bed and any bleeding points can usually be fully visualised either endoscopically, or with palatal retraction and a mirror.
1.8 Signs of Hypovolaemic Shock in Children
Children compensate for a reduction in their circulating blood volume (normally 80–85 mL/kg) with an increase in systemic vascular resistance and heart rate. Their ability to compensate is remarkable, meaning that they can lose up to 30% of their blood volume before becoming hypotensive. Consequently, children decompensate late and rapidly and the clinician must be vigilant for signs of shock to avert a critical situation.
Observe child for the following:
• Tachycardia (age adjusted): Although there may be many confounding causes for a rise in heart rate, for example pain, agitation, fever, etc.
• Tachypnoea (age adjusted): This is a useful and sensitive sign.
• Agitation.
• Signs of impaired organ perfusion: Reduced urine output (usually 0.5–1 mL/kg/h); decreased level of consciousness; delayed perfusion—reduced capillary refill time (> 2 seconds), weak pulses and cool peripheries.
• Hypotension (age adjusted): This is a late sign in children.
1.9 Immediate Management
Confirm the diagnosis of hypovolaemic shock secondary to haemorrhage.
Initial management should follow the ‘ABC’ approach:
• Call for help!
•A Assess airway—ensure airway is patent. If conscious level is decreased, place the child in the recovery position, slightly head down to decrease the risk of aspiration.
•B Assess breathing and apply 100% oxygen—respiratory rate, air entry and oxygen saturations. Alert the anaesthetic team in the face of airway compromise and if a return to theatre is anticipated.
•C Assess circulation. Gain intravenous (IV) access and take blood for full blood count (FBC), group and save for cross-matching (depending on severity).
1.10 Start Fluid Resuscitation
• A 20 mL/kg bolus of Hartmann's solution—assess physiological response.
• Repeat 20 mL/kg bolus of Hartmann's solution if no response/partial response/initial response followed by deterioration.
• Children who require further fluid resuscitation after these two boluses will require blood as the next resuscitation fluid at an initial dose of 10 mL/kg.
• Institute measures to arrest the bleeding (return to theatre, etc.).
1.11 Follow-Up and Aftercare
In view of the problems with accurate diagnosis, and the potential long-term complications, it is reasonable to review an adenoidectomy child in the outpatient clinic post-operatively.
Further Reading
Lock C, Wilson J, Steen N, et al. North of England and Scotland Study of Tonsillectomy and Adeno-tonsillectomy in Children (NESSTAC): a pragmatic randomised controlled trial with a parallel non-randomised preference study. Health Technol Assess. 2010; 14(13):1–164, iii–iv
MRC Multicentre Otitis Media Study Group. Adjuvant adenoidectomy in persistent bilateral otitis media with effusion: hearing and revision surgery outcomes through 2 years in the TARGET randomised trial. Clin Otolaryngol. 2012; 37(2):107–116
Robb P. The adenoids and adenoidectomy Chapter 26, Volume 2. Scott Browns Otolaryngology, Head and Neck Surgery. 8th edition. CRC Press, 2018
Related Topics of Interest
Suppurative otitis media—acute
Otitis media with effusion
Snoring and sleep-related breathing disorder
Tonsillectomy
Tonsil disease
2 Age-Associated Hearing Loss
As with all sensory systems in the human body, there is a progressive degeneration in the auditory system with ageing. Presbyacusis is the term that describes the deterioration of hearing that characterises old age, now replaced by the term ‘age-associated hearing loss’ (AAHL). It may be defined as a progressive bilateral sensorineural hearing loss of mid-to-late adult life, where all other causes have been excluded. Indeed, the definition of AAHL is somewhat arbitrary; there is no agreed age above which an individual suffers from age-related hearing loss and below which one does not. Almost invariably, databases displaying age-related, average hearing thresholds for either screened or unscreened populations show a marked increase in the rate of progression of the hearing loss once into the sixth decade. It is, therefore, reasonable to attribute high-tone hearing loss in an individual over the age of 50 to age-related changes (in the absence of any alternative explanation).
2.1 Pathophysiology
Both the sensory peripheral (cochlea) and central (neural) components of the auditory system are affected and the deterioration appears to become more rapid with increasing age. Peripheral degeneration is reported to be responsible for at least two-thirds of the clinical features of presbyacusis. A variety of possible mechanisms exist. Cellular degeneration gives rise to a reduction in the numbers of inner and outer hair cells, particularly at the basal end of the cochlea. This can lead to secondary neural degeneration in the spiral ganglion. Circulatory changes such as arteriosclerosis, atrophy of the stria vascularis and microangiopathy can lead to metabolic upset and further cell death. This leads to an elevation of hearing thresholds and a loss of frequency selectivity. Degeneration in the central pathways leads to a reduction in performance in terms of signal processing. The net result in most instances will be a combined sensorineural, rather than an isolated sensory or neural impairment.
