Color atlas of ent diagnosis

Bull, Color Atlas of ENT Diagnosis © 2003 ThiemeAll rights reserved. Usage subject to terms and conditions of license.


Color Atlasof ENT Diagnosis4th edition, revised and expanded

Tony R. Bull, FRCSHonorary Consultant SurgeonRoyal National Throat Nose and EarHospital London, UKHonorary Senior Lecturer to the Instituteof Laryngology and OtologyLondon, UKHonorary Consultant SurgeonCharing Cross HospitalLondon, UKConsultant SurgeonKing Edward VII Hospital for OfficersLondon, UK

569 illustrations

ThiemeStuttgart · New York


IV

Library of Congress Cataloging-in-PublicationData is available from the publisher

3rd edition published 1995 by Mosby-Wolfe, London

© 2003 Georg Thieme Verlag,Rüdigerstrasse 14, 70469 Stuttgart,Germanyhttp://www.thieme.deThieme New York, 333 Seventh Avenue,New York, NY 10001, USAhttp://www.thieme.com

Cover design: Cyclus, StuttgartTypesetting by Litoflex srl, Ascoli PicenoPrinted in Germany by Grammlich,Pliezhausen

ISBN 3–13–129391-8 (GTV)ISBN 1–58890–110–6 (TNY) 1 2 3 4 5

Important Note: Medicine is an ever-changing science undergoing continualdevelopment. Research and clinicalexperience are continually expanding ourknowledge, in particular our knowledgeof proper treatment and drug therapy.Insofar as this book mentions any dosageor application, readers may rest assuredthat the authors, editors, and publishershave made every effort to ensure thatsuch references are in accordance withthe state of knowledge at the time ofproduction of the book.

Nevertheless, this does not involve,imply, or express any guarantee orresponsibility on the part of the publishersin respect to any dosage instructions andforms of application stated in the book.Every user is requested to examinecarefully the manufacturer’s leafletsaccompanying each drug and to check, ifnecessary in consultation with a physicianor specialist, whether the dosage schedulesmentioned therein or the contraindicationsstated by the manufacturers differ from thestatements made in the present book. Suchexamination is particularly important withdrugs that are either rarely used or havebeen newly released on the market.Every dosage schedule or every form ofapplication used is entirely at the user’sown risk and responsibility. The authorsand publishers request every user to reportto the publishers any discrepancies orinaccuracies noticed.Some of the product names, patents, andregistered designs referred to in thisbook are in fact registered trademarks orproprietary names even though specificreference to this fact is not always madein the text. Therefore, the appearance ofa name without designation asproprietary is not to be construed as arepresentation by the publisher that it isin the public domain.

This book, including all partsthereof, is legally protected by copyright.Any use, exploitation, or commercializationoutside the narrow limits set by copyrightlegislation, without the publisher’s consent,is illegal and liable to prosecution. Thisapplies in particular to photostatreproduction, copying, mimeographing orduplication of any kind, translating,preparation of microfilms, and electronicdata processing and storage.


V

Preface

A further 8 years have passed since the previous publication of Color Atlasof ENT Diagnosis, and developments in this specialty call for an updatedand revised edition. The format of this book remains a pictorial survey ofear, nose, and throat conditions, combined with a succinct text that aimsto be of practical help in diagnosis. It is not an illustrated textbook, andfurther reference is required for more information on the conditionspresented. This atlas will, I hope, continue to stimulate the interest ofmedical students in the specialty and also provide useful, practicalinformation to ENT trainees and those in general practice and casualtywhere ENT conditions so commonly present. It will also be of relevanceand help to those in allied specialties.

T R Bull, FRCS, London


VI

Acknowledgments

Many of the photographs in this book were taken by myself but I amgrateful for the expertise of the Photographic Department of the RoyalNational Throat Nose & Ear Hospital for many of the better illustrations. My thanks also go to my colleagues who have contributed illustrations tothis edition: Professor Lund, Mr Croft, Mr Nasser, Mr Gault, Mr Bailey, MrHoward, Professor Ramsden, Mr Proops, Professor Weerda, ProfessorWright, Dr Glyn Lloyd, Dr AH Davies, Dr Van Hasselt, Dr J Brennand, Dr GScadding.Figure no. 4.58 has been reprinted with permission from: Farthing CF,Brown SE, Color Atlas of Aids and HIV Disease, 2nd edition, 1998, MosbyWolfe, London. This book has been perused by my colleague at the Royal National ThroatNose & Ear Hospital, Mr Jeremy Lavy, whom I would like to thank, and alsomy senior audiologist, Mrs Jean Rousell, for her advice on the audiometrysection.


VII

Contents

Chapter 1 ENT Examination. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1Examination of the Ear. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4

Referred Ear Pain. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8Hearing Loss. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 10Tests of Balance. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 20Otoacoustic Emissions. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 20

Examination of the Nose. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 29Examination of the Pharynx and Larynx. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 36

Taste and Smell. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 39

Chapter 2 The Ear. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 43The Pinna. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 44

Deformities. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 44Earrings. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 52

The External Auditory Meatus. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 62The Tympanic Membrane and Middle Ear. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 72Microsurgery. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 96Facial Palsy. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 97

Chapter 3 The Nose. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 99Deformities. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 100Cysts. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 103Adenoids. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 109Trauma. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 112

Complications of a Fractured Nose. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 113Rhinoplasty. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 119Deviated Nasal Septum. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 125

Inflammation: nasal vestibulitis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 131Polyps. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 144Epistaxis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 150Neoplasms. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 156

Malignant Nasal Tumors. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 156


VIII Contents

Chapter 4 The Pharynx and Larynx. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 165The Oropharynx, Mouth, and Lips.. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 166The Tongue. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 176The Fauces and the Tonsils. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 184

Infections of the Tonsils, Pharynx, and Oropharynx. . . . . . . . . . . . . . . . . . . . 195The Larynx. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 210

Inflammation of the Larynx. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 210Neoplasms of the Larynx. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 220Laryngeal Surgery. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 222

The Hypopharynx and Esophagus. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 232

Chapter 5 The Head and Neck. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 237Salivary Glands. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 238Swelling of the Neck. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 245

Inflammatory Neck Swellings. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 245Mid-line Neck Swellings. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 247Lateral Neck Swellings. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 249

Index. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 252


IX

Sir Morrell MacKenzie

This painting shows the austere Scottish physician and surgeon whofounded Ear, Nose and Throat as a specialty and wrote the first standardtextbook on Rhinology and Laryngology. Sir Morrell MacKenzie alsofounded one of the first hospitals for Nose and Throat diseases in Londonin 1863 (today the Royal National Throat Nose and Ear Hospital). Themost common condition he treated in this hospital was laryngealtuberculosis, at that time invariably fatal, but today rare and curable.



titoletto sopra 1

Chapter 1ENT Examination


2 ENT Examination

Fig. 1.1 The instruments needed for an ENT examination: The laryngeal andpostnasal mirrors require warming to avoid misting, and hot water or a spirit lampis necessary. An angled tongue depressor or wooden spatula is needed for examin-ing the oropharynx and postnasal space. Angled forceps are used for dressing thenose or ear. A tuning fork is essential for the diagnosis of conductive or sen-sorineural (perceptive) hearing loss. A C1 or C2 (256 or 512 cps) is needed. Thevery large tuning forks used to test vibration sense are unsatisfactory, and may givea false Rinne test. A Jobson–Horne probe is widely used in ENT departments. A loopon one end is for removing wax (and foreign bodies) from the ear or nose. Cottonwool attached to the other end is used for cleaning the ear.

An auriscope, nasal and aural specula complete the basic instruments. A sterileswab and media are necessary for throat, nasal, or ear specimens to be taken forculture and sensitivity. A “narrow” swab holder as shown here is extremely usefulfor aural specimens, as the more common swab is too wide and can be traumaticfor the deep meatus and middle ear.


Examination of the Ear 3

Fig. 1.2 Lighting. The head mirror (a) gives effective lighting for examining theupper respiratory tract and ear, and leaves both hands free for using the instru-ments. Initially, the technique of using a head mirror is not easy, and some mayprefer a fiberoptic or electric headlight (b).

Fig. 1.3 Rigid and flexible fiberoptic endoscopes.These are important additional examination instru-ments. The flexible endoscope is of value to see thelaryngeal region (see Fig. 1.62) in those with amarked gag reflex in whom indirect laryngoscopy(see Fig. 1.61) with a mirror is difficult. The rigidendoscope is important in examination of the nasalcavities.

a

b


4 ENT Examination

Examination of the Ear

Fig. 1.4 Retracting the pinna. Themeatus is S-shaped. To see the drummore clearly, therefore, the pinna isretracted backwards and outwards. Theindex finger may be used to hold the tra-gus forward. If this step of straighteningthe meatus accentuates the pain insomeone presenting with an earache,one can be virtually certain that the diag-nosis is either a furuncle or furunculosis(see Fig. 2.43).

Fig. 1.5 Head mirror and speculum. These are used for the initial examination ofthe meatus and drum.



Fig. 1.6 The auriscope. Thisis best held like a pen. In thisway, the examiner’s little fin-ger can rest on the patient’scheek; if the patient’s headmoves, the position of the earspeculum is maintained inthe meatus.

Fig. 1.7a Preferred way tohold the auriscope. Whenthe left ear is examined, theauriscope is held in the lefthand and vice versa. b Incorrect way to hold theauriscope.

a

b


6 ENT Examination

Fig. 1.8 Pneumatic otoscope. A hand-held air-filled bulb attached to theauriscope enables air to be gently inflat-ed against the drum to demonstratedrum mobility.

Reduced mobility is conspicuousand is evidence of middle ear fluid.Reduced mobility is also seen, however,with tympanosclerosis, which increasesthe rigidity of the drum. Malleus fixationis a rare cause of reduced mobility of adrum of normal appearance.

The fistula test may be done withthe pneumatic otoscope. Pressurechange by pressing on the bulb willcause dizziness in those with erosion ofthe labyrinth by cholesteatoma (see Fig.2.63) or with a perilymph fistula.

Fig. 1.9 A normal drum. The mainlandmarks seen on the pars tensa of anormal drum are the lateral process(top arrow) and handle (middle arrow)of the malleus, and the light reflex(lower arrow). The drum superior to theshort process is the pars flaccida or atticpart of the drum. A normal drum is greyand varies in vascularity and translucency.

Fig. 1.10



Fig. 1.10 A tympanic membrane showing the panoramic view obtained with afiberoptic endoscope. Fiberoptic auriscopes are not in common use and the con-ventional auriscope is widely used. For this reason most drums are shown as theyare seen with an auriscope. It is interesting to compare the appearance of a normaldrum with the auriscope and the appearance with a fiberoptic. A thin posterior scarindrawn onto the stapes is clearly seen (arrow) and would not be so apparent withmost conventional aurescopes.

For the most clear view of the eardrum, and for fine use of instruments, themicroscope (Fig. 1.14) is used.

Fig. 1.11 A more vascular drum. Thishas vessels extending down the handlesof the malleus to the umbo (arrow).These vessels may also be more conspic-uous following mild barotrauma to theear, e.g., rapid descent in an airplane inwhich delayed eustachian tube openingcauses pain. More severe trauma leadsto hemorrhage into the drum or perfo-ration.

Fig. 1.12 The incus (lower arrow) mayshow as a shadow through a thindrum, as may the round window andopening of the eustachian tube,although this is less common. The chor-da tympani nerve may also be seenthrough the drum (top arrow).


8 ENT Examination

Referred Ear PainIf examination of the drum and meatus is normal in a patientcomplaining of earache, the pain is referred. Referred ear pain may befrom nearby structures such as the temporo-mandibular joint, neckmuscles, or cervical spine. It may also be from the teeth, tongue, tonsils,or larynx. Cranial nerves V, IX, and X which supply these sites have theirrespective tympanic and auricular branches supplying the ear. Earachealso frequently precedes a Bell’s palsy.

Fig. 1.13 The chorda tympani nerve isthe nerve of taste to the anterior twothirds of the tongue (excluding the cir-cumvallate papillae), and is also thesecretomotor nerve to the submandibu-lar and sublingual salivary glands. Thechorda tympani nerve usually lies behindthe pars flaccida. It is not normally visi-ble, but if the nerve is more inferior, itshows through the drum (arrow).



Fig. 1.14 Microscope examination of the drum. a Although most drums can bewell seen and conditions diagnosed with the auriscope, the increased magnifica-tion that is obtainable with the operating microscope and easier instrumentation,make this apparatus standard in any well-equipped outpatient department. A videocamera or tutor arm may be attached to the microscope for demonstration.

The auricular branch of the vagus nerve supplies part of the deep meatus andeardrum, as well as some skin in the post auricular fold. Therefore, instrumentationof the ear may produce a sensation of faintness from a vasovagal episode; also acough may be triggered. Many therefore prefer to have the ear examination withthe patient lying down, particularly for procedures such as difficult suction clear-ance of wax and debris from the deep meatus. Routine examination of the drumwith the microscope may be carried out with the patient sitting up (b).

a

b

Fig. 1.15 Siegle’s specu-lum has been displaced bythe pneumatic otoscope(see Fig. 1.8), but Siegle’sspeculum with plain (notmagnifying) glass is usefulto test drum mobility withthe microscope.


10 ENT Examination

Hearing LossMost hearing loss is easy to diagnose as either a well-defined conductiveor sensorineural type. (“Mixed” hearing loss may occur, but this diagnosisis usually non-contributory, and the term is better avoided.)

Lesions to the left of the red line (Fig. 1.16) cause conductive hearingloss, and are frequently curable. Hearing loss to the right of the blue lineis due to a sensorineural lesion, and is usually not so amenable totreatment.

Fig. 1.16 Conductive and sensorineural hearing loss. Hearing loss is either con-ductive or sensorineural in type. It is an essential basic step in diagnosis of hearingloss to distinguish between these two. Sensorineural hearing loss is either due to acochlear or retrocochlear lesion.

SensorineuralConductive

Cochlear Retrocochlear



Tests for Conductive and Sensorinural Hearing Loss

Fig. 1.17 The Rinne test.Tuning fork tests are essen-tial preliminary tests for thediagnosis of hearing loss.The Rinne and Weber testsenable the diagnosis of aconductive or sensorineuralhearing loss to be made. Ifthe tuning fork is heard loud-er on the mastoid processthan in front of the ear, theRinne test is negative, andthe hearing loss conductive.If the tuning fork is heardbetter in front of the ear, theRinne test is positive, and thehearing is either normal orthere is sensorineural hearingloss.

Fig. 1.18 The Weber test.The tuning fork, when held inthe mid-line on the forehead,is heard in the ear with theconductive hearing loss. Thistest is very sensitive, and ifthe meatus is occluded withthe finger, the tuning forkwill be heard in that ear. A conductive loss of as little as 5 dB will result in the Weber test beingreferred to that ear.


12 ENT Examination

Total Hearing Loss in One EarTotal hearing loss in one ear is frequently wrongly diagnosed as aconductive hearing loss. The Rinne is negative because the tuning fork,although not heard in front of the ear, is heard by the better ear whenplaced on the mastoid process of the deaf ear, with the sound beingtransmitted by the bone (false-negative Rinne). The Weber test gives theclue that the Rinne is false, as the sound will not lateralize to the deaf ear.

Total hearing loss in one ear may be congenital or the result of a skullfracture. Meningitis is also a cause, but mumps is probably thecommonest cause, and an acoustic neuroma must be excluded.

Fig. 1.19 Barany box. This is used to confirm total hearing loss. It is placed on thegood ear and produces a noise totally masking this ear. The patient will be unableto repeat words clearly spoken into the deaf ear.

Fig. 1.20 The occlusion (Bing). This isalso helpful. The tuning fork is held onthe mastoid process and the tragus light-ly pushed to occlude the meatus. Thetuning fork is heard louder, in conductivehearing loss, even of a slight degree,there is no change when the meatus isoccluded. The Rinne test does notbecome negative until there is a markeddegree of conductive loss (about a 20-dBair—bone gap). It is therefore possible tohave a slight conductive hearing losswith a positive Rinne test. The more sen-sitive occlusion test will help in the diag-nosis.



Hearing Aids

Fig. 1.21a-c Hearing aids. Aids worn to both ears may be helpful. The better earmay be preferred if only one aid is used. Conductive hearing loss that is notamenable to surgical treatment responds well to conventional hearing aids, as maysensorineural hearing loss with a “flat” tracing, in which the hearing loss is equal atmost frequencies. Most commonly, however, sensorineural hearing loss affects thehigh tones, with relatively good hearing at low frequencies.

There are still difficulties to overcome in designing a hearing aid that can pro-vide good speech discrimination for this type of hearing loss, although the moverecent digital aids have made a significant improvement. Aids containing a micro-phone, amplifier, battery, and earphone can be fitted either behind the ear, to spec-tacles, or as an in-the-ear aid.

a

b c


14 ENT Examination

Fig. 1.22 Modern hearing aids are so small that they may be fitted completelywithin the ear canal, either adjacent to the tympanic membrane or “semi-deep.”With very severe hearing loss, a behind-the-ear aid is needed. The new range ofdigital hearing aids are, in many cases, much more efficient and effective at reduc-ing background noise. The problem with background noise has, in the past, beenthe main complaint of many hearing aid users.

Patience and advice are needed to adapt to the use of a hearing aid, and inthis and other forms of hearing loss management, hearing therapists have animportant role.

Fig. 1.23 Bone-anchored hearing aid.The aid clips onto osseo-integrated tita-nium screws fixed to the mastoid bone. Itis an efficient sound conductor for thosewith congenital absence or deformity ofthe ear canal and pinna, in whom a con-ventional hearing aid cannot be fitted.

With ear discharge not controlledmedically or surgically, the fitting of aconventional aid for conductive hearingloss is also not practical, and bone-anchored aids may be used.



Fig. 1.24 The cochlear implant has proved a great advance in the management ofprofound hearing loss in children and adults, where conventional aids are ineffec-tive to restore hearing. An ear-level microphone is fitted like a hearing aid. Sound isconverted to electric signals to a processor and transmitted to electrodes insertedinto the cochlear (a). The nuclear contour electrode contains a stylette (b). Whenthe stylette is removed, the coil forms a curl which conforms to the cochlear (c).The nuclear contour device contains 22 electro-terminals, which can be seen onthe radiograph showing the implant in place in the inner ear (d). e This imageshows the complete device with the electrode, reference electrodes, receiver core,and microchip packet.

a

b

c

d e


16 ENT Examination

Magnetic resonance imaging is the single most important investigation foracoustic neuroma. Early diagnosis is important for a small neuroma (lessthan 1 cm in diameter). This can be removed with preservation of thefacial nerve to which it is adjacent in the internal auditory meatus, andthe hearing too may be preserved.

Neuromas arise from the nerve sheath of the vestibular nerve (strictlytermed “schwannomas”), and may be dissected from the auditory nerve.The prognosis for larger neuromas is less good, with risk of permanentdamage to the facial nerve and increased morbidity from intracranialsurgery.

Investigation of Hearing Loss: Radiology

Fig. 1.25 Acoustic neuroma. The mostcommon early presentation of anacoustic neuroma is a unilateral sen-sorineural hearing loss. An MRI scan isan essential investigation to exclude thistumor in all cases of unilateral sen-sorineural hearing loss unless there is acertain other cause, e.g., trauma,mumps, meningitis. There is now a

marked awareness that sensorineuralloss, particularly if unilateral and even ifminimal, requires investigation toexclude an acoustic neuroma.

Fig. 1.26 The MRI and CT scan are twoimportant radiograph innovationsdeveloped in Great Britain. The MRI scangives the diagnosis of acoustic neuroma(arrows).



Fig. 1.27 Audiometry. A pure-tone audiogram ist the standard test of hearinglevel. The readings are recorded on a chart with intensity (0–120 dB) and frequency(usually 250–8000 cps). A normal tracing is between –0 dB and +10 dB at all fre-quencies. This test is accurate to about 10 dB only, as there are variables due to thepatient’s responses and the accuracy of both the audiometrician and the machine.Hearing is tested in front of the ear (air conduction—recorded in black) and over themastoid process (bone conduction—recorded in red). A silent or soundproof room isnecessary for accurate pure-tone audiometry.

Investigation of Hearing Loss: Audiometry

Fig. 1.28 Audiogram. The audiogram on the left shows a typical sensorineuralhearing loss; a sharp dip at 4000 cps, as on this chart, is typical of inner ear damagedue to noise trauma. A loss of high frequencies is commonly seen in hearing loss ofold age (presbycusis). The audiogram on the right shows a conductive hearing losswith the sound heard better on the bone, typical of otosclerosis or otitis media.


18 ENT Examination

Audiometry requires skill and training, particularly to test children. Anaudiogram is obtainable from most children by age three to four. Withunilateral hearing loss, noise is used to mask the better ear, so that thisear does not hear the sound transmission from the deaf ear and give afalse reading. Hearing assessment under the age of three years, or inchildren who are unable to cooperate with audiometry, requires specialskills and techniques.

The response of a baby or toddler to meaningful sounds, such as aspoon “chinked” against a cup, gives an indication of hearing.Electrocochleography (ECoG) involves placing fine electrodes through thedrum to pick up auditory nerve reaction potential in response to sound.This refined test gives a good hearing assessment for infants in whom ahearing loss is suspected. Anesthesia is required for ECoG. This objectivetest of hearing acuity is also of help in the diagnosis of psychosomatichearing loss or malingering. The auditory brain stem response (ABR), inwhich electroencephalogram recordings are made following auditorystimulus, is another useful audiometric test.

Fig. 1.29 Speech discrimination audiometry. A criticism of pure-tone audiometry is that an assessment of the ability to hear pure-tone sounds may not reflect the ability to hear speech. A phoneticallybalanced list of words is used. The percentage of those correctlydetected is used as the index to plot a speech discrimination chart.The ability to understand speech is obviously reduced with all hearingloss but particularly with sensorineural loss in which the high tonesare involved. An additional help in the diagnosis of acoustic neuromasmay be poor speech discrimination, in excess of that expected fromthe level of the pure-tone audiogram.



Fig. 1.30 Impendance audiometryinvolves performing several measure-ments to obtain a wide range of infor-mation about the middle and inner ear.A probe with a rubber tip and contain-ing three small patent tubes is fittedinto the meatus to make an airtight seal.One tube delivers the tone to the ear, asecond tube is attached to a micro-phone to monitor the sound pressurelevel within the ear canal, and a thirdtube is attached to a manometer to varythe air pressure in the ear.

Fig. 1.31 Impendance measurementsare particularly helpful in the differentialdiagnosis of conductive and sensorineur-al hearing losses, as they give informa-tion about middle-ear pressure, eustachi-an tube function, middle-ear reflexes,and the level of a lower motor neuronfacial nerve palsy. Impendance testing is

widely used to confirm the presence ofmiddle-ear fluid, and the “flat” tracing ischaracteristic. A “glue ear” may be diag-nosed in babies and younger childrenusing impedance measurements whenthe cooperation required for a pure-toneaudiogram is not possible.

Normal tracing.

Flat tracing of middle-ear fluid.


20 ENT Examination

Otoacoustic EmissionsIn children or babies who are suspected of having a hearing loss who aretoo young for audiometry, otoacoustic emissions give a valuable objectiveassessment of hearing. A “click” noise introduced into the ear triggers thecochlear to admit a sound which can be recorded. With marked hearingloss this sound emitted by the cochlear is not detected. This test is alsohelpful in the diagnosis of nonorganic hearing loss.

Fig. 1.32 Observation for nystagmusis one of the clinical tests for abnormali-ties of balance. Nystagmus due to alabyrinth disorder is characterized by aslow and quick phase of eye movementin which the eye moves slowly awayfrom the side of the involved labyrinth,then flicks rapidly back to that side; thenystagmus is said to be in the directionof the quick phase. The eye movementin nystagmus is fine.

Fig. 1.33 Frenzel glasses. Observationof nystagmus is facilitated by fitting thepatient with glasses with magnifyinglenses, such as Frenzel glasses.

Tests of BalanceVertigo is most commonly due to a disorder of the labyrinth. A sensationof unsteadiness may occur, however, with hypoglycemia, orthostatichypotension, hyperventilation, and cerebral ischemia. Tumors or multiplesclerosis involving the vestibular system also cause imbalance.



Abnormalities in these preliminary clinical tests of balance will indicatethe need for further investigation.