2.2 Clinical Features
Moderate hearing impairment (45-dB hearing level averaged over 0.5, 1, 2 and 4 kHz) occurs in 4% of the 51 to 60 age group, and in 18% of those aged 71 to 80. Men and women are both affected, although men tend to have a slightly worse loss for the same age group.
Initially, patients will complain of difficulty in hearing, particularly in the presence of background noise, so that they find conversations difficult to follow. As the hearing loss progresses, they will become aware of not hearing words and sounds. Recruitment is a frequent problem and adds to the distortion. In addition, the problems and consequences of AAHL are compounded in the elderly because of additional degenerative processes in the central nervous system. This can result in a relative loss in neuronal plasticity, a loss of cognitive abilities and other sensory modalities, particularly sight.
Decreasing hearing acuity also correlates with an increased incidence of falls, depression and dementia in the elderly. The feelings of imprisonment and anxiety that result from the consequent social isolation lead to reduced higher cognitive functioning and psychological well-being, which can in turn increase the economic and societal burden of AAHL. Therefore, it is important, as the life expectancy of our population increases, to make the diagnosis and offer treatment early.
In the absence of any other otological pathology, clinical examination is normal.
2.3 Investigations
In the presence of an appropriate history and a symmetrical sensorineural hearing loss on pure-tone audiometry, little further investigation is required. Hearing loss in a young patient, asymmetry on a pure-tone audiogram, unilateral tinnitus or a conductive component to the audiogram may require further investigation.
MRI scanning may be necessary to exclude a cerebellopontine angle tumour, such as a vestibular schwannoma, in any patient thought to be at risk (as suggested by significant asymmetry or persistent unilateral tinnitus). Most departments will have their own guidelines.
The National Institute for Clinical Excellence (NICE) state that an MRI of the internal auditory meati should be considered for adults with sensorineural hearing loss and no localising signs if there is an asymmetry on pure tone audiometry of 15 dB or more at any 2 adjacent test frequencies, using test frequencies of 0.5, 1, 2, 4 and 8 kHz.
Although several different audiological patterns of hearing loss have been described, depending on the pre-dominant histological changes, a sloping high-frequency loss is the commonest pattern found.
2.4 Management
As there is no curative treatment for deafness associated with ageing, the main aims in management are to assess the degree of disability, to provide a hearing aid and to rehabilitate the patient. There is now some evidence that reducing the accumulation of free radicals within the cochlea may reduce the rate of hearing decline. Antioxidants may therefore have a significant role to play in reducing progression of presbyacusis in the future. These include vitamins A, C and E and also magnesium and zinc.
2.4.1 Hearing Aids
Although about 75% of hearing aid users are over the age of 60, only 18% of the elderly with hearing loss have used hearing aids. There are several reasons for this, including denial of hearing impairment, vanity, acoustic feedback, recruitment and difficulty with manipulating the aid. Many elderly patients live alone and therefore do not see the need to wear a hearing aid unless they are socialising or out shopping. They therefore do not get used to the nuances of the aid, which are initially seen as a nuisance, and in turn they become less likely to wear it in situations where they would benefit from using one. In those with neural presbyacusis, poor speech discrimination may limit the benefit of amplification, as may the performance of the aid itself. Some patients have minimal handicap from their hearing difficulty despite a significant loss and therefore do not present themselves to medical services. Binaural aiding has been shown to produce an additional 10-dB signal-to-noise-ratio advantage, and so is recommended. The evidence suggests that digital aids are preferable to analogue. Loop systems offer an additional benefit to hearing aid users and are available in many public places such as churches, concert halls and lecture theatres. Amplified sounds are transmitted by a fitted induction loop and are picked up by the patient's aid when switched to the appropriate receiving position. Obtaining a hearing aid has become straightforward for patients since the introduction of direct referral from general practice to the chosen local hearing aid provider.
2.4.2 Accessory Aids
Practical measures for individuals with a more severe hearing loss include infrared headphones for use with their television, volume-controlled telephones, louder doorbells, often with an alternative alerting system such as a flashing light or vibrating pager system. Hearing dogs can take on such a role as well as providing a valuable source of companionship in the elderly.
2.4.3 Rehabilitation
Some patients may be helped by rehabilitation in the form of lip reading classes or auditory training. The role of rehabilitation and its benefits for the average hearing-impaired individual are not proven. The presence of comorbidities that affect cognition (e.g. dementia) can significantly impact on an individual's ability and readiness to adapt to the use of hearing aids. In these situations, co-operation is required from caregivers and family members to support ear and hearing aid hygiene and assist with insertion of hearing aids. Early provision of hearing aids is likely to shorten the time required for the individual to gain tolerance of aided speech and grasp the benefits of hearing aid technology. This may also reduce the development of the psychosocial comorbidities that can occur with hearing loss. And finally, whether cause or effect, there is a lower prevalence of depression and dementia symptoms in hearing aid users when compared with a similar elderly group of non-users.
2.5 Follow-Up and Aftercare
There is very good evidence of the importance of follow-up and rehabilitative support after fitting to ensure maximum benefit and hearing aid use. In the longer term, access is required for repairs and replacements, which may be dictated by further hearing deterioration with the passage of time. Routine ENT clinical follow-up is not required.
Further Reading
Alvarado JC, Fuentes-Santamaría V, Melgar-Rojas P, et al. Synergistic effects of free radical scavengers and cochlear vasodilators: a new otoprotective strategy for age-related hearing loss. Front Aging Neurosci. 2015; 7:86
Baguley DM, Reid E, McCombe AW. Age related sensorineural hearing impairment. In: Gleeson M, ed. Scott-Brown's Otolaryngology, Head and Neck Surgery. 8th ed. London: Hodder Arnold; 2008;3:3539–3547
Ferguson MA, Kitterick PT, Chong LY, Edmondson-Jones M, Barker F, Hoare DJ. Hearing aids for mild to moderate hearing loss in adults. Cochrane Database Syst Rev. 2017; 9:CD012023
NICE guidance for the management of adult hearing loss. https://www.nice.org.uk/guidance/ng98/resources/hearing-loss-in-adults-assessment-and-management-pdf-1837761878725; June 2018. Accessed December 11, 2018
Related Topics of Interest
Evoked response audiometry
Hearing aids
Noise-induced hearing loss
Pure-tone audiometry
3 Anaesthesia—General
General anaesthesia (GA) for ear, nose and throat (ENT) surgery accounts for about 5% of anaesthetic practice in the United Kingdom. While many of the operations are straightforward from the anaesthetist's point of view, others may present significant challenges. The nature of the pathology found in ENT patients may make airway management and intubation difficult. In many cases, specific consideration will be needed as to how best to provide optimal surgical conditions and access to the ‘shared airway’, while maintaining safe and effective anaesthetic conditions. This requires communication and cooperation between the surgeon and the anaesthetist so that each understands the concerns, aims and objectives of the other and a mutually acceptable plan of action can be agreed.
3.1 Techniques for General Anaesthesia
General anaesthesia can be classified according to whether ventilation is spontaneous or controlled.
•Spontaneous ventilation: The patient is permitted to continue breathing spontaneously throughout the operation. This technique is commonly employed when there is no need to intubate the patient to facilitate surgery, for example during grommet insertion, removal of simple skin lesions under GA and other simple surgery. The patient is rendered unconscious before a laryngeal mask airway is inserted to maintain airway patency.
•Controlled ventilation: Positive pressure ventilation is applied to the airway to oxygenate the patient. Controlled ventilation is commonly used following tracheal intubation which, in adults, usually follows the administration of a neuromuscular blocking drug, which relaxes the muscles and renders the patient paralysed. Tracheal intubation (either oral or nasal) is chosen to manage the airway for a host of different reasons depending on the situation, for example a cuffed tracheal tube provides protection against airway soiling; it provides a more ‘secure airway’ which is less susceptible to being dislodged or moved during surgery; it allows for more reliable delivery of positive pressure ventilation with negligible leakage of anaesthetic gases.
Induction, maintenance and emergence describe the inevitable sequence of all general anaesthetics.
3.2 Induction of Anaesthesia
Propofol is the drug most commonly used to induce anaesthesia. It is presented as a white lipid emulsion for intravenous administration and its effects are dose dependent; at low plasma concentrations, it causes sedation, which becomes deeper with increasing plasma concentrations until consciousness is lost entirely.
Induction of anaesthesia may be achieved using other hypnotic agents, which might be chosen in place of propofol because of a specific desirable characteristic. For example, ketamine may be useful in the hypotensive patient.