Vertigo due to a labyrinth disorder may occur with or without hearingloss.

Fig. 1.34a Tests to demonstrate abnormalities of gait. One of these is heel–toewalking along a straight line. A person with normal balance is stable without look-ing down at the feet. b The Romberg test is another basic test of balance. Thistest, in which the patient is asked to stand still with feet together and eyes closed,is made more sensitive by asking the patient to mark time, when instability is obvi-ous, indicating a significant balance disorder.

a b


22 ENT Examination

Positional VertigoBenign paroxysmal positional vertigo is a sudden and severe rotary vertigooccurring when lying down in bed or upon looking upwards, when thehead is placed backwards and to one side. There is no hearing loss, and itmay follow a head injury. Although common, it is frequently notrecognized, and unnecessary neurological investigation may be carried out.

The positional history is typical, and diagnosis is confirmed by a positivepositional test. When the head is placed backwards and to one side there isnystagmus which fatigues within several seconds, but recurs temporarilywhen the patient sits up.

This is a self-limiting condition, and advising the patient simply to avoidthe position that triggers off the attack may suffice as treatment. With benignparoxysmal positional vertigo the episodes may vary in severity, duration,and frequency, and also tend to recur. The Epley maneuver (Fig. 1.36a–d) iseffective in curtailing benign paroxysmal positional vertigo. The condition isbelieved to be caused by displaced calcium particles from the utricle formingdebris in the semicircular canals of the labyrinth. Head positions of the Epleymanouver aim to reposition these particles in the labyrinth so they do notaffect the canal dynamics. Positional vertigo may also occur with space-occupying lesions involving the cerebellum and cerebello-pontine angle.Nystagmus may be induced with the positional test, but there is no latentperiod and the nystagmus does not fatigue.

Fig. 1.35 Positional test for benignparoxysmal positional vertigo.



Fig. 1.36a–d The Epleymanouver. The patient liesdown with the head in theposition to trigger positionalvertigo (a). After 30-60 sec-onds, when the nystagmushas settled, the head isturned through 90° to theopposite side (b), andremains there for a furtherminute. The patient is thenrolled on to that side withthe head maintained in thisposition, and the head isthen rotated so that thepatient is facing obliquelydownwards for a furtherminute (c). The sitting posi-tion is then resumed whilemaintaining head rotation,and the head is finally rotat-ed to the central position (d)and moved 40° downwardsto complete the Epleymanouver. Advice to keep the headerect and avoid the triggerposition is given. Three ormore pillows are advisedwhen sleeping. The Epleymanouver may be repeatedif ineffective in the firstinstance.

a

b

c

d


24 ENT Examination

Fig. 1.37 Vertebro-basilar ischaemia.Vertigo with head movement, or tran-sient sudden loss of consciousness(“drop” attacks), occur with temporaryinterruption of the blood supply to thelarbyrinth or cerebral cortex. This condi-tion is seen in older patients with cervi-cal osteoarthritis, and with evidence ofhypertension and atherosclerosis. Move-ment of the irregular cervical spine tem-porarily occludes the tortuous athero-sclerotic vertebral vessels which lead tothe basilar and internal auditory arter-ies. This vertebral angiogram shows thekinking of the vertebral artery.

Fig. 1.38 The caloric test. Irrigation ofthe external meatus with water 7°above and later 7° below body tempera-ture sets up convection currents of theendolymph in the semicircular canals.This causes nystagmus, and the dura-tion of the nystagmus gives an index ofthe activity of the labyrinth. The nystag-mus can be directly observed or record-ed electrically (electronystagmogra-phy). This test is particularly valuable inthe diagnosis of Ménière’s disease andacoustic neuroma. A reduced or absentnystagmus is found (canal paresis).



Sudden severe rotary vertigo often with nausea and vomiting, a tinnitusincreasing prior to the vertigo, and a sensorineural hearing loss (cochleartype), which may fluctuate, form the triad of symptoms characteristic ofMénière’s disease.

Distorted hearing (diplacusis) and a sensation of “pressure” in the earare often further symptoms.

In this curious condition, there is an increase in the endolymphvolume, but the cause is unknown. The disease has a reputation for beingserious, which is not justified. Although the vertigo may occasionally besevere and incapacitating, the symptoms are frequently mild, usually self-limiting, and not progressive. It is never fatal, and medical treatment withlabyrinthine sedatives, for example, prochlorperazine, commonlycontrols the vertigo. Oral histamine-like drugs which aim to increase theblood flow to the inner ear (e.g., betahistine) may also be effective, as maya low salt diet and diuretics. There is, however, no proven specific medicaltherapy at present available for Ménière’s disease.

In one more recent treatment of Ménière’s disease, Gentamycininstilled into the middle ear either directly through the drum or via acatheter, is absorbed through the round window membrane into theinner ear. Gentamycin is more toxic to the vestibular apparatus than thecochlear and the dose can be titrated to destroy vestibular function withminimal effect on the hearing. All patients are, however, warned thatthere is a risk to hearing with this treatment. Good control rates forvertigo have been reported with the treatment.

Fig. 1.39 The triad of Ménière’s disease.

Ménière’s Disease


26 ENT Examination

Many innovative surgical procedures have been tried for Ménière’sdisease; none of them has proved to be totally successful, althoughdecompression of the endolymphatic sac in an attempt to reduce thepressure in the scala media may prove effective conservative surgery.Surgery to destroy the labyrinth is effective in controlling the vertigo, butan irreversible total hearing loss with accentuated tinnitus is one of thefactors that make this treatment a last resort.

Fig. 1.40 Normal ear.



Fig. 1.41 Ménière’s disease.

Fig. 1.42 Illustration of normal ear. Fig. 1.43 Illustration of ear withMénière’s disease, showing atrophicstria vascularis and organ of Corti.


28 ENT Examination

TinnitusTinnitus is commonly associated with hearing loss, although it may rarelybe troublesome with normal hearing. Tinnitus with conductive hearingloss is usually less distressing than tinnitus with sensorineural hearingloss, as in the latter the tinnitus may cause serious psychiatricdisturbance. The full physiology and pathology of tinnitus remainsunknown, and there is no entirely effective treatment. Explanation andreassurance are helpful in the patient’s acceptance of tinnitus (patientsfrequently associate it with serious intracranial disease), and the use of atranquilizer may be necessary. A tinnitus associated with sensorineuralhearing loss is usually a continuous tone (frequently described as “likelistening to a sea shell”). Tinnitus may, however, be pulsatile and needsinvestigation (e.g., computed tomography [CT] or magnetic resonanceimaging [MRI] scan), to exclude a vascular lesion, for example, glomusjugulare (Fig. 2.86). No cause may be found for pulsatile tinnitussynchronous with the pulse.Tinnitus-maskers, in which a hearing aid–like device feeds a noise

that has been matched with the tinnitus into the ear, may mask thetinnitus to a greater or lesser degree and be effective as a treatment.Surgical treatment of tinnitus with section of the acoustic nerve ordestruction of the inner ear has been tried and is unsatisfactory.


Examination of the Nose 29

Examination of the Nose

Fig. 1.44 Examining a child. Instru-ments are best avoided in children. Agood anterior view of the nose can beobtained simply by pressing on the tip ofthe nose. In this case, a clear view isobtained of a pedunculated papilloma ofthe nasal vestibule (arrow).

Fig. 1.45a Speculum examination shows the nasal vestibule, the septum anteri-orly (particularly Little’s area—see Fig. 3.80), and the inferior and middle turbinatesanteriorly. b There are several different types of nasal speculum used throughoutthe world. The ones demonstrated here are Thudicum (left) and the Killian (right)speculums.

a b


30 ENT Examination

Fig. 1.46 Nasal speculum examination.

Fig. 1.47 A nasal endoscope is necessary for a thorough examination of the nasalcavities, the mucosa having been sprayed with surface anesthetic.



Fig. 1.48 Mirror examination of thepostnasal space. This is not easy, par-ticularly in children. With a patient whogags easily, or whose soft palate is closeto the posterior wall of the oropharynx,a view may be impossible. With afiberoptic endoscope (Fig. 1.47), how-ever, a clear view of the postnasal spaceis obtained, and instrumentations forbiopsies of the postnasal space via thefiberoptic endoscope are available.

With the endoscope, however, the postnasal space may be seen more clear-ly, and a soft tissue lateral x-ray shows theadenoids or other pathology in this region.


32 ENT Examination

Fig. 1.50 Acoustic rhinometry. Noise introduced into the nasal vestibule isreflected from the interior of the nose. With a widely patent nasal airway, thereflection of sound is delayed and less intense than with nasal obstruction. Hence, agraph of normality can be made, and acoustic rhinometry is one recent objectivemeasurement for nasal airway.

Fig. 1.49 Rhinometry techniques gives a quantitative measurement of nasal air-ways. Many methods have been employed, but the anterior active method hasgained most acceptance. The pressure is measured through one nostril, while theflow is measured through the opposite side using a face mask and pneumotach.Rhinometry has yet to become of sufficient clinical value to be of routine use in theassessment of nasal obstruction, as the threshold of nasal obstruction or “conges-tion” of which the patient complains correlates poorly with air pressure measure-ments.



Fig. 1.51 Sinus radiographs havelargely been displaced by CT scans forthe investigation of sinus disease.Plain radiographs are, however, helpfulin diagnosis, showing opacity, indicatinginfection or polyposis and bone expan-sion or erosion, suggestive of neoplasm.Plain radiographs are also inexpensiveand involve minimal radiation comparedto CT scans.

Fig. 1.52 A CT scan of thesinuses gives precise detail,particularly of the eth-moids, which are not wellseen on the plain radi-ograph. The CT scan isimportant prior to sinussurgery. The left maxillaryantrum is seen to beopaque on this radiographfrom infection, but the leftethmoids are clear. Someminimal mucosal thicken-ing (which would not bedetected on plain radi-ographs) is seen in the rightethmoid sinus.

Ethmoid sinus

Middle turbinate

Maxillary antrum

Inferior turbinate

Nasal septum

Ethmoid sinus

R L


34 ENT Examination

Fig. 1.54 Sinus endoscopy (antroscopy). A narrow endoscope inserted into themaxillary antrum, either through the thin bony wall of the canine fossa intraorallyor via the inferior meatus of the nasal fossa under the inferior turbinate, gives agood view of the interior of the maxillary sinus, and is helpful in diagnosis.

Fig. 1.53 Transillumination. A brightlight held inside the mouth in a darkroom is an investigation very rarelyused. A dull antrum is, however, an addi-tional sign in the diagnosis of maxillarysinus disease. Transillumination is usefulto assess whether a sinusitis is settling.Dental cysts involving the antrum tran-silluminate brightly.



Fig. 1.57 The postnasal space.Enlarged view of Fig. 1.56 to show theeustachian orifice (1) and posterior endsof the middle (2) and inferior (3)turbinate.

Fig. 1.58 A postnasal cyst (Thorn-valdts, arrow) demonstrated with afiberoptic photograph of the post-nasal space.

Fig. 1.55 The ostium of the maxillarysinus seen through the endoscope.

Fig. 1.56 The postnasal space seen witha fiberoptic endoscope. A panoramicview showing most of the anatomical fea-turees photographed through the fiberop-tic endoscope (see Figs. 1.3, 1.47). (Leftarrow: Eustachian orifice; middle arrow:posterior end of inferior turbinate; rightarrow: posterior border of septum.)

12

3


36 ENT Examination

Examination of the Pharynx and Larynx

Fig. 1.59 Examination ofthe pharynx. A tonguedepressor is necessary toobtain a clear view of thetonsil region in most cases.Patients vary however in howeasily the fauces and posteri-or aspects of the tongue canbe seen. On occasion a veryclear view is obtained (Fig.1.60).

Fig. 1.60 Circumvallate papillae. These are oftenprominent on the base of the tongue. A patient maybe alarmed when looking at the tongue to noticethese normal structures and mistake them for a seri-ous disease. The foliate linguae on the margin of thetongue near the anterior pillar of the fauces maycause similar concern. The top arrow indicates thecircumvallate papillae. The bottom arrow points tothe foliate linguae.


Examination of the Pharynx and Larynx 37

Fig. 1.61 Examination of the larynx using the laryngeal mirror (indirect laryn-goscopy). A good view of the larynx is obtained with most patients. The valleculae,pyriform fossae, arytenoids, ventricular bands, and cords should all be clearly seen.It requires some inhibition of the gag reflex by the patient, and a local anestheticlozenge or spray may be necessary. The tongue is held between the thumb andmiddle finger, and the upper lip retracted with the index finger. This examination isdifficult in children, not only because they may be uncooperative, but because theinfantile epiglottis is curved, unlike the “flat” adult epiglottis, and occludes a clearview of the larynx. Therefore, direct laryngoscopy under anesthetic may be neces-sary to diagnose the cause of hoarseness in a child. Fiberoptic laryngoscopy is nec-essary for seeing the larynx, which cannot be clearly seen on indirect laryngoscopy.


38 ENT Examination

Fig. 1.62 Fiberoptic endoscopy of the upper respiratory tract. When the post-nasal space and larynx are not clearly seen with routine mirror examination, thefiberoptic endoscope, which can be inserted through the nose, gives a view of thenasal fossae, postnasal space, and the larynx. A topical anesthetic is used on thenasal mucosa before the endoscopy is introduced. The field is small, however, and aTV camera may be attached to the endoscope so that a large view may be seen onthe TV monitor—a view that may be shown to the patient.

Fig. 1.63 Lateral radiograph of theneck. A lateral radiograph of the neckgives helpful information about theanatomy of the base of the tongue, lar-ynx, trachea, and upper esophagus. Theupper esophagus (upper arrow) is nor-mally approximately the width of thetrachea (lower arrow). An increase in thewidth of the esophagus is suggestive ofsignificant pathology needing furtherinvestigation, such as a barium swallowradiograph or esophagoscopy.



Taste and Smell

Fig. 1.64 Solutions used to test taste and smell. Four solutions are used to testtaste. The solution is placed on one side of the tongue and the patient is asked toidentify the taste: Sweet, salt, sour, or bitter. This is a relatively crude qualitativetest. Testing for anosmia is done with a series of smell solutions for the patient torecognise.


40 ENT Examination

Fig. 1.65 Anosmia “scratch card” tests: A disk impregnated with a specific odorwhich is released when the disk is scratched with the fingernail. The smell identityis then marked on the card. Quantitative tests are not in routine clinical use,although “olfactometers” with measured odors for smell assessment are described.

Anosmia may be a complication of fracture of the anterior cranial fossa, or itmay follow influenza; recovery is uncommon. Temporary anosmia will occure withsevere nose obstruction. Anosmia is often linked with a complaint of impairedtaste. This is usually found to be normal on testing.

The sensation of smell is an adjunct to the full subtle appreciation of taste. Thedependence on smell for taste appreciation varies from person to person, so that acomplaint of taste loss may or may not accompany anosmia.

One is dependent on the integrity of the patient’s response to smell and tastetests. It is, therefore, often impossible to be certain in medicolegal cases whetheranosmia or ageusia is genuine. With smell, a failure to identify a very strong stimu-lus such as ammonia suggests malingering, as cranial nerve V rather than I isinvolved.



Fig. 1.66a, b Electrogus-tometry. Electricity has ametallic taste, and when asmall current in µa is appliedto the tongue, a quantitativereading can be obtained.The normal threshold on themargin of the tongue isbetween 5 and 30 µa. Thismore refined test of taste isalso of interest in conditionssuch as facial palsy oracoustic neuroma, in whichthe chorda tympani nervemay be involved.

Fig. 1.67 The taste buds. These aremainly situated on the tongue andpalate, and are centered on the fungi-form and circumvallate papillae. Thefungiform papillae (arrowed) degener-ate with age, and are prominent on achild’s tongue. They also atrophy, asseen here, from the right side of thetongue to the mid-line, with the loss ofthe chorda tympani nerve, which may bedivided in ear surgery. The filiform papil-lae account for the rough surface of htetongue and are not related to the tastesensation.

a

b



titoletto sopra 43

Chapter 2The Ear


44 The Ear

The Pinna

DeformitiesThe pinna is formed from the coalescence of six tubercles, anddevelopment abnormalities are common.

Fig. 2.1 Minor deformities. These areof little importance. This shows duplica-tion of the lobule.

Fig. 2.2 Hillocks (or accessory lobules).These are commonly found anterior tothe tragus, and are excised for cosmeticreasons. A small nodule of cartilage maybe found underlying these hillocks.

Fig. 2.3 Darwin’s tubercle (arrow). Adeformity of the pinna of phylogeneticinterest. It is homologous to the tip ofthe mammalian ear and may be suffi-ciently prominent to justify surgicalexcision. Although Darwin’s name isused for this tubercle, Woolmer gavethe first description.


The Pinna 45

Fig. 2.4 Microtia. Absence of the pinnaor gross deformity is often associatedwith meatal atresia and ossicular abnor-malities. Faulty development of the 1st

and 2nd branchial arches results in auraldeformities which may be associatedwith hypoplasia of the maxilla andmandible, and eyelid deformities(Treacher–Collins syndrome, Fig. 2.6b).This type of pinna deformity is difficultto reconstruct.

Fig. 2.5 Surgical reconstruction for microtia. Multiple surgical procedures areusually necessary, and a near-normal pinna is difficult to achieve. Rib cartilagegrafts (1) are taken and fashioned (2) to act as a scaffold for local skin rotation flapsand free skin grafts. The reconstruction is a challenge for the innovative surgeonand results vary with the severity of pinna deformity.

1

2


46 The Ear

Fig. 2.6a, b Gross microtia with a bone-anchored prosthesis and hearing aid.If microtia is gross, a prosthesis rather than reconstruction is to be considered.Prosthetic ears (b) have improved greatly in recent years. It is possible for these tobe attached to the cranium using screws and plates (osseo-integrated implants,see Fig. 1.23) with a bone-anchored hearing aid.

Fig. 2.7 Preauricular sinuses, whichare closely related to the anterior crus ofthe helix, cause many problems. Dis-charge with recurrent swelling andinflammation may occur. The smallopening of the sinus (arrow) is easilymissed on examination, particularlywhen it is concealed, as may rarely bethe case, behind the fold of the helix,rather than in the more obvious anteriorsite.

a b


The Pinna 47

Fig. 2.8 An infected preauricular sinus. A furuncle or skin ulceration in this site isdiagnostic of an underlying infected preauricular sinus. Quite extensive skin losscan occur in this site with recurrent infection of a preauricular sinus. The variationin the appearance of an infected preauricular sinus is striking—but the site in thepreauricular region is constant.


48 The Ear

Fig. 2.9 Preauricular sinus excision. A furuncle or skin inflammation, which maybe quite extensive in this preauricular site, is invariably related to a preauricularsinus. Careful examination for the sinus must be made. Excision when the infectionis quiescent is necessary and this, although minor surgery, is not easy.

A long-branched and lobular structure must be excised. Incomplete excision ofthe tract leads to further infection and the need for revision surgery. To ensurecomplete excision of the preauricular sinus, the extension of an endaural incision asshown is needed, with reflection of the skin anteriorly down to the temporal facia.If the sac is injected with a dye it is better defined, and it is possible to be certain ofcomplete excision. The sac is dissected from its deep aspect towards the sinuspuncture, which is excised with an elipse of skin.


The Pinna 49

Fig. 2.10 Prominent ears. The fold of the antihelix is either absent or poorlyformed in a prominent ear; it is not simply that the angle between the posteriorsurface of the conchal cartilage and the cranium is more “open.” Parents and childmay be offended by the diagnosis of “bat or lop” ears, although these terms arecommonly used.

Fig 2.11 Surgical correction aims to give a natural-looking ear. Techniques aim toavoid a “pinned back” appearance with a sharp, tender antihelix. Reshaping of thecartilage of the pinna is necessary, and recurrence follows simple excision ofpostauricular skin.


50 The Ear

Prominent ears are best corrected between the ages of four and six yearsat the beginning of school. There is, however, no additional surgicalproblem in correcting adult ears. Youngsters may be the subject ofconsiderable ridicule in early years because of bat ears and, therefore,surgical correction is not to be deferred.

Fig. 2.12 Bat ears are often familial (a). The son (b) has the firm ear dressing required for five to ten days after opera-

tion for prominent ears.

a b


The Pinna 51

Fig. 2.13 Prominent ears are often apparent either at or soon after birth. Inthe first six months of life the elastic cartilage of the ear is “moldable.” a–d demon-strate how a baby’s ear can be molded to give a normal shape and produce an anti-helix. After the age of one year, however, the cartilage spring is usually resistant to“molding” techniques.

a b

c d


52 The Ear

Earrings

Fig. 2.14a-c Keloid formation is com-mon in black patients, and is difficult totreat.

Recurrence follows excision, andrepeated excision may lead to hugekeloid formation (c).

Radiotherapy or local triamcinoloneinjections following excision reduce theincidence of recurrence of the keloid.Pressure at the site of keloid excision hasalso been shown to reduce recurrence.Special pressure clip-on earrings areavailable to apply to the ear lobe afteroperation. Keloid formation is commonnear the ear and on the neck, but isalmost unheard of in the middle third ofthe face.

a

c

b


The Pinna 53

Fig. 2.15 Keloid formation may beunpredictable: a normal ear punctumfrom an earring puncture is adjacent toa large earring keloid.

Fig. 2.16 An infected granuloma atthe site of earring insertion.

Fig. 2.17 Nickel sensitivity limits theuse of certain earrings and has causedeczema on the lobule (arrow).


54 The Ear

Fig. 2.18 “High” ear piercing(Fig. 2.17, arrow) complicated by infec-tion (frequently pseudomonas) may leadto abscess formulation. The puncturewith high ear piercing (unlike the lobule)punctures cartilage and may lead to theadditional problem of cartilage infec-tion—perichondritis. Abscess incisionwith drainage, splinting, and antibiotictherapy (e.g., ciprofloxacin) is needed.Permanent deformity of the pinna mayresult, requiring a difficult plastic surgi-cal repair (a). This involves taking a ribgraft and modeling this to reconstructthe absent helix, antihelix, and scaphoidfossa of the pinna (b; c, post-op.).

Fig. 2.19 Trauma. Traumatic “cutting-out” when the earring is pulled by ababy or adult in ill-humor. Infection atthe time the sleepers are inserted isanother hazard (see Fig. 2.16).

a c

b


The Pinna 55

Fig. 2.20a-d Trauma to the pinna. The projecting and obvious pinna is a frequentsite for trauma. Partial or complete avulsion is common. This loss of tissue is from abite. Although small loss of the periphery of the helix can be closed with a wedgeexcision, larger loss (c) requires more complex surgical repair involving cartilagegraft reconstruction of the helix (d).

a

b

c d


56 The Ear

Fig. 2.21 A sebaceous cyst near thesite of an earring puncture. The punc-tum is just apparent and is diagnostic.Sebaceous cysts are common behind theear, particularly in the postaural sulcus.

Fig. 2.22 Hematomas of the pinnafollowing trauma. Bruising with mini-mal swelling settles (a). A hematoma orcollection of serous fluid, however, iscommon, and these, particularly ifrecurrent from frequent injury and leftuntreated, will result in a “cauliflowerear.” The fluid, if aspirated with asyringe (b, c), usually recurs, and inci-sion and drainage may be necessary.Some thickening, however, of theunderlying cartilage invariably takesplace, and a return to a completely nor-mal-shaped pinna is not usual.

b

a

c


The Pinna 57

Fig. 2.23 Perichondritis. A painful red,tender, and swollen pinna accompaniedby fever, following trauma or surgery,suggests an infection of the cartilage.The organism is frequentlyPseudomonas pyocyanea.

Fig. 2.24 Collapse of the pinna carti-lage following perichondritis. Thishappened prior to the availability ofeffective antibiotics. However, perichon-dritis is still a worrying complicationwhich requires intensive antibiotic treat-ment. Collapsing or alteration of theshape of the pinna cartilage may alsooccur in relapsing polychondritis.

Fig. 2.25 Relapsing polychondritis.This is a rare inflammatory conditioninvolving destruction and replacementwith fibrous tissue of body cartilage. Theelastic aural cartilage is replaced byfibrous tissue so that the ear has anunusual “felty” feel and does not haveany “spring” on palpation.