‘Gas induction’ of anaesthesia is done when a patient inhales a mixture of oxygen/air or oxygen/nitrous oxide and sevoflurane which is a volatile anaesthetic agent (see later). Gas induction is most commonly, although not exclusively, used in children who are resistant to having an intravenous cannula sited.
3.3 Neuromuscular Blocking Drugs
If tracheal intubation is required, it is commonplace to give a neuromuscular blocking drug (NMBD) (muscle relaxant) to cause abduction of the vocal cords and allow placement of the endotracheal tube (ETT). Various drugs are available for this purpose and the anaesthetist chooses according to the desirable properties and side effects of each drug, patient factors and the clinical situation. Table 3.1 lists a few examples.
The effects of a full intubating dose of atracurium, rocuronium or vecuronium last for approximately 30 minutes. It is generally not possible to reverse profound neuromuscular blockade by administering neostigmine, the anti-cholinesterase which is traditionally used as a ‘reversal’ agent. Instead, sufficient time must pass to allow the concentration of the NMBD to fall at the neuromuscular junction. Once a sufficient number of receptors are left unoccupied by the NMBD, it is possible to reverse its effects by giving neostigmine. Neostigmine increases the availability of acetylcholine at the neuromuscular junction. The acetylcholine can then bind to the available receptors at the junction and facilitate muscle contraction once again. There are ways around this; for example, the anaesthetist might choose to give a smaller dose of muscle relaxant to begin with. Sugammadex binds to and inactivates rocuronium and vecuronium molecules to reverse their effects. It is, however, expensive enough for many departments to restrict its use.
3.4 Maintenance of Anaesthesia
Anaesthesia is most commonly maintained using inhalational anaesthesia. Volatile anaesthetic vapours are stored in ‘vaporisers’ which are attached to the anaesthetic machine. Oxygen + air, or oxygen + nitrous oxide, flow through the vaporising chamber where they are mixed with the volatile agent. The mixture is subsequently delivered to the patient via the anaesthetic breathing system. The anaesthetist controls the amount of volatile agent delivered to the patient as a percentage of the total volume of gas delivered, and the depth of anaesthesia increases in a dose-dependent fashion. Commonly used volatile agents are listed below. Again, each might be chosen because of the specific advantages it has to offer:
•Sevoflurane (yellow vaporiser): Faster onset and offset of action than isoflurane, not irritant to the airways and so can be used for gas induction.
•Isoflurazne (purple vaporiser): Slower onset and offset than sevoflurane, irritates the airways and so less suitable for gas induction. Cheaper than sevoflurane.
•Desflurane (blue vaporiser): Very fast onset and offset of action, irritant to the airways and so unsuitable for gas induction, useful when rapid emergence is desirable, for example in morbidly obese patients and those with sleep apnoea.
Anaesthesia can also be maintained using total intravenous anaesthesia (TIVA). This usually consists of a continuous infusion of propofol and remifentanil (a very short-acting analgesic drug). Each agent is delivered by an infusion pump and controlled by pharmacological drug algorithms based on the individual patient demographics. This would be used in cases such as those at risk of malignant hyperthermia from inhalational anaesthesia.
3.5 Emergence
To reverse the patient at the end of surgery, the anaesthetist needs to discontinue any inhalational agents, reverse any residual neuromuscular block, and most importantly, provide timely and adequate analgesia appropriate to the surgical situation. It is obviously important not to be giving ‘top-up’ doses of NMBDs just prior to reversal and communication with the surgeon is needed to prevent this. Care of the airway at reversal is important and referred to in the next section.
3.6 Special Anaesthetic Considerations
3.6.1 Airway Assessment
Airway assessment forms part of the standard anaesthetic pre-operative assessment. Anaesthetic teaching relies on simple ‘bedside tests’ (e.g. the Mallampati score, range of movement of neck flexion/extension, mouth opening, etc.). However, their predictive accuracy is poor. If a patient has had surgery before, his or her previous anaesthetic notes can provide invaluable information about any difficulties encountered and how these were resolved.
3.6.2 Anticipated Difficult Intubation
Securing the airway in patients for certain types of ENT surgery might prove especially challenging, for example those with tumours obstructing/encroaching on the airway, following surgery or radiotherapy to the head and neck which has caused deformity/restricted neck movement or mouth opening, abscesses restricting mouth opening, inhaled foreign bodies or conditions causing airway soiling such as posttonsillectomy bleeding. When managing these high-risk patients, clear communication between the surgeon and the anaesthetist is vital. Information should be sought and shared, for example radiological imaging, nasendoscopy findings, clinical drawings or photo graphs of the airway/tumour morphology, and a clear, stepwise management plan agreed upon and communicated to the whole theatre team. More recent emphasis has been placed on the objective of decreasing the risk of hypoxia during difficult intubations either by continuous oxygen delivery by nasal catheters during laryngoscopy or the application of high-flow ventilatory exchange systems (‘Thrive’). The final common pathway of any airway plan might be emergency surgical airway creation, and so the anaesthetist may request that the ENT surgeon be present in theatre, scrubbed and ready to perform an emergency tracheostomy should attempts at oral/nasal intubation fail. In a small number of cases, it may be decided that it is safest to secure the airway by performing an elective awake surgical tracheostomy.
3.7 Hypotensive Anaesthesia
In the past, it was fashionable to induce severe hypotension during anaesthesia to improve the surgical field by rendering it bloodless. This has fallen out of favour, however, because of the risk of critically reducing cerebral perfusion resulting in permanent brain injury. When it is considered necessary, however, there may be an agreement to induce modest hypotension, targeting a mean blood pressure appropriate for each individual patient. This can usually be achieved by controlling depth of anaesthesia, remifentanil infusion, postural adjustments (i.e. slight head-up tilt), adjusting ventilatory parameters, appropriate use of NMBDs, use of specific hypotensive agents, for example β-blockers, etc.
3.8 Recovery from Anaesthesia
The Royal College of Anaesthetists National Audit Project 4 conclusively demonstrated that planning for emergence and extubation was often poor and anaesthetists frequently failed to give due consideration to this perilous time. As a result, airway problems were often more serious in the postoperative period than at induction of anaesthesia.
A strategy for emergence and extubation should be made for every patient. If there is concern that this might be a particularly high-risk time for the patient, then a plan should be made and discussed with the whole team ahead of time, in the same way as for anticipated difficult intubation. Reverting to normal breathing with pharyngolaryngeal competency is not necessarily straightforward either when recovery is slow or incomplete (i.e. anaesthetic factors) or when the surgery has interfered with normal airway function. The anaesthetist may choose to lengthen the time to wakefulness by extubating the tracheal tube and replacing it with a laryngeal mask airway (LMA). The LMA is generally better tolerated and can be left in place till the patient is more awake.
Injury of the recurrent laryngeal nerve may lead to airway problems following extubation. This should always be considered following surgery to the neck, and thyroid surgery in particular because of the anatomy of the nerves in relation to the thyroid gland. Unilateral nerve injury may not cause any airway embarrassment, but bilateral nerve injury can result in adduction of the vocal cords causing total airway obstruction. This might only become apparent once the ETT is removed and may necessitate emergency reintubation. It may then be necessary to perform a tracheostomy, even if the nerve injury has the potential for recovery.
Post-operative bleeding, either in or around the airway, can lead to airway distortion and airway edema which can be rapid in onset. These complications can be exacerbated by coughing or retching, which cause a rise in intracranial and intrathoracic pressure by the Valsalva effect, by hypertension, which can result from pain and anxiety, and posture, particularly lying flat. Uncontrolled bleeding should be managed actively and if doubt exists as to its cause, nasoendoscopy should be considered. If the airway is in danger, appropriate and timely action should be taken to secure it before the clinical situation deteriorates further. If there is bleeding into the neck which is causing airway obstruction, it may be necessary to remove sutures/staples and evacuate any haematoma. While this may immediately improve airway distortion, it should be remembered that laryngeal oedema may also be a factor causing airway compromise. Consequently, early reintubation should be considered. It may be necessary to use an ETT smaller than that used for the original intubation.
3.9 Special Considerations
1. Laser surgery
Laser surgery to the airway has increased in popularity in the last decade. Lasers are hazardous because they make use of concentrated, non-divergent, high-intensity energy. When using lasers in the airway, operators must always remain alert to the rare, but significant, risk of airway fires. Risks should be minimised by the following:
• The use of a laser-resistant ETT, which has two inflation cuffs (so that airway protection is maintained one of the cuffs should be punctured).
• Inflating the cuffs with saline, rather than air, which might ignite if hit by the laser.
• Packing the throat with wet gauze.
• Air should be used in the oxygen mix rather than nitrous oxide, which is more flammable.
• Keeping the fraction of inspired oxygen below 25%, while the laser is in use, if the patient can tolerate this.