The larynx cartilage also may beaffected, causing hoarseness which mayproceed to stridor. The nasal septum maycollapse with a nasal saddle deformity(Figs. 3.23a–d). One or more of the lowerlimb joints are usually swollen and painful.


58 The Ear

Fig. 2.26 Iodoform sensitivity. Anantiseptic ear dressing commonly usedcontains bismuth, iodoform, and paraf-fin (B.I.P.). Sensitivity to iodoform mayoccur, and a red ear with marked irrita-tion suggests this complication (ratherthan perichondritis, which is character-ized by pain). Neomycin is one of themore commonly used topical antibioticsthat may give rise to a skin sensitivity.

Fig. 2.27 Burn scars in the ear regionare evidence of the past use of cauteryto relieve ear symptoms in childhood. Inthe Arab world, these burns are stillcommon, and are known as chowes.

Fig. 2.28 Erysipelas is caused byhemolytic streptococci entering fissuresin the skin near the orifice of the earmeatus (fissures such as those in otitisexterna). A well-defined, raised erythe-ma spreads to involve the face. This con-dition, which is often accompanied bymalaise and fever, was serious in thepreantibiotic era, but settles rapidly withpenicillin.


The Pinna 59

Fig. 2.29 The herpes zoster virus inthe head and neck may affect thegasserian ganglion of cranial nerve V.Here the mandibular (a) and the maxil-lary (b) divisions are involved. The vesic-ular type of skin eruption is confined tothe distribution of the nerve. The oph-thalmic division of V is most frequentlyinvolved, but all three divisions of V arerarely affected at the same time. Theherpes zoster virus also involves thegeniculate ganglion of cranial nerve VII(Ramsay–Hunt syndrome or geniculateherpes). Herpes affects the pinna andpreauricular region (c), and is associatedwith a facial palsy. In most cases, thereis also vertigo and sensorineural deaf-ness. There is less likelihood of a fullrecovery of the facial palsy than in Bell’spalsy (Fig. 2.100). Treatment is withantiviral agents, e.g., acyclovir, and oralsteroids if not contraindicated.

a

c

b


60 The Ear

Fig. 2.30 Basal cell carcinoma. Ulcerson the helix are common. A long historysuggests a basal cell carcinoma. This istreated with wedge resection. An ulcerof short duration suggests a squamouscell carcinoma or more rarely amelanoma, both of which require moreextensive surgical resection.

Fig. 2.31 Solar keratoses (arrows).These warty growths affect the skin ofthe fair-headed when exposed to strongsunlight. They may become malignant.The skin of the helix may be affectedwith several of these keratoses.


The Pinna 61

Fig. 2.32 Gouty tophi (arrow) from acharacteristic lesion on the helix.

Fig. 2.33 Inflammatory ulcers(arrows) affect the helix and occasional-ly the antihelix. The lesions on the helixare blessed with a lengthy diagnosis—chondrodermatitis nodularis helicischronicis—which presents as a long-standing intermittent ulceration.

It is primarily a chronic chondritiswith secondary skin infection. A wedgeresection of the ulcer and cartilage maybe necessary, as the ulcer only healstemporarily with ointments.

Pressure on the ulcer, e.g., from ahard pillow, is a perpetuating factor.Relief of pressure with a soft “padding”dressing may lead to healing.

Fig. 2.34 Ulcers of the antihelix areusually traumatic (on a particularlyprominent antihelix fold). A basal orsquamous cell carcinoma, however, maypresent on the antihelix.


62 The Ear

The skin of the external auditory meatus is migratory and does notdesquamate.

Cleaning of the ear canal is therefore unnecessary—those whodiligently clean their ears, or those of their children, with cotton buds, forexample, hinder the migration of skin, predisposing to wax accumulationand otitis externa.

Some people have nonmigratory skin of the external auditory meatusand are susceptible to episodes of otitis externa. The meatus tends tobecome occluded with desquamated skin wax and debris, and periodiccleaning of the ear is necessary. The migration of meatal epithelium isalso abnormal in keratosis obturans. In this condition, desquamatedepithelium accumulates and may form a large impacted mass in themeatus, causing erosion of the bony canal.

In the past, skin grafts initially used for myringoplasty often failed orled to otitis externa, because skin taken from elsewhere on the body didnot take on this migratory role. Fascia is used to graft the ear drum.

Although wax normally does not accumulate because of meatal skinmigration, it may impact and cause a hearing loss, which may necessitatesyringing, or suction clearance.

The External Auditory Meatus

a

bFig. 2.35a, b A migrating ink dot.


The External Auditory Meatus 63

dc

e fFig. 2.35c-f A dot of ink, if placed near the center of the drum (c), is found to lienear the margin of the drum after three weeks (d), and between 6–12 weeks thedot migrates outwards on the meatal skin (e, f) to emerge in wax at the orifice ofthe meatus.


64 The Ear

Fig. 2.36 Syringing. The rather largesyringe of old-fashioned appearance haschanged little in the past 100 years, andremains a simple and effective treat-ment for wax impaction. The pinna ispulled outwards and backwards tostraighten the meatus, and water atbody temperature is irrigated along theposterior wall of the ear. The water findsa passage past the wax, rebounds offthe drum and pushes the wax outwards.Hard wax may require the use of soften-ing oily drops before syringing.

Fig. 2.37 A modern ear syringe withan electronically operated pump.

Fig. 2.38 Syringing of the ear. An earshould be syringed without undue forceand with care. A perforation, particularlyin the presence of a thin drum may becaused by over-penetration of thesyringe nozzle. Trauma to the ear canalwith resulting pain occur if the nozzle isclumsily inserted. Care must also betaken to ensure that the nozzle is firmlyconnected to the syringe.

Syringing is not painful, therefore pain means either an error in techniqueor that there is an otitis externa or a perforation. If there is a perforation, theear should not be syringed; pain with vertigo may occur with subsequentotitis media and otorrhea, and a past history of discharge suggests aperforation. Coughing (from the vagal reflex—the auricular branch of thevagus supplies the drum) or syncope may complicate syringing. Vertigowith nystagmus will occur if the water is too hot or too cold.



The main danger of a foreign body in the ear lies in its careless removal.Syringing is effective and safe for small metallic foreign bodies.

Vegetable foreign bodies, such as peas, swell with water and are betternot syringed. Insects not uncommonly become impacted in the meatus,particularly in the tropics. Maggots cause a painful ear, and their removalis difficult. Insufflation of calomel powder is effective treatment.

Previous attempts to remove a piece of plastic wedge in the child’smeatus have led to bleeding in the meatus. The drum against which theforeign body impinges can be seen deep to the plastic.

One must not persevere in attempts to remove an aural foreign body,particularly in a child, as a perforation is easily caused. If immediateremoval with a hook or syringe is not effective, the patient must beadmitted for removal under general anesthetic with the help of themicroscope. It is often dangerous to use forceps to remove an auralforeign body, since the object easily slips from the jaws of the forceps togo deeper into the meatus.

Fig. 2.40 A tick foreign body in theear. The insect was adherent to thetympanic membrane, giving a sensationof discomfort and a deceptive drumappearance on examination; this insectwas removed with syringing.

Fig. 2.39 Foreign body in the ear.


66 The Ear

Otitis ExternaEczema of the meatus and pinna (see Fig. 2.41) may be associated witheczema elsewhere, particularly in the scalp, or it may be an isolatedcondition affecting only one ear. Itching is the main symptom, withscanty discharge. The eczematous type of otitis externa usually settleswith the use of a topical corticosteroid and antibiotic drop. Cleaning ofthe meatus may also be necessary, either with cotton wool on a probe, orsuction and the Zeiss microscope. Otitis externa tends to recur.

The patient should avoid over-diligent cleaning of the meatus, orscratching the ear with the finger, probes, or cotton wool buds. Cottonwool buds, if used, should only be used to the orifice of the meatus. Waterentering the ear during washing or swimming also predisposes to therecurrence of otitis externa.

Fig. 2.41 Eczematous otitis externa.Eardrop sensitivity may worsen an otitisexterna. Chloramphenicol drops causedthis condition. Neomycin less common-ly causes similar reactions. Patientsshould be advised to discontinueeardrops that cause an increase in irri-tation or that are painful.

Fig. 2.42 A furuncle in the meatus isthe other common type of otitis exter-na. It is characterized by pain; pain onmovement of the pinna or on insertingthe auriscope is diagnostic of a furuncle.Diabetes mellitus must be excludedwith recurrent furuncles.



Fig. 2.43 Furunculosis. This is a gener-alized infection of the meatal skin. Painis severe and the canal is narrowed oroccluded so that examination with theauriscope is extremely painful and noview of the deep meatus is possible. Aswab of the pus should be taken, andtreatment is with systemic antibioticsand a meatal dressing (e.g., glycerineand ichthyol, or a corticosteroid creamwith an antibiotic).

The organism may be transferred bythe patient’s finger from the nasalvestibules, and a nasal swab is a relevantinvestigation, particularly with recurrentfuruncles. The lymph nodes adjacent tothe pinna are enlarged with a furuncleor furunculosis, and a tender mastoidnode may mimic a cortical mastoidabscess.

Fig. 2.44 Chronic otitis externa per-sisting for years may eventually lead tomeatal stenosis and rarely to closure ofthe ear canal.


68 The Ear

Fig. 2.45a-c “Deep” otitis externa. Anuncommon form of chronic otitis exter-na involves predominantly the skin ofthe deep bony meatus and the surfaceof the tympanic membrane. The drumepithelium may become replaced withsessile granulations (granularmyringitis) infected with Pseudomonaspyocyanea.

In protracted cases of this type ofotitis externa, the skin of the deep mea-tus and drum becomes thickened and“funneled” with meatal atresia. Theresulting conductive hearing loss isextremely difficult to treat surgicallyonce this condition is quiescent.

a

c

b

Middle ear



Fig. 2.46 “Malignant” otitis externa isa rare and serious form of otitis externato which elderly diabetics are particular-ly susceptible. Granulation tissue isfound in the meatus infected withPseudomonas and anaerobic organisms.This granulation tissue tends to erodedeeply, involving the middle and innerear, the bone of the skull base withextension to the brain, and also thegreat vessels of the neck. If uncon-trolled, the condition may be fatal.

Intense antibiotic therapy some-times associated with surgical drainageof the affected areas is necessary. It isnot a “malignant” condition in the histo-logical sense, for the biopsies of granu-lation tissue show inflammatorychanges only. “Necrotizing” otitis exter-na may be more accurate, but “malig-nant” indicates the serious clinicalnature.

Fig. 2.47 Otitis externa secondary todischarge via a drum perforation is ini-tially treated (an ear swab having beentaken for culture and sensitivity) withcleaning of the meatus and the instillationof the appropriate antibiotic and corticos-teroid drops. If the condition persists withmarked irritation and pain, a fungal otitisexterna should be suspected. In persist-ent infection, the meatus contains a cock-tail of drops, pus, and desquamated skin.In fungal infections, as shown here, thedark spores of Aspergillus niger and whitemycelium of Candida albicans can be seen.Thorough cleaning of the meatus precedestreatment with a topical antifungal agent.

The meatal skin infection is intro-duced from outside—usually from thepatient’s finger, or from water, particularlyafter swimming.

The infection, however, may be fromthe middle ear if there is a perforation,and discharge from chronic otitis mediamay be the cause of a persistent otitisexterna. Otitis externa rarely damagesthe tympanic membrane. With fungalotitis externa, however, and the presenceof a granular myringitis, a perforationmay ensue.


70 The Ear

Fig. 2.48 Bullous otitis externa (bul-lous myringitis). This unusual otitisexterna frequently follows influenza oran upper respiratory tract infection. Acomplaint of earache followed by bleed-ing, then followed by relief of pain isdiagnostic of this condition.

Examination shows hemorrhagicblebs on the drum and meatus, similarto the vesicular eruption of herpes. Ifthere is pyrexia with a conductive hear-ing loss, the otitis externa is associatedwith an otitis media, and systemicantibiotics are necessary. In the absenceof pyrexia and hearing loss, this condi-tion settles spontaneously withouttreatment.

Fig. 2.49 Otitis externa with herpeszoster. Otitis externa occurs with her-pes zoster (see Fig. 2.29c) involvingeither the gasserian or geniculate gan-glion, and the vesicles may be hemor-rhagic.

Carcinomas and melanomas in theskin of the external auditory meatus arerare, but any persistent granulation orskin lesion should be biopsied.



Fig. 2.50 Osteomas. White, bony, hard swellings in the deep meatus are a com-mon finding during routine examination. They usually remain small and symptomfree, and tend to be symmetrical in both ears.

Swimmers are susceptible to these lesions, which are sometimes called “swim-mer’s osteomas.” There is experimental evidence to show that irrigation of thebony meatus with cold water produces a periostitis that leads to osteoma forma-tion. Histologically, these bony lesions are hyperostosis, rather than a bony tumor,so that the term “osteoma,” although established, is not strictly correct.

Fig. 2.51 Large osteomas may narrowthe meatus to a chink so that wax accu-mulates and is difficult to syringe. Otitisexterna is also a complication.

These osteomas, therefore, mayrequire surgical removal with a micro-drill. They should not be removed with agouge, for a fracture with bleeding inthe remaining osteoma is a probablecomplication, causing damage to thefacial nerve and resulting in facial palsy.

It is rare for osteomas to occludethe meatus completely, and in almost allcases no treatment is required.


72 The Ear

The Tympanic Membrane and Middle Ear

Fig. 2.52 “Chalk” patches. White areasof tympanosclerosis (arrows) are com-mon findings on examination of thedrum. They are of little significance inthemselves, and the hearing is oftennormal. A past history of otorrhea inchildhood or grommet insertion isusual. Chalk patches do occur with noapparent past otitis media.

Extensive tympanosclerosis with arigid drum is a sequela of past otitismedia, and the ossicles, too, may befixed or noncontinuous.

Fig. 2.53 Scarring of the drum. a A gossamer-thin membrane can be seen toclose this previously well-defined central perforation (arrow). At first sight with theauriscope, a central perforation would appear to be the diagnosis; more carefulexamination with a pneumatic otoscope will show that this thin membrane movesand seals the defect, giving reassurance that the drum is intact.

b Scarring of the drum with retraction onto the round window, promontory,and incus (arrows) is also evidence of past otitis media. It is sometimes difficult tobe sure whether this type of drum is intact; a thin layer of epithelium indrawn ontothe middle-ear structures may seal the middle ear, and examination with the oper-ating microscope may be necessary to be certain of an intact drum.

a b


The Tympanic Membrane and Middle Ear 73

Fig. 2.54 Scarred tympanic mem-brane. A scarred tympanic membranein which the drum has becomeatelectatic and indrawn onto the longprocess of the incus and promontory(arrows).

Fig. 2.55 A retracted tympanic mem-brane which is thin and indrawn ontothe long process of the incus (a), headof the stapes (b), promontary (c), andround window (d). The stapedius ten-don is also seen in this panoramic viewobtained with a fiberoptic endoscope.

ab

c

d


74 The Ear

Fig. 2.56 Traumatic perforation. Ablow on the ear with the hand is a com-mon cause of traumatic perforationwhich has an irregular margin (a), andthere is fresh blood or a blood clot (b) on the drum.

The defect is frequently slit-shaped (c). Pain and transient vertigo at the time ofinjury are followed by a tinnitus andhearing loss.

c

b

a



Fig. 2.57 Healing perforation. Almostall traumatic perforations heal sponta-neously within two months, a thinmembrane growing across the defect.Traumatic perforations are usually cen-tral, but if the perforation extends tothe annulus, healing may not occur. Theextremely large traumatic perforationsmay also fail to close spontaneously.

Taking care to avoid water enteringthe middle ear and avoiding inflatingthe middle ear with the Valsalva maneu-ver are the only precautions the patientneed take.

A middle-ear infection with dis-charge is the commonest complication,usually settling with a course of topicaland systemic antibiotics. Blast injuries,barotrauma, foreign bodies or theircareless removal, and even over-enthusi-astic kissing of the ear may also causetraumatic perforations.

Fig. 2.58 Central perforation. Acuteotitis media with pus under pressure inthe middle ear may rupture the drum,and although healing usually occurs, apermanent perforation can result. Theseperforations are usually central. A smallperforation may be symptom-free, butepisodes of otorrhea with head coldsand after swimming are common, alongwith a conductive hearing loss.

The otorrhea tends to be profuseand mucopurulent, and may be inter-mittent or persistent. This type of cen-tral perforation, when dry, is successful-ly closed with a fascial graft(myringopalsty).

Other complications with centralperforations are rare, so they aredescribed as “safe” perforations. Acentral perforation may persist after anepisode of acute otitis media and otor-rhea in childhood. Myringoplasty is usu-ally delayed in children since closure bypuberty is common. If, however, theupper respiratory tract is free of infec-tion, and the perforation is the site ofrecurrent infections with impaired hear-ing, these are indications to proceedwith myringoplasty in childhood.


76 The Ear

Fig. 2.59 Marginal perforation. A per-foration may reach the annulus posteri-orly and is called marginal. The middle-ear structures are frequently seenthrough the perforation.

The well-defined margin of theround window is particularly obvious,and the promontory, incudostapedialjoint, and stapedius are also apparent.

Fig. 2.60 A posterior marginal perfo-ration of the eardrum, taken with thefiberoptic camera, showing the roundwindow and head of the stapes. A thinfibrous connection can be seen (arrow)which connects to the necrotic longprocess of the incus. This type of ossicu-lar discontinuity is a common cause ofconductive hearing loss following otitismedia (with or without a perforation).Ossicular reconstruction surgery willrestore the hearing.

Fig. 2.61 Squamous epithelium onthe incus. The marginal perforationmay enable squamous epithelium tomigrate into the middle ear. In this ear,white squamous epithelium has formedon the incus. Marginal perforations,therefore, are described as “unsafe”since there is a risk of cholesteatoma(see Fig. 2.63).



Fig. 2.62 Attic perforation. Debrisadherent to the pars flaccida of thedrum (arrow) suggests an underlyingattic perforation. Perforations of thepars flaccida (attic perforations) areinvariably associated withcholesteatoma formation.

Fig. 2.63 Cholesteatoma. The debris,when removed, exposes a white mass ofepithelium characteristic of acholesteatoma (arrow). Cholesteatomais not a neoplasm; it is simply squamousepithelium in the middle ear.

If ignored, it increases in size,becomes infected, and is associatedwith a scanty, fetid otorrhea. It mayerode bone, leading to serious compli-cations. Extension to involve the durawith intracranial infection may occur,and the facial nerve and labyrinth toomay be eroded. The extent of thecholesteatoma determines the danger:A small attic pocket of epithelium is rel-atively harmless, and can be removedwith suction, but an extensive mass ofepithelium is dangerous and needsexploration and removal via a mas-toidectomy approach.

A chronic discharging ear is notpainful, and persistent pain andheadache, or severe vertigo, stronglysuggest an intracranial complication orlabyrinth.


78 The Ear

Fig. 2.64 Cholesteatoma.Cholesteatoma erodes the bony wall ofthe deep meatus so that a pocket con-taining white debris forms in the poste-rior–superior aspect of the drum(arrow).

The complete etiology of thecholesteatoma is not understood.Migration of epithelium into the middleear via an attic or posterior marginalperforation certainly accounts for mostcholesteatomas. However,cholesteatoma may occur behind anintact drum, and may form with centralperforations. Eustachian tube dysfunc-tion with a negative pressure in the mid-dle ear, if long-standing, leads to achronic middle-ear effusion (chronic oti-tis media with effusion) and a retracteddrum. The pars flaccida retracts andmay give the opportunity for a pocketof cholesteatoma to develop. In this pic-ture of cholesteatoma, the remainder ofthe drum is a golden color and fluid ispresent in the middle ear. This long-standing effusion may have beenresponsible for this cholesteotoma for-mation.

Fig. 2.65 A cholesteatoma of 2 cmdiameter removed at mastoidectomypresents the typical well-defined massof white epithelium. The bone erosionthat this mass causes shows on mastoidradiographs and computed tomography(CT) or magnetic resonance imaging(MRI) scans.



Fig. 2.66 Aural granulation. In thesame way that epithelium may migratethrough a perforation into the middleear, mucous membrane may extrudeoutwards to the meatus. Middle-earmucous membrane extruding through aperforation (arrow) becomes infectedand presents with a discharging ear. Anaural granulation is seen in the deepmeatus. Granulation may also form onthe drum of the margin of the perfora-tion, and rarely granulation tissue formson an intact drum in otitis externa(granular myringitis) (see Fig. 2.45).

Fig. 2.67 Aural polyp. If the growth ofgranulation tissue is exuberant, apedunculated polyp develops, whichmay present at the orifice of the meatus(arrow). Granulations and polyps com-monly arise from the tympanic annulusposteriorly, but the originating site mayalso be the mucous membrane of thepromontory, eustachian tube orifice,and antrum and aditus. Careful andthorough removal of polyps and granu-lation tissue to their site of origin is nec-essary. If the polyp is associated withcholesteatoma, removal by mastoidapproach is required.


80 The Ear

Fig. 2.68 Mastoid abscess. A red,acutely tender swelling filling thepostauricular sulcus (arrow), and push-ing the pinna conspicuously forwardsand outwards, is characteristic of a mas-toid abscess.

In the past, mastoidectomy wasneeded for an acute mastoid abscesscomplicating acute otitis media. Thiswas extremely common in the prean-tibiotic era, and required exenteration ofthe mastoid air cells (cortical mas-toidectomy). The operation is nowrarely performed in countries whereantibiotics are available.

Fig. 2.69 Enlarged meatus after mas-toidectomy. A more extensive type ofmastoidectomy is, however, still neces-sary for cholesteatoma which hasextended beyond the middle ear. Thisoperation often alters the anatomy ofthe ear. Examination after operation willshow an enlarged meatus. At operationthe meatus is enlarged with a meato-plasty to allow access to the mastoidcavity, so that wax can be removed witha Jobson–Horne probe or with suction.This is usually necessary once or twice ayear, as the skin of the mastoid cavitydoes not migrate satisfactorily andtherefore wax accumulates. Waterentering in the ear following mastoidec-tomy should be avoided; infection andotorrhea tend to follow. Syringing of amastoid cavity is also to be avoided, notonly because of the possibility of subse-quent otorrhea but because irrigation ofwater over the exposed lateral semicir-cular canal causes vertigo.



Surgical techniques aim to remove cholesteatoma without exteriorizingthe mastoid cavity, so that relatively normal anatomy is maintainedpostoperatively, and hearing is maintained or improved (intact canal walltympanoplasty), although this operation is not suitable for every case.Although avoiding a mastoid cavity, the intact canal wall tympanoplastytechnique tends to conceal a recurrence of cholesteatoma. There are alsosurgical techniques to obliterate the mastoid cavity with muscle, fascia, orbone grafts.

Fig. 2.70 Auriscope view. With theauriscope, a ridge (containing the facialnerve) can be seen separating the drumanteriorly from the epithelized cavityposteriorly. Failure of the mastoid cavityto epithelize results in an infected cavitywith discharge.

(Top arrow: mastoid cavity; middlearrow: facial ridge with the bone overly-ing the descending portion of the facialnerve; bottom arrow: tympanic mem-brane.)

Fig. 2.71a, b Postaural and endaural incisions. These are two commonly usedincisors for access to the middle ear and mastoid. The postaural incision (a) is pre-ferred if extensive mastoid exenteration is planned. The incision lines are delineatedhere, but in these sites the scars are imperceptible.

a b


82 The Ear

Otitis Media with Effusion (So-called “Glue ear” in Children)A middle-ear effusion is a common cause of conductive hearing loss. Itmay occur when either a head cold or barotrauma interferes witheustachian tube function, and it often follows acute otitis media. Apostnasal space neoplasm may also cause eustachian tube dysfunction,and is to be excluded in any adult with a persistent otitis media witheffusion.

In children, otitis media with effusion is very common when adenoidtissue interferes with the eustachian tube. The middle-ear fluid tends tobe tenacious (“glue ear”), unlike the thin, straw-colored exudate of adults.

The appearance of the drum is altered and the mobility reduced.