Should a fire occur, the surgeon should switch off the laser and flood the surgical field with water to cool the tissues. Oxygen delivery should be suspended till the fire is out. A badly damaged or melting tracheal tube may need to be removed. Once the fire is out, oxygen should be reintroduced and anaesthesia reestablished, by face mask if necessary. Examination of the airway with a rigid bronchoscope, reintubation and bronchoscopy with lavage may all be indicated. If damage is severe, a tracheostomy might be necessary.
2. ‘Tubeless’ anaesthesia
For certain procedures, the surgeon may request ‘tubeless’ anaesthesia. There are various ways that the anaesthetist can facilitate this:
•Use of low-frequency jet ventilation (LFJV): The jet ventilation device (e.g. Sander's injector or Manujet) is attached to a side port of the rigid bronchoscope used by the surgeon. The anaesthetist intermittently jets high-flow oxygen down the scope at a rate of 8 to 10 per minute. As the high-flow oxygen jets through the scope, air is entrained, increasing the tidal volume. Anaesthesia is usually maintained using TIVA. LFJV has the disadvantage of requiring surgical pauses while the jet of gas is delivered because there is movement of the pharynx/larynx during gas delivery as a result of the high pressure.
•High-frequency jet ventilation (HFJV): This limits distortion of the airway during gas delivery. High-frequency ventilators deliver jets at a rate of 1 to 10 Hz via a very thin, non-distensible catheter, which is placed above or into the trachea. Airway resection or end-to-end anastomosis can be achieved around this small-lumen catheter.
With either form of jetting, it is essential that there is an exit for the gases used else intrathoracic pressure will build up and lead to pneumothoraces. HFJV machines incorporate pressure monitors, but for the manual situation, diligent clinical surveillance is mandatory.
Further Reading
Arné J, Descoins P, Fusciardi J, et al. Preoperative assessment for difficult intubation in general and ENT surgery: predictive value of a clinical multivariate risk index. Br J Anaesth. 1998; 80(2):140–146
Patel A, Nouraei SAR. Transnasal humidified rapid-insufflation ventilatory exchange (THRIVE): a physiological method of increasing apnoea time in patients with difficult airways. Anaesthesia. 2015; 70(3):323–329
http://www.rcoa.ac.uk/system/files/CSQ-NAP4-ES.pdf. Executive Summary of National Audit Project 4, Royal College of Anaesthetists. Accessed July 28, 2017
Related Topics of Interest
Anaesthesia—local
Anaesthesia—sedation
4 Anaesthesia—Local
The use of local and ‘regional’ anaesthesia, where local anaesthetic (LA) is infiltrated around a specific nerve to produce numbness in the region it supplies, is gaining popularity in anaesthesia because patients can enjoy the benefits of pain-free surgery without being exposed to the risks of general anaesthesia. While the scope for regional anaesthesia is fairly limited in the field of ENT, soaking of the nasal mucosa in Moffat's solution (which contains the local anaesthetic agent, cocaine), infiltration of skin with local anaesthetic agents to facilitate the removal of ‘lumps and bumps’ and infiltrating the surgical site with local anaesthetic to provide post-operative analgesia are all commonplace. For this reason, a working knowledge of commonly used local anaesthetic agents is useful to the ENT surgeon. Despite their relatively good safety profile, fatalities have resulted from LA overdose, so all doctors administering these drugs must be aware of the signs and symptoms of toxicity and how to manage it.
The Association of Anaesthetists of Great Britain and Ireland (AAGBI) advises that standard monitoring (blood pressure, electrocardiography [ECG] and pulse oximetry) should be employed when administering LA. Consideration should be given, when appropriate, to inserting an intravenous cannula, to allow for treatment of any LA toxicity that might occur.
4.1 Local Anaesthetic Agents
Pharmacologically, local anaesthetics can be classified into ester and amide types. Esters have an increased likelihood of precipitating hypersensitivity reactions when compared with amides (Table 4.1).
Maximum dosages are adjusted for lean body weight as described by Specialists in Obesity and Bariatric Anaesthesia (SOBAUK) with up to a maxi mum of 100 kg for males and 70 kg for females.
4.2 Mechanism of Action
Local anaesthetic drugs enter the nerve fibre and bind to sodium channels located on the internal surface of the membrane. Once bound, they inhibit the movement of sodium across the membrane and so prevent the propagation of the nerve impulse. LAs bind more avidly to sodium channels that are open or inactivated and so preferentially affect nerves that have a rapid discharge rate. This means sensory nerve fibres are more susceptible than motor nerves, because they fire at a higher frequency.
In order to pass through cell membranes, any drug must be in its unionised form. The degree of ionisation of any drug depends on its pKa (drugs with a lower pKa—close to pH 7.4—will have a higher unionised fraction than those with a higher pKa) and the pH of the local environment. For this reason, LAs are less effective at producing satisfactory operating conditions in infected areas, such as abscesses, because the reduction in pH in these areas results in a higher proportion of ionised drug, making it unable to cross into the nerve cells to exert its effect.
Certain other drugs can be mixed with LA solution to produce a desired effect, for example adding sodium bicarbonate solution will speed up onset of action, by increasing environmental pH and so increasing the fraction of unionised drug; adding adrenaline to the solution causes local vasoconstriction, thereby decreasing washout of the LA and so extending its duration of action. Adrenaline is contraindicated in sites supplied by end arteries (digits and appendages) and should be used with caution in patients with ischaemic heart disease, hypertension and cardiac arrhythmias. The anaesthetist should always be informed that LA is about to be injected so that any immediate adverse events can be observed and drug administration stopped.
4.3 Features of Specific Agents
1.Lignocaine (Xylocaine)
Lignocaine has an immediate onset of action. It is typically presented as a 1% (10 mg/mL) or 2% (20 mg/mL) solution for injection. It is a mild vasodilator and is often given mixed with adrenaline. It is also available as a spray (4 or 10% formulation) and ointments (2–5%) and as a spray is pre-mixed with the vasoconstrictor phenylephrine as ‘cophenlycaine’. This is useful for preparing the nostril for endoscopy.
2.Bupivacaine (Marcaine)
Bupivacaine is a vasodilating amide with a slower onset (takes up to 20 minutes for the block to develop) and longer duration of action than lignocaine. It is useful for regional techniques and postoperative analgesia. It tends to produce more motor block than lignocaine. At toxic levels, the drug binds avidly to cardiac sodium channels and so cardiac events tend to be resistant to treatment.
3.Levobupivacaine (Chirocaine)
Levobupivacaine is the single levoisomer of bupivacaine and is less cardiotoxic than the parent drug, bupivacaine. The sensory block lasts longer than that of bupivacaine.
4.Ropivacaine (Naropin)
Ropivacaine is a single isomer of bupivacaine. Ropivacaine is less cardiotoxic than either bupivacaine or levobupivacaine and is also more selective for sensory nerves, producing less motor block.
5.Prilocaine (Citanest)
Prilocaine has no vasodilating effect and lower systemic toxicity. Metabolism to o-toluidine may cause methaemoglobinaemia in susceptible patients. Prilocaine is a component of EMLA skin cream (2.5% lignocaine with 2.5% prilocaine).
6.Cocaine
Cocaine is used as a constituent of Moffat's solution to cause vasoconstriction and anaesthesia of the nasal mucosa. In addition to its LA effect, it inhibits the re-uptake of noradrenaline, serotonin and dopamine resulting in greater concentrations of these neurotransmitters in the brain causing predictable consequences: increase in heart rate and blood pressure, which can precipitate myocardial infarction in those with ischaemic heart disease, euphoria, hallucinations and disinhibition.
7.Tetracaine
Tetracaine is available as a 4% gel and is used only topically on intact skin in preparation for intravenous cannulation. It should not be used on inflamed or infected skin.
4.4 Local Anaesthetic Toxicity
Local anaesthetic toxicity is a rare but potentially fatal complication. Several factors may contribute to the development of LA toxicity including the drug used, the site of injection and rate of entry into the circulation and peak plasma concentration. In addition, the physiological state of the patient will affect drug toxicity, with hypoxia, hypercarbia and acidosis all potentiating cardiac toxicity.
4.4.1 Signs of Toxicity
Clinical signs will increase in severity with increasing plasma concentration:
• Light-headedness.
• Tinnitus.
• Perioral tingling and tongue numbness.
• Visual disturbance.
• Agitation.
• Muscular twitching.
4.4.2 Signs of Severe Toxicity
• Sudden alteration in mental status, severe agitation, loss of consciousness.
• Tonic–clonic convulsions.
• Cardiovascular collapse: sinus bradycardia, heart block, asystole or ventricular tachyarrhythmia.
4.4.3 Management
• Stop injecting LA.
• Call for help—crash call if appropriate.
• Make a rapid but thorough assessment of airway, breathing and circulation.
• Open. airway and administer 100% oxygen.
• Confirm or establish intravenous access.
• Correct physiological abnormalities.
• Begin advanced life support if indicated.
• Administer Intralipid according to guidelines.