Fig. 2.72 Otitis media with effusion with minimal drum change. The drum maylook only slightly different, with a brown color and some hyperemia. A confidentdiagnosis of middle-ear fluid can only be made if reduced mobility is demonstratedand impedance audiometry (Figs. 1.30, 1.31) is needed for confirmation.

a

a b



Fig. 2.73 Otitis media with effusion (“glue ear”). a The color change in this con-dition is often diagnostic, as well as the reduced mobility. The golden-brown colorshowing through the translucent drum is readily apparent in the inferior part of thetympanic membrane.

b A photograph with a fiberoptic camera gives a panoramic view of the deepmeatus and membrane. Bubbles within the fluid and levels appearing as a hairlinein the drum may be seen. A “chalk” patch is also seen (arrow).

a b

Fig. 2.74 Otitis media with effusionwith marked drum change. Thechange is frequently gross, making thediagnosis obvious, with a golden color, aretracted membrane, and a prominentmalleus.

Fig. 2.75 A vesicle on the drum (arrow)often occurs in children’s glue ear.


84 The Ear

The full etiology of the eustachian tube dysfunction causing otitis mediawith effusion is at present unknown. Opinions, therefore, differ on thetreatment, particularly that of children’s “glue ears.” Adenoid tissue in theregion of the eustachian tube orifice predisposes to “glue ears,” andadenoid removal is frequently necessary.

Glue Ear“Glue ear” is common between the ages of three and six years, anduncommonly persists after 11 years. The hearing loss is often slight andvaries with colds. The self-limiting nature of the condition calls forconservative treatment, but “glue ears” are not to be ignored.

A marked and persistent hearing loss, interfering with schooling,necessitates surgery. Episodes of transient otalgia are common with “glueears,” and frequent attacks of acute otitis media may occur. The drum mayalso become retracted and flaccid with prolonged middle-ear fluid. Thesefeatures may necessitate insertion of a grommet to reventilate the middle ear.

With glue ear associated with upper respiratory tract symptoms orwith proven atopy, the use of an antihistamine and nasal steroid sprayassist the resolution of the middle-ear effusion.

Fig. 2.76 Blue drum. The middle-eareffusion alters in composition, and atsome stages in otitis media with effu-sion the drum appears blue in color—theso-called “blue drum.”

A similarly blue appearance of thetympanic membrane is seen followinginjury when bleeding occurs in the mid-dle ear (hemotympanum). The conduc-tive hearing loss associated with thisinjury resolves with resorption of themiddle-ear hematoma. A persisting con-ductive hearing loss following injury,however, suggests injury to the ossicleswith an ossicular discontinuity (see Fig. 2.88).

Otitis media with effusion often set-tles spontaneously.



Fig. 2.77 Myringotomy. If otitis mediawith effusion with poor hearing persistsfor over three months, myringotomy(under general anesthetic in children)with aspiration of the fluid is often necessary.

An arrow indicates the radial incisionof the myringotomy into which thegrommet may be inserted. The posteri-or/superior quadrant of the drum is notused to avoid injury to the underlyingincus and stapes.

Fig. 2.78 Grommets. a The insertion of a grommet, a flanged teflon tube, is fre-quently needed to avoid a recurrence of middle-ear fluid. b A mini-grommet causesless drum trauma, but extrusion is more rapid.

a b


86 The Ear

Fig. 2.79 Grommet insertion. Amyringotomy incision in the posteriorhalf of the drum may damage the incud-ostapedial joint or round window, and agrommet inserted posteriorly maycause incus necrosis from pressure onthe long process: An anterior or inferiorradial myringotomy is a safer incision.

Fig. 2.80 A grommet in place. Thegrommet tube ventilates the middle earand acts instead of the eustachian tube.Hearing and the appearance of thedrum both return to normal.

The grommet usually extrudesspontaneously between 6–18 monthsto leave an intact drum, and is found inwax in the meatus. With recurrent mid-dle-ear fluid, repeated grommet inser-tion may be needed. If normal eustachi-an tube function has not returned andotitis media with effusion recurs, thegrommet is replaced.

Tympanosclerosis and drum scar-ring ensue. This complication is alsoseen in untreated “glue ear.” Minimalsurgical trauma during grommet inser-tion is advisable. However, with a nar-row ear canal, grommet insertion is notalways technically easy.



The Patulous, or “over-patent” Eustachian TubeObstruction of the eustachian tube is a common and frequently diagnoseddisorder. Abnormal patency of the tube (the patulous eustachian tube),however, is also not uncommon, and the diagnosis is frequently missed.

The condition tends to occur in people who have lost weight orwomen who are taking “the pill” or are pregnant. The symptoms are of asensation of blockage in the ear, with normal hearing or minimal loss.Patients may comment that they hear themselves breathe and eat, andhear their own voice “echo” in their ear. This sensation may alter withhead movement (wrongly suggesting middle-ear fluid), and often isabsent on lying down. Fortunately, the symptoms are usually minor andsettle spontaneously. Reassurance and explanation suffice as treatment inmost cases. Failure to make the diagnosis, however, and treatment of thecondition as eustachian tube obstruction is common.

Chronic Otitis Media With EffusionMiddle-ear fluid, if persistent, may cause permanent changes in thedrum. An otitis media with effusion can cause hearing loss for decades,and the diagnosis is frequently overlooked in a long-standing hearingloss. Impedance audiometry helps in diagnosis.

Fig. 2.81 Grossly altered drum. Abrown color, with retraction of a flaccidmembrane onto the ossicles andpromontory, is seen with long-standingmiddle-ear fluid. (Bottom arrow:indrawn drum onto the promontory;top arrow: incudostapedial joint.)


88 The Ear

Fig. 2.83a The grommet lumen may also become obstructed with blood if themyringotomy incision bleeds excessively.

b Infection with a granuloma may also occlude the lumen. Although thistype of granuloma may respond to an antibiotic and steroid eardrops, it is fre-quently necessary for the grommet to be removed.

Fig. 2.82 Grommet occluded withexudate. Insertion of a grommet inthese chronic adult cases may restorehearing, but frequently either the lumenof the grommet becomes occluded withexudate, which may extrude throughthe tube into the meatus, or a constantotorrhea occurs.

There is no successful treatment atpresent for chronic otitis media witheffusion when this fails to respond toinsertion of a grommet. A further prob-lem with chronic otitis media with effu-sion is the return of middle-ear fluidwith hearing loss when the grommetextrudes. A larger flanged grommet(long-term grommet) which remains inposition longer, and periodic replace-ment are the present remedies.

a

b



Acute Otitis MediaEarache with conductive hearing loss and fever accompanying a head coldcharacterize acute otitis media. The drum is red and the landmarks areobscured; drum distension and pulsation may be seen.

Otitis media is common in children, probably due to their short, wideeustachian tube and the presence of adenoids which may be infected nearthe orifice. Rupture of the tympanic membrane in acute otitis media is notuncommon and muco-purulent otorrhea ensues with a pulsatiledischarge. Penicillin is invariably curative, and complications are rare.

The middle-ear infection frequently settles without otorrhea, but ifthe drum does rupture, a pulsating muco-purulent discharge filling themeatus is diagnostic of otitis media. A swab for culture and sensitivity istaken in these cases, although the ear usually becomes dry within 48hours of penicillin therapy, and the perforation closes in most cases withlittle or no scarring.

Acute mastoiditis, previously serious and common, is almost unheardof where antibiotics are available. Myringotomy and corticalmastoidectomy are operations of the past for acute otitis media.

Otitis media with effusion after the acute attack is the maincomplication today.

Fig. 2.84 Occlusion of thegrommet lumen. Excessbleeding at the time of inser-tion may cause this problem,or subsequent occlusionwith serous exudate. Thereare various designs of grom-met or ventilation tube, andthis Y-shaped tube showsthe narrow lumen to beoccluded.


The histology of a glomus jugulare tumor (Fig. 2.86) is similar to thecarotid body tumor, with which it may coexist. If the glomus tumoroccupies the middle ear, it can be removed via a tympanotomy ormastoidectomy approach. When the jugular foramen is involved with lossof the cranial nerves IX, X, and X (often XII from the anterior condylarforamen is also affected), the treatment is difficult. A surgical approach tothe skull base is needed via the mastoid and neck, with a neurosurgicalexposure if there is an intracranial extension.

If the tumor is surgically inaccessible, radiotherapy does slow thegrowth of an already very slow-growing tumor, and has an importantplace in the management, particularly in the more elderly patient.Microembolism under radiographic control of the vessels supplying thetumor is a further modality used in the treatment of these very vascularlesions, prior to surgery.

90 The Ear

Fig. 2.85 Acute otitis media withbulging and hyperemia of the posteri-or–superior quadrant of the tympanicmembrane. This is the typical earlyappearance of acute otitis media pho-tographed with a fiberoptic camera.

Fig. 2.86 Glomus jugulare tumor. Aphotograph, via the fiberoptic endo-scope, showing a glomus jugularetumor presenting, as is characteristic,with a hyperemia in the lower half of thedrum. Middle-ear fluid is often present,and a meniscus is also seen (arrow).



Fig. 2.88 Injury to the ear ossicles.This may follow head injury. Dislocationof the incudostapedial joint is common-est (approx. 75%) (arrow), but fractureof the stapes crura and disruption of thestapes footplate also occur.

Barotrauma causing marked mid-dle-ear pressure change, e.g., from div-ing or flying, may also disrupt the stapesfootplate ligament or rupture the roundwindow, causing perilymp fluid from theinner ear to pass into the middle ear(arrow)—a perilymph fistula. A fluctuat-ing sensorineural hearing loss and verti-go ensue.

Fistulae often heal spontaneously,but a persistent perilymph leak needs tobe sealed surgically.

Fig. 2.87 Bleeding. Bleeding from theear or a red or “blue” drum (see Fig.2.76), if the tympanic membrane doesnot rupture, may also follow a base-of-skull fracture with bleeding into themiddle ear.


Otosclerosis: Hearing Loss Due to Fixation of the Stapes Bone

92 The Ear

Fig. 2.89 Otosclerosis. This is a common cause of bilateral symmetrical conduc-tive hearing loss in adults.

The stapes footplate is ankylosed in the oval window by thick vascular bone.This curious bony lesion is usually an isolated middle-ear focus. It may be associat-ed, however, with osteogenesis imperfecta tarda, and blue sclerae are occasion-ally seen with otosclerosis.

Otosclerosis is familial and more common in women (otosclerotic hearing lossincreases during pregnancy, which may account for the apparently higher inci-dence in women). Patients frequently notice paracusis, in which there is improvedhearing with background noise. The cause of otosclerosis remains unknown.

Fig. 2.90 The stapes. The smallestbone in the body. It is, like the otherossicles, adult size at birth.



Fig. 2.92 There are several types ofprosthesis, of which teflon (left) andteflon-wire are commonly used.

Fig. 2.91 The stapedectomy opera-tion. The operation for hearing loss dueto otosclerosis involves removal or per-foration of the ankylosed stapes boneand replacement with a mobile prosthe-sis. This very successful operation wasdevised by John Shea of Memphis, Ten-nessee, United States, in 1957, and wasa great advance in surgery, with goodhearing achieved in over 90% of cases.

The diagram shows the attachmentof the stapes prosthesis to the longprocess of the incus; the distal end ofthe prosthesis is placed through theopening made in the ankylosed stapesfootplate. The lower diagram shows theexposure of the middle ear forstapedectomy. The drum is reflectedanteriorly, hinging on the long processof the malleus. The stapes superstruc-ture and part of the footplate areremoved, and the prosthesis inserted.(M: malleus; I: incus;VIII: vestibulocochlear nerve.)


94 The Ear

Fig. 2.94 A teflon-wire prosthesis(top arrow). The distal end is enteringthe inner ear through the hole in thefootplate (bottom arrow).

Fig. 2.93 Stapedectomy—opening inthe fixed footplate. An opening ismade in the fixed footplate (arrow). Thewhite marks to the right of this openinginto the inner ear are the otoliths.

The prosthesis is attached to thelong process of the incus, and the distalend of the prosthesis is placed into theinner ear.



Fig. 2.95 Fat-wire prosthesis. The wireloop is closed on the incus (top arrow)and a fat graft (middle arrow) seals theoval window. The bone covering thefacial nerve (bottom arrow). It is impor-tant for the stapedectomy prosthesis tobe closed like a ring on the finger on thelong process of the incus.

This ensures that the prosthesis willnot slip, but also that pressure does notpredispose to incus necrosis. Thelentiform nodule on the incus is pre-served and is a further factor ensuringthat the prosthesis/incus attachment issecure.

Fig. 2.96 The distal end of the pros-thesis must not only lie precisely inthe stapedectomy (or stapedotomy)opening but a “seal” is required toavoid a perilymph fistula and leakagefrom the inner ear fluid into the middleear. A vein graft (arrows) is one of theoptions for this seal.

Fig. 2.97 Conductive hearing lossvery similar to otosclerosis is seenwith Paget’s disease. The bonychanges seen with Paget’s disease, how-ever, tend to affect the entire ossicularchain and not specifically the stapes.

Surgery for conductive hearing losswith Paget’s disease is usually not advis-able and hearing aids are to be pre-ferred.


96 The Ear

Microsurgery

Fig. 2.98 The middle-ear operating microscope. Middle-ear surgery is possiblebecause of the development of the middle-ear operating microscope. This appara-tus makes the drum, ossicles, and other middle-ear structures easy to manipulatewith fine instruments. The microscope is sterilized with a drape, and a camera andvideo camera and tutor arm can be attached.

Fig. 2.99 Operating microscope.A TV camera can also be attached tothe microscope, with a monitor givingthe surgeon and observers a goodoperative view.


97

Facial Palsy

Facial palsy may follow skull fracture or facial nerve laceration near thestylomastoid foramen, and is also an uncommon complication of middle-ear surgery and superficial parotidectomy. An extensive cholesteatoma ormiddle-ear carcinoma may also damage the facial nerve. In the absence ofa careful examination of the tympanic membrane, such a case may bewrongly diagnosed and treated as Bell’s palsy. All facial palsies shouldhave an otological assessment.

Bilaeral facial palsy is an interesting rarity. It is the facial asymmetryof facial palsy that is conspicuous and makes the diagnosis obvious; abilateral facial palsy may not be so readily diagnosed.

Fig. 2.100 Bell’s palsy is the common-est cause of facial palsy and is a lowermotor neuron lesion of the facial nerve,of unknown etiology, involving a loss ofmovement of facial muscles, usuallytotal, of one side of the face. Thisincludes the muscles of the forehead(with facial paralysis due to an uppermotor neuron lesion, such as a stroke,these muscles continue to function dueto cross innervation distal to the cortex).

Pain in or around the ear frequentlyprecedes Bell’s palsy, and a history ofdraught on the side of the face may besignificant. Bell’s palsy may be recurrentand associated with parotid swelling(Melkersson–Rosenthal’s syndrome).

The etiology and management ofBell’s palsy is controversial, althoughthe cause is almost certainly viral.

Edema of the facial nerve near the stylomastoid foramen has been demonstrated.Most Bell’s palsies recover completely and spontaneously within 6 weeks. If seen inthe early stages, however, antiviral treatment and prednisolone orally should begiven. Providing there is no general medical contraindication to steroids, “a” sug-gested dose of prednisolone is: *20 mg q.d.s. five days: 20 mg t.d.s. one day: 20mg b.d. one day: 20 mg o.d. one day: 10 mg o.d. one day. Physiotherapy main-tains tone in the muscles during recovery and also has a place in the managementof Bell’s palsy. Bilateral facial palsy is very rare. These cases, however, require inves-tigation to exclude underlying disease, e.g., Lyme disease, sarcoidosis.


98 The Ear

Fig. 2.101a, b Tests of facial nerveinvolvement. The level of involvementof the facial nerve in facial palsy can bedetermined by:1 Taste (electrogustometry): if taste isabsent or impaired, the lesion is proxi-mal to the chorda tympani.2 Stapedial reflex (impedance audiome-try).3 Lacrimation (Schirmer’s test, b). Lit-mus paper is placed under the lower lid.If the facial nerve lesion is proximal to,or involves the geniculate ganglion, thetears are reduced. These tests are reliable in traumatic sec-tion of the facial nerve to detect thelevel of injury. In Bell’s palsy, the testsare of little value.

a

b


titoletto sopra 99

Chapter 3The Nose


100 The Nose

Deformities

Fig. 3.1 Congenital deformities.Abnormal fusion of the nasal processesis uncommon, and may result in varyingdegrees of deformity.

In this case, the nose is bifid withhypertelorism (the distance betweenthe eyes being greatly increased). Inmilder cases, the bifid appearance of thenose is less marked, and may justappear as a rather “wide” nose.

Fig. 3.2a, b Congenital absence of the nose is a rarity. With total atresia, thiscondition, as with bilateral atresia of the posterior choanae, presents an airwayobstruction emergency.

a b


Deformities 101

Fig. 3.3a, b Congenital atresia of one posterior choana. This congenital defor-mity may not present until adult life. A total unilateral obstruction from birth maycause suprisingly little trouble to the patient. If, however, the symptoms aremarked, the atresia can be treated surgically with removal of the bony obstruction.

Bilateral atresia presents with dyspnea soon after birth. Immediate surgicalcorrection is required. A membranous atresia may be perforated and dilated usingmetal sounds, but if the atresia is bony it must be opened with a drill, using either atransnasal or transpalatal approach. Indwelling portex tubes are left in place for upto six weeks postoperatively to prevent a recurrence of the stenosis. Choanal atre-sia is well demonstrated on a computed tomograph (CT) scan, which is diagnostic.The arrow indicates the bony choanal atresia, which can be compared with the nor-mal size. Closure of the posterior choanae with choanal atresia is well seen on thisfiberoptic photograph of the postnasal space (b).

Fig. 3.4a, b Hemangiomas of the face and nose present in babies and are a cos-metic problem. Treatment is deferred, for regression in about 70% of affected chil-dren is completed by age seven.

a b

a b


102 The Nose

Fig. 3.5 Nasal glioma. This curiouspolypoid swelling presents in the nosesof children or babies. A biopsy confirmsthe nasal glioma, which is usually an iso-lated entity attached to the septum. ACT scan is needed to exclude the possi-bility of an intracranial attachment, butthis is rare. This is a benign lesion.


Cysts 103

Cysts

Fig. 3.6 Nasoalveolar cysts have aconstant anatomical site and spot diag-nosis is possible. Externally, there is flat-tening of the nasolabial fold and flaringof the alae nasi. In the anterior nares thecyst extends into the floor of the noseand displaces the inferior turbinateupwards. Excision via a sublabial incisionand enucleation is the treatment. Surgi-cal rupture of the cyst usually meansincomplete removal, and predisposesto recurrence. The arrow indicates “flar-ing” of ala.

Fig. 3.7 Nasoalveolar cysts.


104 The Nose

Fig. 3.8 Dermoid. A cystic swellingnear the glabella is probably a dermoid;excision may not be straightforward. Thedifferential diagnosis in childhood is thenasal glioma. There is commonly a sinusconnecting the cyst to a punctum onthe skin near the nasal tip, and theremay be extension of the cyst deep to thenasal bones as far as the cribriform plate.


Cysts 105

Fig. 3.10 Nasal papilloma excision. Excision is not straightforward. An ellipticalexcision with closure will produce an obvious nasal asymmetry, and more elaboratetechniques are required to ensure a satisfactory result, e.g., an island sliding flap (a,b, c,).

Fig. 3.9 Nasal papilloma. Benignlesions on the nose such as a mole orpapilloma are common. If large, howev-er, the obvious site on the nose necessi-tates excision and biopsy.

a b

c d


106 The Nose

a bFig. 3.11a, b Rhinophyma, in which the skin becomes thickened and vascular,may produce gross nasal deformity in which the skin epithelium becomes thick-ened and vascular. “Shaving” of the excess skin (without skin grafting) is the surgi-cal treatment. Irregular areas of epithelium (arrow) should be sent for histologysince basal- or squamous cell carcinoma may occur within a rhinophyma.


Cysts 107

a

bFig. 3.12a, b Basal cell carcinoma (rodent cell carcinoma) are common on thenose, face, and ear. Any persistent ulcer, which may bleed, or area of indurationshould arouse suspicion.

Excision, radiotherapy, or laser treatment is curative for early lesions. Moresuperficial lesions respond to fluorouracil cream. Deeply erosive basal cell carcinomasmay be difficult to resect or cure. Many basal cell carcinomas require wide excision.

A simple elliptical excision leads to unnecessary scarring, which is to be avoid-ed on the face. Incisions are made in the relaxed skin tension lines of the face and anumber of flaps devised, e.g., the rhomboid as demonstrated here to minimizescarring.


108 The Nose

a

c

b

dFig. 3.13 Scar revision. a When a scar on the face is prominent, simple excisionand resuturing does not always give an improved result. b The “breaking-up” of theline when the scar is excised makes a scar considerably less evident. Facial scars maybe improved markedly with techniques such as these but complete eradication israrely possible. c One month after scar revision. d Nine months after scar revision.


Adenoids 109

Persistent snoring in a child is the main symptom of enlarged adenoids.In day-time there is mouth breathing. Purulent rhinorrhoea (if there issecondary sinusitis) and epistaxis also occur, with or without nasalsymptoms. There is hearing loss due to otitis media with effusion, orearache from recurrent acute otitis media.

Adenoids normally regress before puberty and adults with largeadenoids are rare. If an adult has nasal obstruction due to postnasallymphoid tissue, the histology is essential to exclude a lymphoma.

Nasal obstruction may occur from birth due to large adenoids, and thebaby has difficulty with bottle and breast feeding. It is occasionallynecessary to remove these “congenital adenoids” in toddlers.

A conservative attitude should be taken, however, with removal ofadenoids awaiting regression of the lymphoid tissue. Adenoidectomyalone is not common surgery. Tonsillar enlargement is usually alsopresent, and is an additional cause of the upper respiratory tractobstruction and snoring.

Adenoids

Fig. 3.14 Adenoids. A mass of lym-phoid tissue shaped like a bunch ofbananas occupies the vault of the post-nasal space in children. If the adenoidsare large, nasal obstruction occurs.


110 The Nose

Fig. 3.15 Lateral radiograph of adenoids. The postnasal space is often difficult orimpossible to see in a child, and a lateral radiograph clearly shows the size of theadenoids and degree of obstruction. In this radiograph, a small airway is present(lower arrows) despite a large adenoid shadow (upper arrow).

Fig. 3.16 Accurate lateral radiographs are necessary. A wrongly angled radi-ograph (a) is not infrequently erroneously reported as showing “large adenoids.” Itis not easy to maintain a child in the correct position; patience and skill are requiredby the radiographer. When checking the lateral radiograph for adenoids, therefore,it is essential to be sure that the lateral picture is true (b) before assessing the bulkof the adenoid lymphoid tissue.

a b


Adenoids 111

Fig. 3.17 Fractured nose.This common injury onlyrequires treatment if the sep-tum is dislocated or involvedin hematoma, or if there is anexternal deviation of the nosewhich is of cosmetic concernto the patient (a: seenfrontally; b :most obviouswhen examined from above).It is important to reducenasal fractures within twoweeks, lest the bones cannotbe manipulated and a subse-quent rhinoplasty or refrac-ture may be necessary.Reduction, therefore, is eithercarried out soon after thefracture or delayed until theedema, which makes assess-ment of the deformity diffi-cult, has settled (usually with-in four to 10 days). Manyfractured noses, however, are“chip” or undisplaced crackfractures with hematoma,and require no treatment.

a

b


112 The Nose

Trauma

Fig. 3.18 Surgical emphysema of theorbit. An alarming and unusual compli-cation of a nasal fracture is surgicalemphysema of the orbit when thepatient blows the nose or sneezes. Thisis due to a fracture through the eth-moidal cells and lamina papyracea, link-ing the nasal cavity to the orbit. There isno cause for alarm, and if care is takennot to inflate the orbit, spontaneoushealing follows. The characteristic crepi-tus on palpation is diagnostic. A facialinjury that has caused a nasal fracturemay also have involved the maxilla andanterior cranial fossa (with cerebrospinalfluid rhinorrhea), and precautionsshould be taken to exclude such anassociated fracture as well as any possi-ble injury to the eye.

Fig. 3.19a, b Radiographs of nasal bones showing complete separation of onebone. In this case, the nasal bone radiograph shows some obvious and significantinjury. In almost all instances, however, the radiographs for a fractured nose are oflittle practical value, although they may be of medicolegal significance.

a b


Trauma 113

Complications of a Fractured Nose

Fig. 3.20a-c A septalhematoma following trau-ma to the nose. Blood col-lects under the subperichon-drium on both sides, causing“ballooning” of the septumand total nasal obstruction.If the nasal obstruction istotal, early drainage of thehematoma is required. Awarning must be given pre-operatively that nasal sad-dling of the dorsum mayensue, the hematoma havingled to necrosis of the septalcartilage. Septal swellingwith partial nasal obstruc-tion usually settles sponta-neously, and drainage is notnecessary. The hematoma, ifleft, may become infected.Pain and malaise accompanythe total nasal blockage.Draining is necessary, andsaddling is then common(see Fig. 3.21).

a

b

c


114 The Nose

Fig. 3.21 Nasal saddling.Minimal saddling, as inthis patient (a) may accen-tuate a previous nasalhump. Simple lowering ofthe nasal bones restoresthe appearance of a nor-mal nose (b).

Fig. 3.22a, b A saddle nasal deformity following trauma, and a septalhematoma. This was repaired with cartilage graft taken from the concha of the ear.

a

a b

b


Trauma 115

Fig. 3.23a-d Grafts. With more severe saddling, a graft is needed to restore thenasal contour. Cartilage, bone, or a synthetic are alternative grafting materials.

a b

c d


116 The Nose

Fig. 3.24 Iliac crest bone graft. An iliaccrest bone graft (arrow) used for a sad-dle deformity is demonstrable on thisradiograph.

Fig. 3.25 Synthetic graft. A syntheticgraft (silastic) seen on radiograph(arrow), is also used to correct nasalsaddling.


Trauma 117

Fig. 3.26 Septal hematomas in childhood. Septal hematomas are not uncom-mon in children, and may follow trauma or be spontaneous, in which case a blooddyscrasia needs to be excluded. The parents should be warned that the develop-ment of the nose may be retarded, and may lead to a “small” nose in adult life. Inthe past, surgical correction was left until the nose was fully grown at age 16–17,but it is now apparent that grafting of these saddle deformities in childhood willlead to more normal nasal development. a A childhood saddle deformity beforegrafting (age seven). b After grafting (age seven). c Age 11. d A normal nose andnot an infantile nose has developed as a result of grafting in childhood (age 19).

a b

c d


118 The Nose

a bFig. 3.27 Nasal plastic surgery. a A small infantile nose following a septal abscessin childhood. b Nasal plastic surgery using cartilage and composite ear grafts givessignificant improvement.

Fig. 3.28 Retraction of the columella.Retraction of the columella (arrow) andloss of tip support of the nose are lessusual complications of a septalhematoma.


Trauma 119

Rhinoplasty

a b

e f

c d

Fig. 3.29 Rhinoplasty. The appearance of a nose with a congenital or traumatichump of the nasal bones can be improved with rhinoplasty (a, b; c, d). A deviatednose may be straightened (e, f).


120 The Nose

a b

c d


Trauma 121

Fig. 3.30a-f Nasal tip rhinoplasty. Bulbous or bifid nasal tips can be modified (a,b). Incisions for rhinoplasty are within the nasal vestibule and access to the nasalbones, cartilages, and septum may be obtained with an intranasal (or external, seeFig. 3.31) approach.

e f


122 The Nose

Fig. 3.31a-c External rhinoplasty. Atransverse incision across the columella(with a “notch” to give a minimally per-ceptible scar) enables the skin of thenose to be elevated superiorly with expo-sure of all the underlying structures (b).

This rhinoplasty approach is usedfor many of the grosser nasal deformi-ties, e.g., cleft-lip nasal deformities. Italso enables lesions on the dorsum ofthe nose to be excised without an obvi-ous overlying scar. The lesion beingremoved here is a nasal sinus (c).

a

c

b


Trauma 123

Fig. 3.32 Mentoplasty. The improvement with rhinoplasty in this case has beenaccentuated by mentoplasty.

a

Fig. 3.33 A silastic implant has beeninserted adjacent to the mandible. Areceding chin is not to be overlooked ina patient seeking rhinoplasty, for itaccentuates the nasal deformity, andmentoplasty gives a subtle but strikingimprovement in appearance.This implant may be introduced eitherby an external submental incision or onintraoral incision via the mucosa of thebuccal sulcus.

b


124 The Nose

a

c

bFig. 3.34 Marked mandibular under-development (a) in which a mandibularadvancement to restore dental occlu-sion as well as the esthetics was com-bined with a rhinoplasty (b). The radi-ograph (c) shows the sliding advance-ment and wiring of the mandibularbone.


Trauma 125

Deviated Nasal SeptumA congenital or traumatic dislocation of the septal cartilage into one nasalfossa causes unilateral nasal obstruction. If the obstruction is marked, orcomplicated by recurrent sinusitis, a septal correction is effective surgery.

The time-honored operation for this is a submucous resection (SMR),but a septoplasty in which cartilage is preserved and repositioned—ratherthan removed—is now used. The SMR operation involves removal of muchof the septal cartilage and loss of nasal support with saddling, and septalperforations are occasional complications.

a bFig. 3.35 Deviated nasal septum into the columella. With caudal dislocation ofthe septum, an obvious deformity is coupled with nasal obstruction (a). Reposition-ing or excision of the septal dislocation is necessary to improve the appearance andairway (b).

Fig. 3.36 Deviated nasal septum. Deviated nasal septum with a spur of septalcartilage and maxillary bone occluding the inferior meatus and causing nasalobstruction (see over).


126 The Nose

Fig. 3.38 A posterior spur (arrow)on a deviated nasal septum seenwith the endoscope. Most septaldeviations can be seen with a specu-lum but are seen with greater claritywith the endoscope, and the applica-tion of a nasal vasoconstrictor to themucosa.

Fig. 3.39 The septoplasty operation.An incision through the nasal mucosaand cartilage with elevation of themucoperichondrium (arrow) givesaccess to the septal cartilage, which ispartially resected and repositioned.

Fig. 3.37 Septoplasty technique.


Trauma 127

Perforations of the Nasal Septum

Fig. 3.40 Deviated nasal septum in achild. The diagnosis is obvious withoutthe use of a nasal speculum. Elevation ofthe infantile nasal tip suffices to give aclear view of the anterior nares.

Fig. 3.41 A perforation of the nasal sep-tum. This may not give rise to any symp-toms, and be a chance finding on exam-ination. Crusting usually occurs, howev-er, causing nasal obstruction and dis-comfort, with episodes of scanty epis-taxis.

Fig. 3.42 Prominentblood vessels appearing onthe margin of the perfora-tion, leading to epistaxis. Awhistling noise on breath-ing is another symptom.


128 The Nose

Perforations may result from repeated trauma to the septum (e.g., nosepicking). Chrome workers are susceptible to a septal perichondritiscausing a perforation. An inadvertent tear of the nasal mucous membraneon both sides during septal surgery is another cause of perforation.

Destruction of the vomer and ethmoid bone accounts for a posteriorseptal perforation, and may be due to a gumma. Surgical repair of septalperforations, particularly large ones, is not easy. Composite cartilagegrafts taken from the concha of the ear combined with mucosal rotationflaps of the nasal mucous membrane form the basis of most techniques.Plastic flanged prostheses may be fitted to seal the perforation, but mayextrude, or be incomfortable.

Fig. 3.43 Vestibulitis. When nasal dis-charge and skin involvement affect bothnostrils, a vestibulitis (an eczema of thevestibular skin) is the probable diagno-sis. This condition responds rapidly to anantibiotic ointment. The nasal swab usu-ally grows a staphylococcus.


Trauma 129

Fig. 3.44 Unilateral nasal vestibulitis and discharge (purulent and fetid in a) isalmost always diagnostic of a foreign body in a child's nose, as is unilateral nasalvestibulitis alone (b).

a

b


130 The Nose

Fig. 3.45 Removal of a foreign body.Removal frequently can be managed asan outpatient, when it is necessary tohold the child securely while a probe orhook is placed posterior to the foreignbody. Forceps frequently push the for-eign body posteriorly, and thus shouldbe avoided. A general anesthetic is nec-essary if the foreign body is impacted orinaccessible.

Fig. 3.46 Rhinolith. A foreign bodythat is ignored accumulates a calcare-ous deposit and presents years later as afetid, stony, hard mass—a rhinolith. Thisis well demonstrated on x-ray, and a rhi-nolith may become large, eroding thelateral wall and floor of the nose.

Although at first sight appearingeasy to remove, the impaction may beextremely firm, particularly with thelarger rhinoliths.


131

Inflammation: nasal vestibulitis

Fig. 3.47 Vestibulitis presents as crusting and irritation in the anterior nares withresulting nasal obstruction. Examination shows excoriated vestibular skin and sep-tal mucous membrane. Rubbing or over-diligent cleaning of the nose by the patientusually causes vestibulitis, particularly if, as in this case, the septum is deviatedanteriorly and impinges on the lateral wall of the nose. Advice and the use ofantibiotic and corticosteroid ointment are effective in controlling vestibulitis. Cor-rection of the septum may be necessary.

Fig. 3.48 Nasal vestibulitiswith squamous epitheli-um replacing the mucosa.A deviation of the septumhas predisposed to a chron-ic vestibulitis. Digital irrita-tion, or the use of cocaine,which may also lead to aseptal perforation, mayunderlie this problem.


132 The Nose

Fig. 3.49 Vestibulitis in achild overlying a grosslydeviated anterior septum.Septal surgery is avoided inchildren, but cases in whichthe obstruction is grossrequire a conservative sep-toplasty. Exessive cartilageresection may retard nasalgrowth, predisposing tosaddling or an infantile nose(Fig 3.27a).

Fig. 3.50 Vestibulitis. Painful crusting of the nasal vestibule and anterior naresmay be a simple eczematous type of skin lesion which settles with a topical antibi-otic and steroid ointment. There should, however, be an awareness that thisvestibulitis is a granuloma, or part of the manifestation of systemic disease such aspolyarteritis nodosa or systemic lupus erythematosus. A further possibility is an“irritative” vestibulitis from cocaine snuff, or columellar carcinoma, as in this case

Fig. 3.51 Granular rhinitis.Granulation tissues in thenose requires biopsy. Sar-coidosis not infrequentlyinvolves the upper respira-tory tract mucosa of thenasal fossae and larynx. Inthe nose the granulationsare pale, but tuberculosis,malignant granuloma, andneoplasia are among thedifferential diagnoses.


Inflammation: nasal vestibulitis 133

Fig. 3.52 Nasal adhesion. Adhesion or synechiae may follow nasal trauma (includ-ing surgical trauma) and bridge the lateral wall of the nose, frequently from theinferior turbinate to the septum, causing nasal obstruction. Recurrence follows sur-gical division of the larger adhesions unless an indwelling silastic splint is left in situuntil mucosa underlying the adhesion regenerates.

Fig. 3.53 Furuncles and cellulitis of the columella (a). These may spread toinvolve the skin of the nose and face (b). Treatment is with systemic penicillin.

a

b


134 The Nose

Fig. 3.54a-c Acute rhinitis. In the common cold, the nasal mucous membrane isedematous, so the inferior turbinate abuts against the septum to result in obstruc-tion and an excess of mucous which causes the running nose.

A similar appearance is seen in nasal allergy, either “seasonal hay fever” orperennial allergy, but the edematous turbinate mucous membrane appears gray (c)rather than red (b). A persistent purulent nasal discharge usually means that thereis a sinusitis. Corticosteroid nasal sprays for nasal allergy reduce the obstruction,rhinorrhea, and sneezing that characterize both seasonal and perennial nasal aller-gy. Skin tests to detect specific allergens are of use with grass pollen and housedust allergy related to the house dust mite.

Nasal sprays, along with allergen avoidance where possible, and oral antihista-mines without sedative side effects are the first lines of treatment for nasal allergy.This management of nasal allergy is preferable to desensitization, as there is anincreased awareness and concern regarding anaphylactic shock.

a

b c



Fig. 3.55 Chronic rhinitis. The turbinate mucous membrane frequently reacts to irri-tants, whether tobacco, excessive use of vasoconstrictor drops, or atmospheric irri-tants, by enlarging. Thickened red inferior turbinates are seen adjacent to the septum,limiting the airway. Nasal obstruction, either intermittent or persistent, with a post-nasal discharge of mucus (“postnasal drip”) are the symptoms of chronic rhinitis. Thisis the condition most frequently labeled by the patient as “catarrh” or “sinus trouble.”

If the changes due to chronic rhinitis are irreversible, i.e., the nasal obstructionpersists when the irritants are removed, it is probable that minor surgery to reducethe turbinates in size will be necessary.

A nasal corticosteroid spray and nonsedating oral antihistamines help, but vaso-constrictor drops have no place in the treatment of chronic rhinitis and their con-stant use is a cause of rhinitis medicamentosa.

Rhinitis frequently coexists with asthma (the upper and lower respiratory tractsharing a common epithelium), and about 30% of those with rhinitis have asthma.(About 80% of asthmatics have rhinitis.)

Fig. 3.56 Wegener’s granuloma. Anendoscopic view of the granulomatoustissue seen on nasal endoscopy. Wegen-er’s granuloma is a rare autoimmuneinflammatory disease which often pres-ents with nasal symptoms of obstruc-tion, crusting, and epistaxis. Damage tothe septum may lead to a saddle defor-mity (Fig. 3.21-3.23).

The granulomas may be limited tothe nose, but the respiratory tract maybe involved along with a generalizedvasculitis and glomerulonephritis. Thecondition is characterized by periods ofremission, and treatment with oralsteroids and cytotoxic drugs has dra-matically improved the prognosis of apreviously fatal condition.


136 The Nose

In most inflammatory conditions of the nasal mucous membrane, there isan excess of mucus. An atrophy of the mucosa and mucous glands withfetid crusting of wide nasal fossae, however, is seen with atrophic rhinitis.This is uncommon and idiopathic. It may be an isolated nasal condition,part of Wegener’s granuloma, or disseminated lupus erythematosus.There is also a phase of atrophic nasal crusting in rhinoscleroma.

Nasal surgery in which there is excessive resection of nasal tissue andmucosa also predisposes to atrophic crusting.

Acute Maxillary Sinusitis

Fig. 3.57a, b A CT scan showing total opacity of the left antrum and ethmoidsdue to infection (arrows). Clearing and a return to a normal CT scan of an infect-ed maxillary and ethmoidal sinuses following intranasal antrostomy (arrow). In thisinstance the antrostomy (or opening into the maxillary antrum), has been madethrough the inferior meatus. It is more commonly made through the middle meatus.

a b



Acute Maxillary SinusitisThis is a common complication of a head cold. If a head cold persistsbeyond four to five days with continued nasal obstruction, purulentrhinorrhea, and headache, the probable diagnosis is maxillary sinusitis.Apical infection of the teeth related to the antrum or an oroantral fistulafollowing dental extraction also cause maxillary sinusitis, as may traumawith bleeding into the antrum or barotrauma.

Frontal or facial pain may be referred to the upper teeth; nasalobstruction and purulent rhinorrhea are the other symptoms. The antrumis opaque on computed tomography (CT; Fig. 3.57a). There may betenderness over the sinus, but swelling is rare. Pus is seen issuing fromthe middle meatus (Fig. 3.58a, arrow).

Acute infection may less commonly affect the ethmoid, frontal, andsphenoid sinuses. Systemic antibiotics, a vasoconstrictor spray, or drops

Fig 3.58a, b Maxillarysinusitis with pus (a,arrow) adjacent to the mid-dle turbinate issuing intothe middle meatus, seenwith the endoscope (b).

a

b


138 The Nose

and inhalations are usually curative for acute sinusitis. A persistentmaxillary sinusitis, however, requires surgery.Although frontal headache, and less commonly pain over the cheek, arecharacteristic of maxillary sinusitis, very severe pain suggests either acomplication of the sinusitis, or a neuralgic cause for the pain. Migrainousneuralgia (cluster headaches) characterized by episodes of frontal painwhich increase in severity reaching the level of extremely severe pain,which then regresses. Such a history, without nasal symptoms, suggests adiagnosis of migrainous neuralgia and further investigation is needed.

Fig. 3.59a, b An antral washout may beneeded, albeit rarely today, for a persist-ent maxillary sinusitis. This involvesinserting a trocar and cannula under theinferior turbinate, and puncturing the lat-eral wall of the nose through the maxil-lary process of the thin inferior turbinatebone, to enter the antrum. Water is irri-gated through the cannula, and the pusemerges through the maxillary ostium.

An acutely infected maxillary sinusmust not be washed out until medicaltreatment has controlled the acutephase. Cavernous sinus thrombosisremains a danger. The bad reputationthat antral washout has for pain is notjustified if a good local anesthetic andgentle technique are used.

a

b



Recurrent attacks of acute maxillary sinusitis may require operation. Apermanent intranasal opening into the antrum is made either in themiddle or inferior meatus (intranasal antrostomy). This operation is alsoeffective for those cases of acute sinusitis that fail to respond toconservative treatment and antral washouts.

Fig. 3.60 Dental sinusitis. The apicesof the molar teeth may be extremelyclose to the antral mucosal lining. Theupper wisdom tooth apparent on thisradiograph (arrow), if infected, wouldbe likely to cause maxillary sinusitis or, ifremoved, would be clearly at risk forcausing an oroantral fistula.

Fig. 3.61 Orbital cellulitis. Complica-tions of acute sinusitis confined to theantrum are rare. A severe maxillary sinusi-tis, however, usually involves the ethmoidand frontal sinuses. Infection spreadingvia the lamina papyracea or floor of thefrontal sinus leads to an orbital cellulitis. A CT scan is essential in these cases todefine the extent of infection and toexclude frontal lobe involvement.

Fig. 3.62 An orbital abscess, requiringexternal drainage, may form. Meningitisor brain abscess may also follow thespread of infection from the roof of theethmoid, frontal, or sphenoid sinus tothe anterior cranial fossa.

Infection associated with a rapidlygrowing neoplasm, such as a rhab-domyosarcoma, is the differential diag-nosis in this case.


140 The Nose

Chronic SinusitisChronic sinusitis may develop from incomplete resolution of an acuteinfection. The onset, however, may be insidious and secondary to nasalobstruction (e.g., due to a deviated septum, nasal polyps, or, in children,to enlarged adenoids. Apical infection of the teeth related to the antra canalso cause chronic sinusitis.

Purulent rhinorrhea, nasal obstruction, and headache are the mainsymptoms of chronic sinusitis. Pus in the middle meatus withradiographic opacity of the sinus are confirmatory of infection. Pusconfined to the antrum rarely gives complications, but often there is aspread of infection to the ethmoids and frontal sinuses. It is not commonfor frontal and ethmoid sinusitis to occur without maxillary sinusitis. Pusin the frontal and ethmoid sinus, as with acute infections, may spread toinvolve the orbit and brain. Obstruction of the sinus ostium may lead toencysted collection of mucus within the sinus—a mucocele.

Fig. 3.63 A mucocele. Thefront sinus is commonlyaffected, and erosion of theroof of the orbit leads toorbital displacement down-wards and laterally.



Fig. 3.64 A mucocele. Proptosis also occurs with mucoceles, and is best con-firmed by examination from above (a, arrow). The frontal sinus wall may be erodedboth posteriorly and anteriorly. An eroded anterior wall results in a fluctuantswelling on the forehead (b, arrow). In this case, there is also orbital displacementand proptosis.

Fig. 3.65 Lateral displacement of theorbit. This occurs with a mucocele aris-ing in the ethmoid sinus, and is usuallyaccompanied by a swelling of the medi-al canthus. In this case, the mucocele isinfected—a pyocele.

a b


142 The Nose

Fig. 3.66a, b Maxillary sinus radiographs. In acute and chronic maxillary sinusitis,a fluid level may be seen on radiography. A tilted view is taken to confirm the pres-ence of fluid (b, arrows). A thickened or rather “straight” mucous membrane maylook like a fluid level, as may a bony shadow if the radiograph is wrongly angled.

a b

Fig. 3.67 CT scans to show the sinuses. CT scans give a much more detailed pic-ture of the maxillary, ethmoid, frontal, and sphenoid sinuses. They are routinewhen endoscopic sinus surgery is anticipated, and are also of additional help to theplain sinus radiograph for diagnosis. CT scans, however, involve considerably moreradiation to the orbit and are expensive. Opacity of the ethmoid sinuses character-istic of infection is seen (a, arrow). Also seen is an air cell in the middle turbinate(concha bullosa; b, upper arrow) and a right intranasal antrostomy into the maxil-lary sinus (b, lower arrow).

a b



Fig. 3.70 The Caldwell–Luc operationin which the antrum is opened with asublabial antrostomy, the antral mucousmembrane removed, and an intranasalantrostomy is made. The Caldwell–Lucoperation, previously commonly carriedout, is rare. Antibiotics, endoscopicsinus surgery, and a possible change inthe nature of the sinus disease accountfor this.

Fig. 3.69 View through the sinusendoscope.

Fig. 3.68 Endoscopic sinus surgery. Incases of persistent sinusitis that do notrespond to medical treatment, endo-scopic sinus surgery is now successful incuring most cases. The improvement ofinstruments and techniques for nasaland sinus surgery enable biopsies ofantral mucosa, excision of nasal cystsand foreign bodies in the antrum, e.g., amisplaced apical dental filling, to bedealt with via the sinus endoscope.

The Caldwell–Luc operation (Fig. 3.68)and radical or “open” surgery for chronicfrontal sinus infections are now a rarity.

Mucopus

Middle turbinate

Nasal septum


144 The Nose

Nasal polyps are a common cause of nasal obstruction, and may causeanosmia. They are benign and do not present with bleeding. Examinationshows a gray pendulous opalescent swelling arising from the ethmoid. Apolyp is very different in appearance from the red inferior turbinateadjacent to it.

Polyps may be solitary or multiple, often extending from the nasalvestibule to the posterior choana. They are usually bilateral. Nasal polypsmay become extremely large, causing expansion of the nasal bones andalae nasi. A nasal polyp which is ulcerated and bleeds is probablymalignant.

Nasal polyps result from a distension of an area of nasal mucousmembrane with intercellular fluid. They are due to a hypersensitivityreaction in the mucous membrane, but may also result from sinusinfection. Obstruction of the sinuses by polyps, however, may lead to asecondary sinusitis, and a sinus radiograph is a routine investigation.

Small nasal polyps may cause little in the way of symptoms and maybe chance findings. Usually, however, polyps extend and enlarge, andpresent with nasal obstruction. They do regress with corticosteroid nosedrops and sprays, but in many instances, surgical removal either underlocal or general anesthesia is necessary.

Nasal polyps in children or young adults, particularly if recurrent andassociated with upper respiratory tract infections, suggest cystic fibrosis.In this condition the mucosal cilia of the respiratory tract are poorlymotile (ciliary dyskinesia). (The young adult [Fig. 3.75a] with nasal boneexpansion from extensive nasal polypi was found on further investigationto have cystic fibrosis.)

Nasal polyps tend to recur, and in some instances may be a recurrentlife-long problem, for example, those with the well-recognized triad ofrecurrent nasal polypi, asthma, and aspirin hypersensitivity.

Polyps


Polyps 145

Fig. 3.71 Nasal polyp (arrow). Fig. 3.72 Nasal polyps as seenthrough the sinus endoscope.

Fig. 3.73 Nasal polyp extrudingthrough the anterior nares. Largenasal polyps prolapse into the nasalvestibule with the exposed surface los-ing the opalescent gray color.


146 The Nose

Fig. 3.75 Nasal bone expansion due to extensive nasal polyps in the youngerpatient (a) also requires rhinoplasty to restore appearance (b).

a b

Fig. 3.74 Extensive nasal polyps mayexpand into the nasal bones, and theexternal deformity of the polyps maybecome gross. Surgical removal of thepolyps may suffice in the elderly, inwhom this complication is usually seen.


Polyps 147

Antrochoanal PolypThis is a special type of nasal polyp occurring in adolescents and youngadults. Unilateral nasal obstruction is caused by a gray single polyp seenin the postnasal space. The maxillary sinus is opaque on radiograph.

Fig. 3.76 Nasal polyps in the oropharynx. Extensive nasal polyps may extendbeyond the soft palate and present in the oropharynx (arrow).

a

Fig. 3.77a Antrochoanal polyp seen with the postnasal mirror. A large antro-choanal polyp may present below the soft palate. A solitary polyp in one choana isalmost certainly an antrochoanal polyp, but a vascular polyp that should beremembered as a differential diagnosis is the angiofibroma of male puberty.


148 The Nose

Fig. 3.77b, c The angiofi-broma of male puberty is arare vascular malformationin the postnasal space, whichmay become extremelylarge, presenting with nasalobstruction and epistaxis.Treatment is difficult, butsurgical removal via a midfa-cial “degloving” approach(b,c) allows access via themidfacial skeleton withoutfacial scars. Some facial frac-tures and other midfacialtumours can managed viathis approach. Very largeangiofibroma beingremoved from the postnasalspace.

b

c


Polyps 149

Fig. 3.78 Antrochoanal polyp. This type ofpolyp, which arises from the antral mucosa,extrudes through the ostium to fill the posteriornasal fossa and postnasal space. It frequentlybecomes extremely large and extends below thesoft palate. Removal of the polyp from its originin the antrum through a sublabial antrostomyapproach may be necessary (Fig 3.70).

The polyp is dumb-belled in shape with apedicle connecting the nasal and antral portions.Intranasal removal is followed by recurrence in50% of cases, but may be necessary in early ado-lescence if the permanent dentition is endan-gered by a sublabial antrostomy. (Top arrow:polyp removed from antrum; second arrow:polyp from nasal fossa; third arrow: polyp frompostnasal space; bottom arrow: polyp that hasextended into oropharynx.)

Fig. 3.79 Aspiration from the antrum.This shows straw-colored fluid, and is areliable diagnostic test for an antro-choanal polyp.


150 The Nose

Epistaxis

Fig. 3.80 Epistaxis. Anteriorly on theseptum there is anastomosis of severalarteries (the sphenopalatine, the greaterpalatine, the superior labial, and theanterior ethmoidal). This site is calledLittle’s area or Kiesselbach’s plexus, andis the commonest site of nose bleeds.Although associated with alarm, mostepistaxis is short-lived and trivial. It isbetter to sit upright since the bloodtends to be swallowed, causing nauseaon lying down. There are numerouscauses of epistaxis. Some, such as trau-ma and acute inflammatory nasal condi-tions, are obvious and common, but themore serious local and general causesmust not be overlooked. Diagnosis mustfollow control of the epistaxis. Hyper-tension and blood dyscrasia are impor-tant general causes; neoplasms andteleangiectasia may also be underlyinglocal factors.


Epistaxis 151

Fig. 3.82 Incorrect technique for con-trolling epistaxis. The pressure is overthe nasal bones and ineffective. Thearrow indicates the site where pressureshould be applied.

Fig. 3.81a, b Control of epistaxis. Firm pressure with the finger or thumb on thelateral wall of the nose opposite Little’s area on the side of the bleeding, if main-tained for about four minutes, will control the bleeding.

a b


152 The Nose

Fig. 3.83 Cautery. If epistaxis is recur-rent, cautery (which is painless withlocal anesthetic) to the bleeding point isnecessary, either with galvanocautery orwith a chemical (e.g., trichloracetic acidor silver nitrate). Trichloracetic acid usedin this case causes the bleeding site inLittle’s area to become white.

Care must be taken to avoid thechemicals running onto the skin of thevestibule or face, as scarring will result.A topical anesthetic is applied to thenasal mucous membrane in Little’s areafor galvanocautery but, with silvernitrate and trichloracetic acid, no anes-thetic is needed, and the procedure ispainless providing the vestibular skin isnot touched.

It may be preferable for cantery tobe carried out with the patient lyingdown, and with the help of the operat-ing microscope (see Fig. 1.14a).


Epistaxis 153

Fig. 3.84 Hereditary nasal teleangiectasia. Frequent and often severe epistaxis ischaracteristic of this condition, in which numerous leashes of bleeding vessels areapparent over the nasal mucosa (a). Telangiectasia are also seen elsewhere in thebody—on the skin of the cheek (b), the lips (c), the tongue (d), the hands (e) andfingernails (f).

Cautery may be effective in the early stages, but this condition is difficult tomanage, and may require either extensive skin grafting of the nasal septum toreplace the vascular septal mucosa, or estrogen therapy.

a

c

b


154 The Nose

d

e

fFig. 3.84


Epistaxis 155

Epistaxis from the anterior septum may be profuse and alarming, but firmsustained pressure on the nares is invariably effective. Posterior epistaxisfrom the sphenopalatine artery may be very severe and difficult tomanage. Nasal packing is needed to control the acute phase.

A posterior bleeding site may be identified with the nasal endoscopeand cauterized. With more severe bleeding, the sphenopalatine arterymay be clipped or ligated endoscopically. Ligation of the maxillary orexternal carotid artery is necessary if bleeding persists.

The terminal branch of the anterior ethmoidal artery may be the siteof bleeding superiorly in the nose, particularly with nasal fractures; thisvessel may require ligation. Radiographic techniques enable embolism ofthe terminal vessels to be carried out via an arterial catheter, and this isan option in managing very severe epistaxis, which may become life-threatening.

Fig. 3.85 Septal hemangioma. a A vascular sessile polyp is seen on the septum(hemangioma), which is the cause of severe, recurrent bleeds. Treatment is by exci-sion, or cautery if the lesion is small.

b A large septal hemangioma occluding the nasal vestibule. Sometimes this iscalled a “bleeding polypus of the septum.” Nasal hemangiomas may develop duringpregnancy and be a cause of epistaxis at this time.

a

b


156 The Nose

Neoplasms

Malignant Nasal TumorsA nasal polyp that does not appear gray and opalescent should arousesuspicion, as should a polyp that bleeds spontaneously. A solid-lookinghyperemic polyp may be an inverted papilloma. Granulation tissue in thenose may be malignant granuloma or carcinoma, and biopsy of anysuspicious nasal lesion is necessary.

Prognosis when radiotherapy is followed by maxillectomy is quite goodfor an early maxillary carcinoma, but poor when there is extensiveinvasion. Exenteration of the orbit with maxillectomy is necessary whenthe base of the skull is involved. The use of cytotoxic drugs results inregression in some of these paranasal sinus neoplasms and is a furtherline of treatment. Extension of a neoplasm superiorly into the anteriorcranial fossa involves resection superiorly of the dura and involved frontallobe of the brain in continuity with the nasal and sinus neoplasms(cranio-facial resection).

Fig. 3.86 A pigmented polyp may be amalignant melanoma.


Neoplasms 157

Fig. 3.87 Carcinoma of the antrum or ethmoid. These may extend not only intothe nasal fossa and cheek (a, arrow), but may present in the oral cavity (b, arrow),appearing as a dental lesion.

ba


158 The Nose

Fig. 3.89 Repair following excision of nasal tip basal cell carcinoma. A largedefect may remain in an obvious site (a, arrow). In this instance, a composite graft(a graft of two or three tissue layers) taken from the cartilage and skin of the earwas used as a free graft to repair the nasal tip (b).

Basal cell carcinomas in the groove at the base of the alae tend to erode deeply.Radiotherapy is the alternative treatment to surgery, and with modern super-volt-age therapy, lesions overlying cartilages can be treated with minimal risk of peri-chondritis.

b

a

Fig. 3.88 Basal cell carcinoma of thenose. One should be suspicious of anapparently innocent but chronic skinlesion (arrow) which slowly increases insize and may bleed. Excision with agood margin is curative (see p. 107). If,however, these lesions are ignored—andfrequently they are disguised with cos-metics for months and even years—theirexcision can present considerable prob-lems of reconstruction to avoid deformi-ty in such an obvious site as the regionof the nasal tip.


Neoplasms 159

Fig. 3.90 Carcinoma of the nose. a The apex of the nasal vestibule must be exam-ined extremely carefully in a case of scanty epistaxis, where no obvious bleedingsite is apparent in Little’s area.

Minimal bleeding and occasional serosanguineous discharge were this patient’spresenting complaints.

Later, the carcinoma became obvious, having eroded through the skin of thedorsum of the nose. b Wide surgical excision with forehead reconstruction rhinoplasty or, less common-ly, radiotherapy, are the available treatments.

ba


160 The Nose

Fig. 3.91 Carcinoma of the septumand columella.

Fig. 3.92 Squamous cell carcinoma ofthe nasal vestibule. The history wasshort, and the differential diagnosis of abasal cell carcinoma was made at biopsy.

Fig. 3.93 Carcinoma of the nasal sep-tum. A biopsy of this ulcer on the sep-tum and columella, which presentedwith scanty epistaxis, confirmed squa-mous cell carcinoma.


Neoplasms 161

Fig. 3.94 Chronic inflammation of thenose. Lupus vulgaris is now rare. It pres-ents as a chronic ulcer of the nasalvestibule extending onto the face. Thedifferential diagnosis of inflammatoryulceration anteriorly in the noseincludes sarcoidosis, which may alsocause destruction of the ala. Biopsy isnecessary for the diagnosis.

Fig. 3.95 The effects of lupus vul-garis. Lupus, if ignored, is destructive tothe skin and cartilage of the alae nasiand septum.


162 The Nose

Fig. 3.96 Carcinoma of the postnasal space (nasopharynx). This is uncommonin most countries, but has an unexplained high incidence in the Far East (particular-ly China) and East Africa. There are many presenting symptoms. As the posteriorchoanae are large, nasal obstruction is not common with ulcerated carcinomas,which tend to present with symptoms of nerve involvement or otitis media witheffusion due to interference with the eustachian tube. Lymphosarcomas and papil-liferous carcinomas, however, cause obstruction. Carcinoma invades the skull base,involving nerves V, VI, and the Vidian (pterygoid) nerve, and may cause headacheby invasion of the dura. The nasopharynx is a relatively concealed site, and presen-tation of carcinoma is commonly late, with a cervical node metastasis. The treat-ment is with radiotherapy. The overall prognosis is not good, with about a 30%five-year survival rate. This is, however, mainly related to the late diagnosis. Anawareness of the early presenting symptoms and signs is essential for improvedprognosis.

Eye squintnerve VI

involvement


Neoplasms 163

Fig. 3.97

Fig. 3.99 Carcinoma of the postnasal space (a, arrow) seen well with the endo-scope adjacent to the eustachian cushion. Some bleeding shows the site of a biopsyof the postnasal carcinoma taken via the endoscope (b).

Fig. 3.98

Fig. 3.97 Carcinoma of the postnasal space, presenting with a metastatic cervi-cal lymph node (arrow).

Fig. 3.98 Carcinoma of the postnasal space. A photograph through the fiberop-tic endoscope gives a clear view of this postnasal space carcinoma.

The biopsy forceps also introduced through the anterior nares can be seen.Therefore, biopsy of a postnasal carcinoma can be carried out as an outpatient pro-cedure under local anesthetic, using the fiberoptic endoscope.

Prior to the introduction of this instrument, the postnasal space was a “hidden”site, as this area cannot always be seen with mirror examination (see Fig. 1.48).General anesthesia was necessary for a thorough examination and biopsy.

Fibreoptic endoscope

Biospy forceps

Post-nasal carcinoma

ba



titoletto sopra 165

Chapter 4The Pharynx and Larynx


166 The Pharynx and Larynx

The Oropharynx, Mouth, and Lips

Fig. 4.1 A mucocele of thelip. Mucoceles are cystic,nontender swellings present-ing on the lips or in the oralcavity. They result fromextravasation of mucus froma mucous gland into the sur-rounding tissue. Treatment isexcision, which is not alwayseasy because of theextremely thin wall. Simplemarsupialisation is oftenadequate.

Fig. 4.2 A hemangioma ofthe lip. These may requireexcision or laser surgeryfrom a cosmetic point ofview or on account of bleed-ing with trauma.

Fig. 4.3 Lip ulcers. Lip ulcer-ation has numerous causes,either traumatic, inflamma-tory, or neoplastic. The provi-sional diagnosis can be madefrom the history and type ofulcer. Biopsy is necessary toconfirm the diagnosis. Thislesion is a pyogenic granulo-ma. Although these lesionsare frequently small andrelated to trauma, they mayenlarge from secondaryinfection (see Fig. 4.4) andtake several weeks to heal.


The Oropharynx, Mouth, and Lips 167

Fig. 4.4 Lip ulcer enlargingfrom secondary infection.

Fig. 4.5 Herpes simplex of the lip showing the characteristic vesicles (a) whichlater crust (b).

a b



Fig. 4.6 Keratosis may extend from theangle of the mouth along the occlusalplane of the teeth and is commonly adental problem; it may be self-induceddue to nervous cheek-biting. It is oftenthe result of persistent trauma to themucous membrane.

When occurring in a site notexposed to trauma, e.g., the retromolarfossa, it should arouse suspicion that themucosal change may be malignant and,therefore, a biopsy is necessary.

Fig. 4.7 Angular stomatitis (arrow) occurs with the type of dental hyperkeratosisshown in Fig. 4.6, but it may also be part of the Plummer–Vinson orPatterson–Brown–Kelly syndromes in which glossitis (also seen here) andhypochromic anemia are associated with a postcricoid lesion, either a web or a car-cinoma. This syndrome occurs mostly in women.



Fig. 4.8 The torus palatinus. The bony hard mid-line palatal swelling can be diag-nosed confidently by these characteristics (arrow). It is a common finding, and onlyrequires removal if it interferes with the fitting of a denture.

Fig. 4.9 A large torus palatinus may take on a curious, irregular appearance sus-picious of a carcinoma. Similar bony swellings occur on the lingual surface of thelower alveolus opposite the premolars (torus mandibularis).



Fig. 4.10 Torus mandibularis. A white bony hard lesion arising from the inneraspect of the mandible may present as a swelling in the floor of the mouth (arrow).This is considerably less common than the torus palatinus.

Fig. 4.11 A bilateral torus mandibularis (arrows).



Aphthous Ulcers (see p. 172 ff)An area of white superficial ulceration is surrounded by a hyperemicmucous membrane. These commonly occur in crops of two or more, andheal spontaneously in about one week. They are also acutely tender, andaffect the nonkeratinizd oral mucous membrane. Although there is noinduration on palpation, the histological inflammatory changes are notsuperficial, and may extend into the underlying muscle.

Hydrocortisone pellets to suck, or triamcinolone with Orabaseointments applied to the ulcer, are the most effective present treatmentsto relieve the pain. As the etiology of these extremely common ulcersremains unknown, treatment is empirical.

Fig. 4.12 Ectopic pleomorphic adenoma. A palatal swelling which is not bonyand hard may be a fissural cyst if mid-line, but if placed to one side (as it is here), itis almost certainly a tumor of one of the minor salivary glands. Biopsy is necessary.It is frequently a pleomorphic adenoma, but may be an adenoid cystic carcinomaor other malignant salivary tumor. A tumor extension from the maxillary antrummust also be excluded.



Fig. 4.13a, b Aphthousulcers.

a

b

Fig. 4.14a, b Ulceration and swelling of dental origin. In b an aphthous-likeulcer overlying the apex of this deciduous tooth suggests the diagnosis of an apicaldental abscess.

a b



Fig. 4.15 Aphthous ulcerson the tongue. Aphthousulcers on the tongue marginare often traumatic fromtooth irregularity.

Fig. 4.16 Trauma from adenture. This may be an irri-tating factor, as may anyminor trauma to the mucousmembrane in a person sus-ceptible to aphthous ulcers.

Fig. 4.17 Aphthous ulcers on the soft palate. Aphthous ulcers are not uncom-mon on the soft palate.



Fig. 4.18 Solitary aphthous ulcer. This ulcer (periadenitis mucosa necroticarecurrens) looks similar to a simple aphthous ulcer and is the same histologically,but it behaves differently. It is less common, larger, persists for several weeks ormonths and may leave a scar. It occurs in more varied sites affecting the soft palateand even the pyriform fossa, where it presents with severe dysphagia. Carbenox-olone is used topically for the lesions in the oral cavity.



Fig. 4.19 Multiple oral ulcers. These may be the herpetiform type of aphthousulceration, but are possibly caused by a blood dyscrasia. If the ulcers are crustedand hemorrhagic, the condition is either erythema multiforme or pemphigus.Hemorrhagic bullae may also be seen on the soft and hard palate. An iritis and gen-ital ulceration may be present (Behçet's syndrome). High doses of systemic steroidsare usually needed to control this type of severe ulceration.

The snail-track ulcers of secondary syphilis must be remembered also in thedifferential diagnosis of oral ulceration (see Fig. 4.59).

Fig. 4.20 Parotid salivarycalculus. An ulcer in theregion of the orifice of theparotid duct (a, arrow) sug-gests a possible salivary cal-culus. Parotid calculi are con-siderably less common thanthose in the sub-mandibularduct, but occasionally theymay occlude the orifice ofthe duct, causing painfulintermittent parotid swellingwhich requires incision andremoval (b, c).

a

c

b



The Tongue

Fig. 4.21 “Tongue tie.” Thisis due to a short frenulumlinguae, and apart from thedefect of being unable toprotrude the tongue, thepatient is almost alwayssymptom-free. Speechdefects can rarely be attrib-uted to tongue tie necessi-tating division of the frenu-lum.

Fig. 4.22 Geographic tongue (benignmigratory glossitis). There are smoothareas with no filiform papillae. Theseareas vary in site on the tongue, and theappearance may concern the patient. Itis, however, a condition of no signifi-cance requiring no treatment other thanreassurance.

Fig. 4.23 Black hairy tongue. Patientsnot infrequently regard the appearance oftheir tongue as an index of their generalhealth, and are concerned upon seeing abrown-black staining. This may be fungal(Aspergillus niger) and related to pro-longed antibiotic therapy, but is frequent-ly a chance finding with no other patholo-gy than hypertrophy of the filiform papil-lae. Tobacco may be a cause. Scrapingand cleaning the tongue temporarilyimproves the appearance, but is unneces-sary since this condition is harmless.


The Tongue 177

Fig. 4.24 Hemangiomas ofthe tongue. These may bechance findings and are usu-ally innocuous. If large andgiving rise to bleeding, lasersurgery is the most effectivepresent treatment.



Fig. 4.25a, b Papilloma of the tongue. Benign lesions of the tongue are com-mon, and are either sessile or pedunculated (b). Simple excision under local anes-thetic with biopsy is required.

a

b


The Tongue 179

Fig. 4.26 The ranula is a mucocele occurring in the floor of the mouth (a). A bluecolor and the profunda vein stretched across the surface are characteristic. Thisranula may extend into the tissues of the floor of the mouth and neck (plungingranula). Total surgical removal is difficult because of the thin wall, and marsupialisa-tion, as with the lip lesion (Fig. 4.1), is adequate treatment. Recurrence is notuncommon.

The ranula may also present more in the floor of the mouth than on the under-surface of the tongue, and the diagnosis may not be so obvious. b A less well-defined ranula occupying the floor of the mouth.

Fig. 4.27 Lingual thyroid. Developmental anomalies in the thyroid gland mayresult in thyroid tissue remaining at the foramen caecum or in the thyroglossaltract. The symptom-free swelling at the base of this tongue is thyroid tissue, andwas shown on a radioactive idodine scan to be active. No thyroid gland was palpa-ble in the neck, and there was no iodine uptake other than at the base of thetongue. This lingual thyroid, therefore, was this patient’s only active thyroid tissue.

a b



Fig. 4.28 Tongue ulceration. The site and type of tongue ulcers give the provi-sional diagnosis: A marginal ulcer with a raised edge is probably a carcinoma; anulcer on the dorsum with a punched-out margin may be a gumma. Tuberculosismay be the cause of a tender ulcer on the tip of the tongue in an area where tuber-culosis is prevalent. However, these clinical findings are only guides. Biopsy of thisulcer on the dorsum showed it to be a solitary aphthous ulcer (Fig. 4.18).

Fig. 4.29 An aphthous tongue ulcer of the tongue may be deceptive. A buccalmucosal aphthous ulcer is flat, but on the tongue some swelling due to traumamay make a biopsy necessary in order to be certain of the diagnosis.


The Tongue 181

Fig. 4.30 A Chancre.Tongue ulceration from pri-mary syphilis.

Fig. 4.31 Laser excision of a tonguelesion. This shows the minimal reactionat the excision margin, and the non-bleeding base of the excision.

Fig. 4.32 Median rhomboid glossitis.This rare anomaly results from failure ofthe lateral halves of the tongue to fuseposteriorly, leaving the tuberculumimpar in the mid-line. A smooth, red,usually symptom-free area persists.



Fig. 4.33 Carcinoma of the tongue. This usually occurs on the margin or from theextension of an ulcer on the floor of the mouth (as shown here). Biopsy of this pro-liferative ulcer showed squamous cell carcinoma. Partial glossectomy in continuitywith a neck dissection, or radiotherapy, are the current treatments.

Fig. 4.34 Leukoplakia. This is precarcinomatous on the tongue. It may be second-ary to dental or dietary irritation. Leukoplakia is also characteristic of tertiarysyphilis, and the tongue is a site where the spirochaete predisposes to carcinoma.Leukoplakia, particularly with no apparent underlying traumatic cause, should bebiopsied to exclude carcinoma.


The Tongue 183

Fig. 4.35 Hypoglossal nerve paralysis.Initially, there is fibrillation and lateratrophy of the muscles on one side ofthe tongue. The tongue deviates on pro-trusion to the side of the nerve palsy. Adestructive lesion in the jugular fora-men region may extend to involve thehypoglossal nerve as it emerges fromthe nearby anterior condylar foramen.This paralysis of the tongue shows wrin-kling caused by fibrillation, and is due toa glomus jugulare tumor, which has alsodamaged the cranial nerves emergingthrough the jugular foramen (IX, X, andXI).

The hypoglossal nerve, if involved incervical metastases, may be sectionedin a radical neck dissection (see p. 222).



The Fauces and the Tonsils

Fig. 4.36 The uvula. This obvious anatomical feature in the oropharynx has littlepathological significance. When particularly long, however, as here, it has on occa-sion been thought responsible for various throat symptoms such as discomfort andsnoring. Partial amputation has been recommended.

The uvula is excised along with part of the tonsillar fauces and soft palate in theoperation of uvulopalatopasty for snoring. The appearance of the palate after oper-ation is seen in Figs. 4.38b and 4.66.

Fig. 4.37 Bifid uvula. A common minor congenital deformity of the palate. It is of little significance, but it may be associated with a submucous palatal

cleft. Inflammation of the uvula as an isolated entity may occur, however, and acherry-like enlargement may be the sole presenting sign of a sore throat (uvulitis).


Snoring Snoring, although in most cases a relatively trivial problem, may if grosshave serious implications. Although snoring is commonly associated withobesity, aging, (where the pharyngeal tissues become more lax) alongwith late-night excess food and alcohol intake, there are anatomicalfactors in the upper respiratory tract that contribute to snoring. Nasalobstruction accentuates snoring but is not commonly the prime cause.Surgery therefore for airway problems to the nose may not be curative.

The anatomy of the soft palate and oropharynx however is a cause ofsnoring when the soft palate, uvula and fauces are long and lax. Largetonsils may also cause snoring. Surgery to reduce the size and mobility ofthe soft palate—uvulopalatoplasty—has become established world-wide.The uvula is excised along with shortening of the faucial pillars, eitherwith excision, or laser techniques. (see Fig. 4.38a, b). Sleep studies are carried out preoperatively for assessment of the snoring.Apart from appraising the predominant site causing the snoring, whetherthe oropharynx, tongue base, or nose, sleep studies monitor therespiration rate, cardiac function with O2 and CO2 levels during sleep.

With gross snoring both in children (where upper respiratory tractobstruction from marked adenoids and tonsil hypertrophy may berelevant) and in adults, significant physiological upset may ensure. Withsleep apnea respiration is sufficiently disturbed by snoring to causecardiac arrhythmia and maybe cardiac enlargement, along with periods ofoxygen deficit.

In these instances treatment for snoring either by surgery or byoxygen administration at night is necessary along with other steps, forexample, weight loss. Oxygen supplied at night prevents sleep apnea—continuous positive airway pressure (CPAP; Fig. 4.38c). A mask is firmlyattached to the nose to supply oxygen; the patient's discomfort may limitthe application of this treatment (see over).

The Fauces and the Tonsils 185



Fig. 4.38 Snoring. a, b Uvuloplasty toremove the uvula and shorten the fau-cial pillars. c An oxygen mask may beworn at night to prevent sleep apnea.

a

c

b



Fig. 4.39 Papillomas. These may occur on the uvula (a), fauces, and tonsil. Thepatient often notices these papillomas when looking at the throat, or they arefound at medical examination. Symptoms are uncommon. They are usually pedun-culated and are easily and painlessly removable in outpatients. They should be sentfor histology to exclude a squamous carcinoma. If ignored, a papilloma may causesymptoms on account of size. This large papilloma (b) arises from the base of theright tonsil.

a

b



Fig. 4.40 Tonsil size. There is no recognized “normal” size for a tonsil. It is, there-fore, arguable as to whether tonsils can be described as “enlarged.” The apparentsize of the tonsil can be altered considerably when the tongue is protruded forcibly.This child, whose oropharynx looks normal when the tongue is slightly protruded(a), can make the tonsils meet in the mid-line with maximum protrusion of thetongue (b).

a b

Fig. 4.41a, b Tonsil size affected by tongue depressor. The tongue depressoralso alters the apparent size of the tonsils. If the tongue is firmly depressed, thepatient gags and the tonsils meet in the mid-line (b).

a b



Fig. 4.42a, b Tonsils meet-ing in the mid-line. It isunusual for tonsils to meet inthe mid-line or to overlap.Lymphoid tissue of this bulk,particularly during an acutetonsillitis, may cause respira-tory obstruction and severedysphagia. There is anincreased awareness of theseverity of upper respiratorytract obstruction from thebulk of tonsillar and adenoidlymphoid tissue.

In children, particularly attimes of superimposed tonsil-litis, the interference withbreathing becomes alarming,and obstructive sleep apneasyndrome is now well-recog-nized as an important indica-tion for surgery to removethe tonsils and adenoids. Corpulmonale is seen in childrenwith marked upper respirato-ry tract obstruction.

Fig. 4.43 Lateral radi-ograph of tonsils. The tonsils(arrow) and adenoids shownon lateral radiograph, and thesoft-tissue shadow helps inassessing the degree ofobstruction that the lym-phoid tissue may be causing.The lingual tonsil is unusuallylarge in Down’s syndromepatients and contributes totheir characteristic bulkytongue.

a

b



Fig. 4.44 Unilateral tonsil enlargement. A tonsil can be described as “large”when compared with the other tonsil. A conspicuously large tonsil in the absence ofacute inflammation is an important finding suggesting either a chronic quinsy or alymphosarcoma. A persistent and conspicuously large tonsil, therefore, should beremoved for histology.

Fig. 4.45 A palate and tonsil carcinoma. This presents as an indurated ulcerrather than a diffuse enlargement, and causes referred ear pain. The biopsy is takenfrom the ulcer margin.



Fig. 4.46 Simulated tonsil enlarge-ment. A tonsil may appear to beenlarged by medial displacement from aparapharyngeal swelling, and carefulexamination of the fauces ensures thatthe correct diagnosis is made. It is possi-ble to biopsy a normal tonsil and realizelater that medial displacement is simu-lating enlargement. In this case, theparapharyngeal mass is an internalcarotid aneurysm. This initial diagnosisin Casualty was a quinsy—a dangerouserror if followed by incision.

Fig. 4.47 Tumors of the deep lobe of the parotid gland causing medical displace-ment of the tonsil are other more common parapharyngeal swellings, as are chemod-ectomas, neurofibromata, and enlargement of the parapharyngeal lymph nodes.



Fig. 4.48 Supratonsillar cleft. Thisrecess near the superior pole of the ton-sil, if large, tends to collect debris. Amass of yellow fetid material can beextruded from the tonsil with pressure;discomfort or halitosis are symptomswith which this condition may present.Tonsillectomy may be necessary. Thesurgeon, however, must beware of ton-sillectomy for halitosis.

Although dental or gastric patholo-gy may cause this symptom (as may apharyngeal pouch), the symptom maybe imagined by the patient, or by anoth-er person complaining about the halito-sis.



Fig. 4.49 Keratosis pharyngeus. Yellow spicules due to hyperkeratinized areas ofepithelium are sometimes extensive over the tonsil and lingual tonsil (a). It is usual-ly a chance finding, and it is important in diagnosis to probe the tonsil (b) to be cer-tain that these yellow areas are not exudate. No treatment is required for this con-dition unless it is associated with tonsillitis.

a

b



Fig. 4.50 Tonsillar exudate. Exudate from tonsillar crypts may appear indistin-guishable from keratosis pharyngeus, and hence palpation with a probe is necessary.

Fig. 4.51 Retention cysts. These are common on the tonsil and appear as sessileyellow swellings (a). If small they can be ignored, and although symptoms areuncommon, a concern by the patient or a sensation of a lump in the throat may callfor surgical removal. Retention cysts are also seen following tonsillectomy in theregion of the fauces (b).

a b



Infections of the Tonsils, Pharynx, and Oropharynx

Acute Tonsillitis (see p.196)This condition is characterized by sore throat, dysphagia, and pyrexia. Theappearance of the tonsils varies. An obviously purulent exudate coveringthe tonsils is common, and is either diffuse or punctate (Fig. 4.52a, b). Anapparently less severely infected throat with hyperemia of the tonsilsonly may, however, be associated with severe symptoms. The tonsillarlymph nodes near the angle of the mandible are large and tender.

With acute tonsillitis, the exudate and hyperemia are centered on thetonsils. In an acute pharyngitis, as may be associated with a head cold, themucous membrane of the entire oropharynx is hyperemic.

The gonococcus may cause acute pharyngitis, and a throat swab mustbe placed in Stewart’s medium for laboratory examination if this infectionis suspected. The throat swab in acute tonsillitis commonly grows thehemolytic streptococcus, and a course of oral penicillin (oftensupplemented with an intramuscular injection) is invariably curative. Ananalgesic may also be needed, but lozenges and gargles are usuallyunnecessary.



Fig. 4.52 Acute tonsillitis. The appearance of the tonsils in acute tonsillitis iseither diffuse (a) or punctate (b).

a

b



Quinsy (see p. 198)This is a complication of acute tonsillitis in which a peritonsillar abscessforms. The symptoms may be extremely severe, with absolute dysphagiaand pain referred to the ear and trismus, as well as malaise, fever, andmarked swelling of the tonsillar lymph node. Examination shows thesigns of acute tonsillitis with medial displacement of the tonsils to themid-line.

If the abscess is pointing, incision at the site marked (Fig. 4.53a,b;arrows) releases the pus. Since the advent of antibiotics, there is less needfor incision of quinsies. High doses of intramuscular penicillin for fivedays followed by a further five-day course of oral penicillin is thetreatment. A large tonsil with medial displacement will persist withinadequate treatment, repre-senting a chronic quinsy in whichrecurrence of an acute episode is common. A throat swab of the pus istaken at the time of diagnosis, and the result may later require changingthe penicillin to another antibiotic.

A quinsy is extremely rare in children and is also rarely bilateral.Complications are uncommon, but bleeding from a quinsy is an importantand serious sign: It is due to erosion by the peritonsillar pus of one of theadjacent vessels—either one of the tonsillar arteries or the internalcarotid artery (bleeding quinsy).

Quinsies not infrequently occur in those who have suffered previousepisodes of tonsillitis. Tonsillectomy, which is often indicated after aquinsy, is delayed by four to six weeks until the acute phase has passed.Vascular fibrous tissue found lateral to the tonsil after a quinsy maketonsillectomy technically difficult, and some advocate tonsillectomy atthe time of the acute quinsy (quinsy tonsillectomy).

The pain with a quinsy is frequently so severe that swallowing isalmost impossible and oral antibiotics cannot be given. Intravenousantibiotics, for example, penicillin supplemented with metronidazole (forthere is a high instance of anaerobic organisms on culture) are givenintravenously and usually bring about resolution in 24–48 hours.



Fig. 4.53a, b Quinsy.

a

b



Infectious MononucleosisInfectious mononucleosis should be suspected if a sore throat and malaisepersist despite antibiotic treatment, and a white cell analysis andPaul–Bunnell test are indicated.

A white membrane covering one or both tonsils is characteristic andhelpful in diagnosis. Hypersensitivity to ampicillin is increased ininfectious mononucleosis, and the antibiotic should be avoided as asevere urticaria follows its use. The positive Paul-Bunnell blood test isdiagnostic of infections mononucleosis, and atypical mononuclear whitecells are increased on the blood film.

Fig. 4.54a, b Infectiousmononucleosis.

a

b



Oral Candidiasis (Thrush)Monilla, or oral candidiasis (thrush), is one of the fungal infections of thepharynx. Extensive white areas cover the entire oropharynx, and are notconfined to the tonsil. They are either continuous (Fig. 4.56a) or punctate(Fig. 4.56b). A swab shows Candida albicans and confirms the diagnosis.The condition responds to antifungal mouth washes or lozengescontaining nystatin or amphotericin. It is commoner in neonates, and maycomplicate treatment with broad spectrum antibiotics.

Oral candidiasis is one of the commonest upper respiratory tractmanifestations of AIDS; unexplained oral fungal infection should makethe possibility of AIDS a diagnostic consideration (Fig. 4.57). Nasalvestibulitis and cervical lymphadenopathy may be associated findings.

Fig. 4.55 Infectious mononucleosis in a patientwithout tonsils. In this case, the membrane charac-teristic of infectious mononucleosis is seen either onthe lingual tonsil or, as in this case, on a prominentposterior pharyngeal band of lymphoid tissue. Asimilar white membrane also covers the lymphoidtissue in the postnasal space.

The appearance on examination of the postnasalspace may lead to a suspicion of neoplasm. Theincrease in bulk of the adenoids also causes a “nasalvoice,” which is sometimes characteristic of infec-tious mononucleosis.



Fig. 4.56 Oral candidiasis. a Extensive continuous white areas covering theoropharynx. b Extensive punctate white areas covering the oropharynx.

a

b



Fig. 4.57 AIDS-related oral candidiasis. This is a common presentation of HIVinfection. Oral candida is treated with topical or systemic antifungal agents, e.g.,nystatin, ketoconazole, or fluconazole. If there is dysphagia with oral candida,esophageal involvement should be suspected.

Fig. 4.58 Hairy leukoplakia. Oral candidiasis is the commonest presentation inthe pharynx of AIDS, but hairy leukoplakia (arrows) is a further presentation, alongwith cervical lymphadenopathy.

Oral hairy leukoplakia differs from oral candida in that it is distributed along thelateral borders of the tongue and cannot be scraped off. It is due to Epstein–Barrvirus reactivation. Mouth ulcers also occur with HIV infection and good oralhygiene and dental care are important adjuncts to treatment.



Fig. 4.59 Ulcers on the tonsil and soft palate. Candida was cultured, but theseare snail-track ulcers of secondary syphilis.

Fig. 4.60 Chronic pharyngitis. In this condition there is a generalized hyperemiaof the pharyngeal mucous membrane, with hyperemic masses of lymphoid tissueon the posterior wall of the oropharynx. A persistent, slightly sore throat is themain symptom. The cause is usually “irritative” rather than due to chronic infec-tion. Environment, occupation, diet, and tobacco are the common factors.



Fig. 4.61 Scleroma with scarring ofthe soft palate and oropharynx. This isa specific chronic inflammatory diseaseof the upper respiratory tract mucosapredominantly occurring in EasternEurope, Asia, and South America. A pro-tracted painless inflammation of thenose (rhinoscleroma), pharynx, or lar-ynx is followed after many years byextensive scarring, which is particularlyapparent in the oropharynx. Unlikegummatous ulceration, which is a differ-ential diagnosis, scleroma is notdestructive, the uvula is preserved,although it may be retracted by scarringinto the nasopharynx, and is seen withthe postnasal mirror. The histology ofthe mucosa in scleroma is characteristicand diagnostic.



TonsillectomyTonsillectomy is one of the most frequently performed operations in theworld. Stricter indications for operating, however, are reducing thenumber of tonsillectomies. Recurrent episodes of acute tonsillitis,interfering with school or work, are the main indications. A quinsy orchronic tonsillitis are other indications, along with marked enlargementinterfering with the airway.

Fig. 4.62 The tonsillar fossae following tonsillectomy. These are covered with awhite/yellow membrane for about 10 days until the fossae are epithelialized.

Fig. 4.63 Tonsils after removal todemonstrate the lingual pole (arrow).The pole must be included at tonsillecto-my. A tonsil remnant may be left inadver-tently at this site, giving rise to furtherinfection, but tonsils do not “regrow.”Adenoid tissue is, however, not possibleto enucleate and remove in toto; it mayrecur, particularly when removed beforeage 4.



Fig. 4.64 Secondary infection. A blood clot in the tonsillar fossa is an importantpostoperative finding, and almost certainly indicates secondary infection. Thisoccurs between day three and 10, and is associated with bleeding and increasedpain. The bleeding is usually scanty and settles when antibiotics control the sec-ondary infection. Severe delayed bleeding after tonsillectomy may occur, however.The finding of a blood clot in a tonsillar fossa must not be ignored.



Fig. 4.65a, b Secondary tonsillar infection with bleeding and bruising of thesoft palate. This appearance may be related to an excessively traumatic tonsillecto-my. An infected blood clot is present in the tonsillar fossa; removal may cause morebleeding. A tonsillar blood clot present with primary bleeding, however, should beremoved if possible, as this may settle the bleeding.

a

b



Fig. 4.66 Guillotine tonsillectomy. Tonsillectomy today is by dissection with min-imal injury to the fauces and surrounding structures. Adept use of the guillotinemay also be a rapid and effective surgical technique, but removal of the uvula andfauces is possible in inexperienced hands. Fortunately, postoperative scarring of thepalate and uvula is frequently symptom-free. This appearance of the soft palatewith conspicuous shortening is similar to that following the uvulopalatoplasty oper-ation for severe snoring (see Fig. 4.38a, b).

Fig. 4.67 Palatal trauma.Laceration to the hard andsoft palate are not uncom-mon. The oft-given advice tochildren not to “run with apencil or similar object intheir mouth” is intended tooffset palatal lacerationresulting from a fall. Sutur-ing, however, is usuallyunnecessary, and unlessthere is gross mucosal sepa-ration, the palate andtongue heal well sponta-neously following trauma.



Fig. 4.68 Epiglottitis. This is a serious, life-threatening condition and a diagnosisthat may be missed. The complaint of a sore throat in an ill patient with a history ofdysphagia and fever, often strongly suggestive of a quinsy, is associated with littleamiss on oral examination. Such a situation strongly suggests epiglottitis, and alateral soft-tissue radiograph is frequently diagnostic. This is a diagnosis not to bemissed, and awareness that it also occurs in children is important.

The normal narrow contour of the epiglottis is seen to be replaced by a roundswelling (b: arrow). This condition, if ignored, may lead to stridor, respiratoryobstruction, and death if the airway is occluded.

Early diagnosis, hospital admission, and intravenous antibiotic therapy (e.g.,cefuroxime) is curative. Close nursing observation of the airway is necessary.

a b



Inflammation of the Larynx

LaryngitisWhether acute or chronic, laryngitis presents with hoarseness andgeneralized hyperemia of the laryngeal mucous membrane. Acutelaryngitis commonly follows an upper respiratory tract infection, or istraumatic following vocal abuse. Voice rest is the most effectivetreatment.

Chronic laryngitis may be associated with infection in the upper orlower respiratory tract, but is commonly “irritative” due to occupationand environment, vocal abuse, or tobacco. The unusual laryngitis ofmyxoedema must not be forgotten.

The Larynx

Fig. 4.69 Normal vocal cords. These are ivory-colored and smooth with few ves-sels on the surface. This is the view obtained through a laryngoscope at directmicrolaryngoscopy.


The Larynx 211

Fig. 4.70 A fiberoptic endoscopic view of a normal larynx (see Fig. 1.62).

Fig. 4.71 A laryngeal web. Congenital abnormalities of the larynx are uncom-mon. Webbing of varying degrees of severity is one of the commoner developmen-tal abnormalities, and presents as hoarseness. Similar webbing may follow inadver-tent trauma at endoscopic surgery to both vocal cords near the anterior commis-sure. A mucosal web is treated with surgical division. Most webs, however, are deepand fibrous and need an indwelling “keel” after division to avoid recurrence.



Fig. 4.73 Vocal cord nodule seen through a fiberoptic endoscope. A solitary vocalcord nodule at the characteristic site is not uncommon, although they are usuallybilateral and fairly symmetrical.

Fig. 4.72 Laryngeal nodules (arrows).A specific and localized type of chroniclaryngitis, often seen in professionalvoice users, is laryngeal nodules(singer’s nodules). Initially an edema isseen on the vocal cord between theanterior one-third and posterior two-thirds of the cord. Removal of the nod-ules may be necessary, but attention tothe underlying voice production by aspeech therapist is the most importantaspect of treatment. These nodules arenot an uncommon cause of hoarsenessin children, particularly of large familiesinvolved in competitive shouting(“screamers” nodules'). Vocal cord nod-ules are also seen in those who overuseor misuse their voices.


The Larynx 213

Fig. 4.74 Vocal cord nod-ule with hematoma. Avocal cord nodule withhematoma formation follow-ing vocal abuse.

Fig. 4.75 Juvenile laryngealpapilloma.

Recurrent respiratory papillomatosis must be excluded in a hoarseinfant or child, for if the hoarseness is ignored, stridor will develop aspapillomas accumulate in the laryngeal airway. Nevertheless, vocal cordnodules (“screamers’ nodes”) are the commonest cause of hoarseness inchildren.

In juvenile papillomas, multiple wart-like excrescences develop,usually before the age of five, mostly on or around the vocal cords.Recurrence follows removal, but fortunately eventual spontaneousregression is usual. The cause is now established as the human papillomavirus (types 6 and 11), which produces the disease in children who havean HLA-linked T-cell deficit.Bull, Color Atlas of ENT Diagnosis © 2003 ThiemeAll rights reserved. Usage subject to terms and conditions of license.

Management consists of regular microlaryngoscopy with removal ofpapillomas using the CO2 laser or laryngeal microdebrider. The aim is notto achieve radical removal of all the papillomas, but just to maintain a safeairway and as good a voice as possible while awaiting spontaneousresolution, avoiding damage to the underlying laryngeal tissues whichmight produce scarring and stenosis. In severe cases a tracheostomy maybe necessary, but should be avoided if at all possible as papillomas tendto develop around the tracheal stoma and “seed” further down thetracheobronchial tree. In very severe cases adjuvant chemotherapy withinterferon may be used.


Fig. 4.76 Laryngomalacia. This is the commonest cause of stridor in infants. Theepiglottis is curled (“omega-shaped”) and tightly tethered to the aryepiglotticfolds, which are tall and floppy, resulting in supraglottic collapse on inspiration.

Diagnosis can usually be established from the history and confirmed by awakeflexible fiberoptic laryngoscopy.

Most cases are mild, no treatment is necessary, and the stridor gradually fades,resolving completely by about age 2. However, 10% of cases are severe with failureto thrive (and often associated gastroesophageal reflux). In these patients an endo-scopic aryepiglottoplasty may be required to release the epiglottis and reduce thearyepiglottic folds.


The Larynx 215

Fig. 4.77 Pedunculated vocal cord polyp. A large pedunculated polyp may formon the vocal cord and be missed on examination for it moves above and below thecord on expiration and inspiration. A large polyp (a) is less apparent (b) when it isbelow the cord on inspiration.

a b



Fig. 4.79 Granulomas of the larynxexcision. Here the pedicle of the intuba-tion granuloma is being held with for-ceps. Recurrence frequently followsexcision, but laser beam techniquesappear to lessen the likelihood. Relative-ly large lesions can occupy the posteriorhalf of the larynx with minimal voicechange. Anteriorly in the larynx, howev-er, small lesions cause conspicuousvoice change.

Fig. 4.78 Intubation granulomas of thelarynx. These result from trauma by theanesthetic tube to the mucosa overlyingthe vocal process of the arytenoid; theyare, therefore, posterior. With the skillthat anesthetists have achieved for endo-tracheal intubation, trauma to this regionis uncommon. Granulomas at this sitealso develop after prolonged vocal abusehas caused a chronic laryngitis in whichthe epithelium over the vocal processbecomes ulcerated (“contact ulcers”).Removal at the pedicle is necessary.

Fig. 4.80 Polyp at the anterior com-missure. This site is not always easy tosee on indirect laryngoscopy for it maybe partly obscured by the tubercle ofthe epiglottis. The laryngoscope isplaced against the tubercle, displacing itforwards and a clear view is obtained.

A small lesion near or at the anteriorcommissure of the larynx may produceconspicuous hoarseness. However, alarger lesion posteriorally in the larynxmay not produce such a conspicuousvoice change.


The Larynx 217

Fig. 4.81 Hemangiomas(arrow). These are uncom-mon vocal cord lesions and ifsmall may cause no hoarse-ness or bleeding, and be achance finding on examina-tion. Laser surgery promisesto be the effective treatmentfor larger hemangiomas.

These hemangiomasmay be associated with simi-lar lesions in the head andneck in children (Figs 3.4a,b).

Fig. 4.82 Acute laryngitis showing slight hyperemia and edema of both vocalcords seen with the fiberoptic endoscope.



Fig. 4.83a, b Chronic laryngitis. With this condition, hyperemia of the mucousmembrane may be associated with other changes in the larynx. Edema of the mar-gin of the vocal cords is common (Reinke’s edema), so that the free margin is poly-poid and a large sessile polyp may form. The edema, although affecting both cords,may be more marked on one side (b).

Fig. 4.84 Hypertrophy of the ventric-ular bands. Hypertrophy of the ventric-ular bands is another finding in chroniclaryngitis and they may meet in themid-line on phonation, producing acharacteristic hoarseness. Reinke’sedema is also present. Microlaryn-goscopy and surgical excision of theedematous margins is effective with dis-section or the laser beam. Excision tothe anterior commissure is made on onecord only to avoid webbing.

a b


The Larynx 219

Fig. 4.85 Prolaps of the ventricularmucous membrane. This may alsooccur in chronic laryngitis and presentsas a supraglottic swelling. A supraglotticcyst or carcinoma must be excluded.

Fig. 4.86 Long-standing chroniclaryngitis. The mucous membrane maybecome extremely hypertrophic withwhite patches (leukoplakia). Histologi-cally, the white patches represent areasof keratosis which may precede malig-nant change and be reported as carcino-ma in situ. This patient had smoked over60 cigarettes a day for 50 years.



Neoplasms of the Larynx

Fig. 4.87 Carcinoma of thevocal cord. This usuallyoccurs in smokers. Theindurated leukoplakia on thisvocal cord (arrow) is a well-differentiated squamous cellcarcinoma that has arisen asa result of chronic laryngitiswith hyperkeratosis.The prognosis for vocal cordcarcinoma with radiotherapyis excellent, with a cure rateof over 90% for early lesions.The voice returns to normal,as does the appearance ofthe vocal cord.Fig. 4.88 Supraglotticsquamous cell carcinoma.Carcinoma of the larynxcommonly involves the vocalcord (glottic carcinoma), butlesions may develop belowthe cord (subglottic) orabove the cord (supraglot-tic). The ulcerated area ofgranulation tissue above theedematous vocal cord in thiscase is a squamous cell carci-noma.

Fig. 4.89 Subglottic squamous cellcarcinoma. The prognosis for supra-glottic and subglottic carcinoma isworse than for glottic carcinoma, forhoarseness is delayed until the cord isinvolved and the greater vascularity andlymphatic drainage above and belowthe cord predisposes to earlier metastasis.


The Larynx 221

Fig. 4.90 Carcinoma of the larynx. 70% of laryngeal carcinomas affect the vocal cords.

Fig. 4.91 The laser beam for surgical excision. This may prove to be the tech-nique of choice for certain lesions in the upper respiratory tract. In this case it isbeing used at microlaryngoscopy to excise an intubation granuloma (see Fig. 4.78).The laser is now widely used for the removal of tongue (see Fig. 4.31) and pharyn-geal lesions, particularly hemangiomas and other vascular lesions. The laser alsoappears to have advantages for excision of juvenile papillomas, intubation granulo-mas, and possible laryngeal webs. Use of the operating microscope ensures preciseexcision with the laser beam, which causes considerably less tissue damage thancautery or diathermy.



Laryngeal Surgery

LaryngectomyNearly all cases of early carcinoma of the vocal cord are cured withradiotherapy or laser surgery. Disease, however, may remain withextensive cord carcinomas, with supraglottic or subglottic lesions, or withcarcinoma of the pyriform fossa or epiglottis.

Partial laryngectomy (laryngofissure, extended laryngofissure, orsupraglottic laryngectomy) gives adequate resection of some laryngealcarcinomas, but frequently a total laryngectomy is required. This radicalsurgery, which may be associated with a neck dissection if the nodes areinvolved, means a permanent tracheostome, and an alternative method ofspeech has to be developed. Air is swallowed into the upper esophagus,and coherent speech is achieved by learning to phonate with controlledregurgitation of the air. Even with intensive speech therapy, somepatients remain unable to achieve reasonable voice.

Conservative laryngectomy (supraglottic or hemilaryngectomy) aimsin the smaller laryngeal cancers to preserve part or all of the vocal cordsand to avoid a tracheostome, so that laryngeal voice is preserved. Forthose who are unable to speak after total laryngectomy, or as a primaryprocedure with laryngectomy, a valve fitted between the tracheosteomeand esophagus enables air to be redirected with a more normal voiceproduction (Blom–Singer valve).

Fig. 4.92 Total laryngectomy withleft radical neck dissection.

Fig. 4.93 Stomal stud. Steno-sis of the tracheosteome issometimes a postoperativeproblem, and a small stomalstud can be used.


The Larynx 223

Fig. 4.94a The Blom–Singer voice prosthesis may be inserted at the time oflaryngectomy or placed later in those who are unable to develop coherent speech.b The prothesis shown diagrammatically and positioned into the new opening tothe esophagus at the top of the tracheosteome.

a

b

Fig. 4.95 Laryngectomy specimen.This shows a large laryngeal carcinomaextending above and below the rightvocal cord and across to the left side ofthe larynx. It also shows the hyoid, thy-roid, and cricoid cartilages and upperrings of trachea, which are removed atlaryngectomy.



HoarsenessHoarseness may be due to paralysis of one vocal cord, the left being morecommonly involved. Lack of cord movement on phonation is diagnosedon indirect laryngoscopy or fiberoptic laryngoscopy. Although temporaryidiopathic cord palsy is the single most common cause, involvement ofthe left recurrent laryngeal nerve in chest disease must be excluded. Anyhilar lymph node lesion in the region of the aortic arch may involve thisnerve, such as secondaries from lung carcinoma. The enlarged left atriumof mitral stenosis may also press on the left recurrent laryngeal nerve andcause hoarseness, as may an aortic aneurysm or the enlarged pulmonaryartery of pulmonary hypertension.

The recurrent laryngeal nerves are also occasionally damaged in theneck by severe external injury, or by thyroid carcinoma or surgery. Centrallesions, or lesions near the jugular foramen involving the vagus, may alsocause cord paralysis, and hoarseness is one of the symptoms of posteriorinferior cerebellar artery thrombosis.

Hoarseness, particularly a whispered voice with normal larynx, is afunctional voice problem. Nonorganic aphonia is not uncommon in youngwomen, and stems from a superficial psychiatric upset. Treatment fromthe speech therapist is usually effective without referral to a psychiatristbeing necessary. Curious alterations in the voice or hoarseness may alsobe due to a nonorganic dysphonia.

PhonosurgeryMicrosurgical techniques are effective to restore normal quality of ahoarse voice. Minute lesions on or within the vocal cord can be excised orenucleated with precision.

Phonosurgery is of particular use for established vocal cord palsy. The voiceis weak and “breathy” because the glottis does not fully “close” on phonation.Techniques to medialize or increase the bulk of the immobile cord enablefull closure of the glottis and normal or near-normal voice to be achieved.

StroboscopyStoboscopy is a further technique for demonstrating laryngeal pathologywith the endoscope and video camera (see Fig. 4.96a, b). The rapidmovements of the vocal cords during phonation can be seen magnifiedand in slow motion. Minimal cord lesions causing voice change whichwere hitherto undetectable can be diagnosed and treated, for example,small nodes and cysts within the vocal cord.


The Larynx 225

Fig. 4.96a, b Stroboscopy is a further technique for demonstrating laryngealpathology with the endoscope and video camera.

a

b



Fig. 4.97 Left vocal cordpalsy. The paralyzed vocalcord is seen to lie near themid-line (arrow) and under-goes no movement onphonation at indirect laryn-goscopy (see Fig. 1.61). Theparalyzed vocal cord is seento fall medially towards themid-line and inferiorly, so itis below (inferior to) the cordwith normal movement.

Fig. 4.98 Radiograph ofaortic aneurysm (arrow).Pressure on the left recur-rent laryngeal nerve causesnerve palsy and hoarseness.

An enlarged hilar lymphnode secondary to a lungcarcinoma in this site is acommon cause of hoarse-ness due to left vocal cordpalsy.


The Larynx 227

Microsurgery of the LarynxThe use of the microscope for direct laryngoscopy has greatly increasedthe scope and precision of laryngeal surgery. All small benign lesions ofthe larynx are excised with this technique. Biopsies of malignant diseasecan be taken accurately from the suspicious area with minimal damage toadjacent tissue.

Fig. 4.99 Microlaryngoscopy. The holder for the laryngoscope is clamped (a),enabling the surgeon to have both hands free for instrumentation. The radiographsare seen in the background (b); the chest radiograph and radiograph of the cervicalspine are routine investigations before direct laryngoscopy. Cold light instrumentsgive bright, reliable illumination, and the development of a light-transmitting glassfiber cable has been another advance in endoscopy.

a

b



Obstruction of the larynx causes stridor, and may necessitate atracheostomy. Acute inflammatory conditions of the upper respiratorytract (e.g., epiglottis), foreign bodies or neoplasms limiting the airway arethe commonest causes of stridor.

Tracheosteomy is also required for respiratory failure due to centraldepression of the respiratory center, for example, strokes, barbituratepoisoning, head injury, poliomyelitis, or tetanus. Multiple rib fractures orsevere chest infections may require tracheostomy. Tracheostomy enablesbreathing to be controlled by an intermittent positive pressure respirator,and bronchial secretions can be removed with suction. A prolongedobstruction of the glottis may occur with juvenile papillomas, severetrauma to the larynx, or bilateral cord palsies, making a permanenttracheosteomy necessary. A tracheostomy tube with a speaking valveallows air to enter during inspiration, but closes on expiration so that airpasses through the larynx for phonation.

Emergency tracheostomy may be a difficult operation, particularly ifdone under local anesthetic when a general anesthetic with intubation isnot practical. An opening into the trachea through the cricothyroidmembrane offers a simpler and more direct relief for upper respiratorytract obstruction.

Tracheostomy

Fig. 4.100 A patient after tra-cheosteomy (with speaking valve).


The Larynx 229

Fig. 4.101 Plastic tra-cheosteomy tubes. Theseare also in common use.

Fig. 4.102 Silver tra-cheostomy tubes in com-mon use (Negus).

Fig. 4.103 Cricothyrotomycannula with trocar. Thisinstrument has been devisedfor emergency operations. Atracheosteomy can be per-formed later when the emer-gency of the acute obstruc-tion is past.



Fig. 4.104 Tracheostomy. Openings are usually made between the 2nd and 3rdtracheal rings. A “higher” tracheostomy predisposes to stenosis of the larynx in thesubglottic region. The airway is most accessible and superficial at the level of thecricothyoid membrane, and in acute laryngeal obstruction an opening through themembrane will restore the airway. The cricothyrotomy opening is, however, for anemergency, and is only temporary. Indwelling tubes at this site lead to subglotticstenosis of the larynx.


The Larynx 231

Fig. 4.105 Subglottic stenoses. Slight-ly hyperemic cords (arrows) with an areaof ring-like stenosis below the vocalcords can be seen in this patient. Thisstenosis followed trauma, partly relatedto a road traffic accident in which thetrachea was injured, and also related toa high tracheostomy through the firsttracheal ring. Dilation is rarely effectivefor this type of cicatricial stenosis, andexcision of the stenotic area of the tra-chea with end-to-end anastomosis orgrafting procedures are necessary. Sub-glottic stenosis is also a complication ofprolonged endotracheal intubation.

Fig. 4.106 Subglottic stenosis inbabies and children. This may be con-genital due to a grossly thickenedcricoid cartilage, or acquired secondaryto neonatal intubation with consequentcicatricial fibrosis.

Dilatation is ineffective, and endo-scopic laser treatment is appropriate foronly the mildest cases.

Most of these children will require atracheostomy, followed by a laryngotra-cheal reconstruction with costal carti-lage grafting.



Globus PharyngeusThis is a very common condition in which the patient, not infrequently ayoung girl, complains of a sensation of a lump in the throat. The siteindicated is the cricoid region.

When taking the history, a helpful direct question is to ask whetherthe lump is most apparent on swallowing food, fluid, or saliva. The patientwith globus will consistently reply that saliva is the problem, and that thesymptom occurs between meals.

The Hypopharynx and Esophagus

Fig. 4.107 Globus pharyngeus. Thepatient is indicating the region of thecricoid cartilage which is the site of dis-comfort with globus pharyngeus.

The symptom of discomfort in theregion of the cricoid is not infrequentlyassociated with nasal symptoms of post-nasal discharge or chronic rhinitis wherefrequent swallowing predisposes andaccentuates the globus symptom.

Fig. 4.108 Barium swallow. Globuspharyngeus is a psychosomatic condi-tion, but there is a demonstrable spasmof the cricopharyngeus on barium swal-low, where the barium column is seento be “nipped.” Over-attention by thepatient perpetuates the spasm, and usu-ally reassurance and explanation are theonly treatments required.


The Hypopharynx and Esophagus 233

Globus pharyngeus is not necessarily nonorganic, and “globus hystericus”is a misnomer. It is a condition that may call for investigation, particularlyin the older age group, when it may be the presenting symptom of diseasein the esophagus or stomach. Hiatus hernia and esophageal refluxcommonly cause cricopharyngeal spasm, and gastric ulcers andneoplasms may also present with globus. A barium swallow and meal is,therefore, an important investigation (Fig. 4.108). Cervical osteoarthritis(Fig. 4.109a, b, arrow) with marked changes in the region of the 6th

cervical vertebra may also give rise to globus.

Fig. 4.109 Cervical osteoarthritis. a Projection of cervical osteophytes into thepostcricoid region of the upper esophagus causes cricopharyngeal spasm and thesymptom of globus. b In this radiograph, gross osteophytes have caused “nipping”of the barium (arrow) by the cricopharyngeus muscle.

a b



Pharyngeal PouchThis is a herniation of mucous membrane through the posterior fibers ofthe inferior constrictor muscle above the cricopharyngeus, usuallyoccurring in old age. The defect predisposing to its development is afailure of coordinated relaxation of the cricopharyngeus on swallowing. Apouch is frequently associated with a hiatus hernia.

A small pouch may cause no symptoms, but when large, dysphagiadevelops, varying from slight to absolute. There is regurgitation ofundigested food, gurgling may be heard in the neck after eating, or aswelling may be seen, laterally in the neck, usually on the left.

The pouch accumulates food, and spillage into the respiratory tractmay cause coughing. A pouch may present with respiratory disease—either bronchitis, apical fibrosis simulating tuberculosis, or acutepulmonary infection (bronchitis, bronchopneumonia, or a lung abscess).

The barium swallow is the only investigation required to confirm thediagnosis of pharyngeal pouch. If symptoms are marked, surgery isneeded. Endoscopic stapling techniques with division of the party wall(arrow) has replaced a neck incision with pouch excision and repair.Rarely, a carcinoma occurs within the lumen of a pharyngeal pouch.

Fig. 4.110a, b Pharyngeal pouch.a b


The Hypopharynx and Esophagus 235

Fig. 4.111a-c Foreign bodies in theesophagus. Foreign bodies, such asbones, coins, pins, dentures, and smalltoys, may impact in the upper third ofthe esophagus. A history of possible for-eign impaction must not be ignored asesophageal perforation leads to cervicalcellulitis and mediastinitis, which maybe fatal.

Air seen on radiograph behind thepharynx and esophagus is diagnostic ofa perforation. Persistent dysphagia, painreferred to the neck or back, pain oninspiration, and fever all suggest a for-eign body.

Chest radiography and radiographyof the neck are essential investigations,but even if negative, persistent symp-toms are suspicious and esophagoscopyis necessary. However, coins which passthe cricopharyngeus usually traverse therest of the gut, and rarely requireremoval.

a

c

b



Fig. 4.112a, b Carcinoma of the pyriform fossa and upper esophagus. The pre-senting signs are dysphagia for solids and pain, commonly referred to the ear.There is early metastasis to the cervical nodes. A carcinoma involving mainly themedial wall of the pyriform fossa causes hoarseness.

The prognosis is not good, particularly with upper esophageal carcinoma,whether treatment is with radiotherapy or surgery. Resection for these carcinomasinvolves a pharyngolaryngectomy and the replacement or reconstruction of thecervical esophagus poses technical problems. Immediate replacement with stom-ach or colon, mobilized and brought through the thorax and sutured to the phar-ynx, is one technique.

The delayed use of neck and chest myocutaneous flaps is an alternativemethod of reconstruction. Microvascular surgical techniques have enabled imme-diate reconstruction with a section of the ileum, which is a further option.

a

b


titoletto sopra 237

Chapter 5The Head and Neck


238 The Head and Neck

Salivary Glands

Fig. 5.1 Submandibular calculus. Acalculus obstructing the submandibularduct causes painful and intermittentenlargement of the gland. The swellingoccurs on eating and regresses slowly.Secondary infection in the gland leadsto persistent tender swelling of thegland. The swelling in the submandibu-lar triangle is visible and palpablebimanually with one finger in themouth.

Fig. 5.2 Grossly enlarged submandibular gland. This develops if an impactedcalculus is ignored. A neoplasm of the submandibular gland is the differential diag-nosis if the enlargement is persistent and there is no evidence of a calculus on radi-ograph. The nodular surface and the firm, nontender character on palpation of thisgland are also suggestive of a neoplasm, commonly a pleomorphic adenoma oradenoid cystic carcinoma.


Salivary Glands 239

Fig. 5.3 Tonsillary lymph nodeenlargement. A tonsillar lymph nodeenlargement (arrow) may be similar toan enlarged submandibular gland. Thisnode is frequently palpable in children,being more conspicuous at times of ton-sillar or upper respiratory tract infec-tion, and may become very obvious, asin this case. The node is soft and tender.

Exact location of the site is impor-tant: It is posterior to the submandibu-lar triangle at the angle of themandible, and not within the sub-mandibular triangle.

Fig. 5.5 Submandibular calculus impacted at the orifice of the duct. This is easilyremoved with local anesthesia in the outpatients.

Fig. 5.4 Abscess formation in a sub-mandibular triangle lymph node sec-ondary to dental infection. Mumps mayalso cause a tender submandibularswelling, and an enlarged lymph node inthe submandibular triangle, secondaryto dental infection, simulates glandinvolvement.



Fig. 5.6 Submandibular calculidemonstrated on radiograph impact-ed in the duct. An anterior calculus maybe removed by incision over the duct inthe floor of the mouth, a suture beingplaced posterior to the calculus to pre-vent “slippage backwards” towards thegland.

Fig. 5.7 Excision of the submandibu-lar gland (specimen) is required for cal-culi impacted in the duct or within thegland (arrow). Care is taken in this oper-ation to preserve the mandibular branchof the facial nerve which crosses thesubmandibular triangle to supply themuscles of the angle of the mouth.

Fig. 5.8 Mixed parotid tumor (pleo-morphic adenoma) (arrow). Thesepresent as a firm, smooth, nontenderswelling. The growth is slow, so the his-tory may be long. The bulk of theparotid lies in the neck posterior to theramus of the mandible, and parotidtumors do not usually cause predomi-nantly facial swelling.


Salivary Glands 241

Fig. 5.9 Parotid swelling. A softerswelling in the tail of the parotid (arrow)may be an adenolymphoma (Warthin’stumor), a benign tumor of salivarygland tissue within a parotid lymphnode. The pleomorphic adenoma is alow-grade malignant tumor, and is com-monly in the superficial lobe of theparotid. The treatment is a superficialparotidectomy with preservation of thefacial nerve. A soft parotid swelling witha short history and a partial or completefacial palsy is probably an adenoid cysticcarcinoma or higher-grade malignanttumor of the parotid gland, requiringtotal parotidectomy with sacrifice of thefacial nerve and radiotherapy.

Fig. 5.10 Congenital hypertrophy ofthe masseter muscle. Careful palpationfollows observation of a swelling, andwhat appears as a parotid mass here ispalpable as a congenital hypertrophy ofthe masseter muscle.



Fig. 5.11 Fine needle aspiration (FNA). A needle aspiration is a frequently usedinvestigation for neck swellings. Aspiration from the neck swelling under localanesthetic enables histological examination of the aspirate smear to be made.

This avoids the necessity of an incision and “open” biopsy, or biopsy excision ofthe node.

a b

Fig. 5.12 Mumps. Acute viral parotitis is a common infection, and the diagnosis isusually obvious. Well-defined tender swelling of the parotid gland, first on one sideand shortly after on the other, with associated trismus and malaise, are characteris-tic. However, mumps can be deceptive when it remains unilateral and the swellingis not strictly confined to the parotid. In this case of mumps (a, b), the swellinginvolved the side of the face, causing lid and facial edema. Unilateral total deafnessis a complication of mumps.

a b


Salivary Glands 243

Fig. 5.13 Sebaceous cyst. A swelling inthe parotid region (arrow), but on theface suggests another diagnosis. Thereis a small punctum on the swelling inthis picture, diagnostic of a sebaceouscyst.

Fig. 5.14 Sebaceous cyston the face. Minor lesionssuch as sebaceous cystspresent a problem on theface when excision is need-ed. Particular care is neededto enucleate these cystsmeticulously, through inci-sions made within therelaxed skin tension lines. It may also be necessary to“break-up” the straight inci-sion line so that it is lessobvious.

A keloid is a further con-cern, particularly in blackskin. This followed excisionof a sebaceous cyst in theupper neck.



Fig. 5.15 Sialectasis of the parotidgland. This presents as intermittentepisodes of painful swelling. Calculi inthe parotid duct are uncommon, andare not easily demonstrated on radi-ograph. An intraoral view is necessary.

A sialogram confirms sialectasis,and the punctate dilations of theparotid ducts are similar in appearanceto bronchiectasis. The parotid swellingwith sialectasis is often infrequent andmild, and triggered by certain foods.There is no simple treatment; superficialparotidectomy is reserved for the rare,severe cases.

Fig. 5.16 Normal sub-mandibular sialogram. Thepattern of ducts not involvedwith sialectasis is demon-strated. A parotid sialogramis not difficult to perform,since the duct orifice oppo-site the second upper molartooth is obvious and can bemade more apparent bymassaging over the parotidgland to cause a visible flowof saliva. The submandibularduct orifice anteriorly in thefloor of the mouth is notobvious; cannulation forsialography may be difficult.


245

Inflammatory Neck SwellingsThe spread of dental infection must be remembered as a possible cause ofinflammatory neck swelling.

Swelling of the Neck

Fig. 5.17 Ludwig’s angina. An indurat-ed, tender, mid-line inflammation ischaracteristic of Ludwig’s angina. Biman-ual palpation reveals a characteristicwoody firmness of the normally soft tis-sues of the floor of the mouth, which isan early sign. This acute infection mayspread from the apices of the lower inci-sors, in this case following extraction.

In the preantibiotic era this condi-tion was serious, because spread ofinfection involved the larynx and causedthe acute onset of stridor. This compli-cation is still to be remembered,although extensive neck incisions torelieve pus under pressure are rarelynecessary, and the response to intra-muscular penicillin is good.

Fig. 5.18 Cervical cellulitis may devel-op from a dental abscess in the lowermolars and involve the neck laterally.



Fig. 5.19 Submental sinus. A chronic,localized, mid-line infection under thechin is probably a submental sinus. Thisrecurrent mass of granulation tissueformed at the opening of a sinus, lead-ing to apical infection in a lower incisortooth.

Fig. 5.20 Tuberculous cervicalabscesses. These are uncommon incountries where cattle are tuberculin-tested, as intake of infected milk is theusual cause. A chronic, discharging neckabscess in the posterior triangle is char-acteristic of tuberculosis. Firm, non-tender nodes without sinus formation inthe same site are also suggestive oftuberculosis. Chemotherapy alone usu-ally fails to control this condition, andexcision of the nodes or chronicabscesses is required.


Swelling of the Neck 247

Mid-line Neck Swellings

Fig. 5.21 Thyroglossal cyst. This is amid-line neck swelling forming in theremnant of the thyroglossal tract (a).The swelling is commonly between thethyroid and hyoid, but suprahyroid cystsalso occur. The convexity of the hyoidbone and thyroid cartilage push the cystto one side, so it may not be strictlymid-line. The cyst moves on swallowingand on protrusion of the tongue (b, c,arrows). It is usually nontender but maypresent with recurrent episodes of acuteswelling and tenderness.Treatment is excision with removal ofthe body of the hyoid bone tract. Failureto excise the body of the hyoid predis-poses to recurrence for the thyroglossaltract extends in a loop deep to thehyoid bone.

a

c

b



Fig. 5.22 Thyroglossal cyst. Excision ofthe cyst alone, without the tract andbody of the hyoid bone, leads to recur-rence. The cyst remnant causes inflam-mation and discharge at the scar. Thisappearance is characteristic of an inade-quately excised thyroglossal cyst.

Fig. 5.23 Dermoids. Mid-line neck swellings in the submandibular region (a) orsuprasternal region (b) are commonly dermoids.

a b



Lateral Neck Swellings

Fig. 5.24 Branchial cyst (a, arrow; b).This has a consistent site, is smooth,and, if there is no secondary infection,nontender. It lies between the upperone-third and lower two-thirds of theanterior border of the sternomastoid,and is deep to and partly concealed bythis muscle (c). It can be large by thetime it presents. When excised, the deepsurface is found to be closely related tothe internal jugular vein.

A metastatic lymph node from thethyroid, upper respiratory tract (e.g.,nasopharynx) or postcricoid region, andswellings of neurogenous origin(chemodectomas, neurofibromas, neu-roblastomas) are among the importantdifferential diagnoses of a lateral neckswelling. The ubiquitous lipoma is alsonot uncommon in the neck, and in chil-dren the cystic hygroma is to be remem-bered. Hodgkin’s disease also frequentlypresents with an enlarged cervical lymphnode.

a

c

b



Fig. 5.25 Laryngocele. This is anunusual neck swelling that the patientcan inflate with the Valsalva maneuver.It is an enlargement of the laryngeal sac-cule into the neck between hyoid andthyroid cartilage. It tends to occur inmusicians who play wind instruments,or in glass blowers. Infection may devel-op in laryngoceles (a pyolaryngocele),and presents as an acute neck swellingoften with hoarseness and stridor.

b

a

c

Fig. 5.26 Test for accessory cranial nerve (XI) function. The sternomastoid mus-cle is supplied by the accessory nerve. If the patient is asked to press the foreheadagainst the examiner’s hand (a), the sternal attachments of the muscle stand out(b, arrow). When cranial nerve X is inactive, the sternal head on the side of thelesion remains flat (c, arrow).



Fig. 5.27 Horner’s syndrome. Pressure on the sympathetic nerve trunk in theneck, particularly by malignant disease, causes changes in the eye. Ptosis, with asmall pupil, is apparent in the patient’s left eye; this is also associated with anenophthalmos and a lack of sweating. With a cervical swelling, examination shouldexclude Horner’s syndrome.


252

Abscessbrain 139cervical, tuberculous 246dental 172lymph node 239mastoid 80orbital 139peritonsillar 197pinna 54septal 118

Accessory cranial nervefunction test 250

Acoustic neuroma 12, 16, 18, 24Adenoid cystic carcinoma 171,

238, 241Adenoidectomy 109Adenoids 109–110, 189, 205

glue ear and 84, 89Adenolymphoma 241Adenoma, pleomorphic 171,

238, 240, 241AIDS

candidiasis 200, 202hairy leukoplakia 202

Amphotericin 200Angiofibroma of male puberty

147–148Angular stomatitis 168Anosmia 40, 144

testing 39, 40Antrochoanal polyp 147, 149Antroscopy 34–35Antrostomy 136, 142, 143Antrum

carcinoma 157washout 138

Aortic aneurysm 226Aphthous ulcers 171–175

tongue 173, 180Aspergillus niger 69, 176Aspirin hypersensitivity 144Asthma 135, 144Atherosclerosis 24Audiogram 17