Treatment of local anaesthetic toxicity is with 20% lipid emulsion (Intralipid) which can be found on the cardiac arrest trolley, along with the dosing guidelines. Initial dose is 1.5 mL/kg over 1 minute, followed by an infusion of 15 mL/kg/h. If after 5 minutes, cardiovascular instability persists, the initial bolus should be repeated up to twice more (making three boluses in total) and the infusion rate should be doubled to 30 mL/kg/h. The total dose of Intralipid should not exceed 12 mg/kg. Recovery from LA-induced cardiac arrest may take over 1 hour.
4.5 Allergic Reactions
Amide local anaesthetic drugs have an extremely low incidence of allergic reactions. Patients will often report allergy to LA following its use for dental procedures. This should prompt further questioning, because they usually report tachycardia or chest tightness following administration. These symptoms do not represent allergy to the lignocaine used, but a normal physiological response to the adrenaline in the mixture. Hypersensitivity and cross-hypersensitivity are not uncommon with ester local anaesthetics.
Further Reading
The SOBA Single Sheet Guideline. http://www.sobauk.co.uk/downloads/single-sheet-guideline. Accessed July 31, 2017
AAGBI Safety Guideline: Management of Severe Local Anaesthetic Toxicity. https://www.aagbi.org/sites/default/files/la_toxicity_2010_0.pdf. Accessed September 4, 2017
Related Topics of Interest
Anaesthesia—general
Anaesthesia—sedation
5 Anaesthesia—Sedation
Procedural sedation and analgesia (PSA) is used in ENT surgery to reduce pain and anxiety and to provide amnesia for surgical procedures. PSA involves the administration of sedatives or dissociative agents, with or without analgesics, to induce an altered state of consciousness that allows the patient to tolerate painful or unpleasant procedures while preserving cardiorespiratory function.
5.1 Depth of Sedation
Four levels of sedation are defined by The American Society of Anesthesiologists (ASA).
1.Minimal sedation: A drug-induced state during which the patient responds normally to verbal commands. Cognitive function and physical co-ordination may be impaired, but airway reflexes, ventilatory and cardiovascular functions are unaffected.
2.Moderate sedation: A state where a purposeful response to verbal commands either alone (conscious sedation), or accompanied by light tactile stimulation, is maintained. The airway is normally unaffected and spontaneous ventilation is adequate.
3.Deep sedation: A state where the patient cannot easily be aroused but responds purposefully to repeated or painful stimulation. It may be accompanied by clinically significant ventilatory depression. The patient may require assistance to maintain a patent airway, and may require positive pressure ventilation.
4.General anaesthesia: A controlled state of unconsciousness accompanied by a loss of protective reflexes, including loss of the ability to maintain a patent airway or to respond purposefully to physical stimulation or verbal command.
5.2 Use of PSA in ENT Surgery
Where possible, PSA may be considered in patients unfit for general anaesthesia (GA), for patients who express a preference for it, and for procedures when patient co-operation is useful, for example vocal cord medialisation. When considering this technique, it is imperative to evaluate the surgeon's operative needs and to select the patients carefully. PSA will not be suitable for some, nor provide adequate operating conditions for many ENT procedures.
Middle ear surgery: Tympanoplasty, mastoid-ectomy, myringotomy, grommet insertion and cochlear implantation can be performed under local anaesthesia and sedation. Under local anaesthesia, many patients experience discomfort including a sense of noise, anxiety, dizziness, backache, claustrophobia or earache. Sedation may help alleviate some of these symptoms.
Nasal surgery: Functional endoscopic sinus surgery, septoplasty, balloon dilation of frontal sinus duct, dacryocystectomy and reduction of fractured nasal bones can all be successfully performed under local anaesthesia with sedation using various intravenous sedatives and/or analgesics.
Head and neck surgery: Excision of head and neck skin lesions, lip lesions, oral, oropharyngeal lesions and laryngeal procedures might lend themselves to PSA.
5.3 Pre-Operative Assessment
The very young and old, frail, morbidly obese, those with obstructive sleep apnoea (OSA), pulmonary and cardiac disease, and patients with significant kidney or liver disease are, amongst others, at higher risk of complications when receiving sedation. These patients may be best served by an anaesthetist administering their PSA. Patients should be carefully assessed for the presence of predictors of difficult bag-mask-ventilation, for example dysmorphic facial features, the presence of a beard, significant cachexia, morbid obesity, history of snoring or limited neck extension. Again, it may be prudent for an anaesthetist to manage these patients. Any patient receiving anything more than minimal sedation should be fasted to reduce the risk of aspiration of stomach contents into the airway. Fasting guidelines for general anaesthesia should be followed.
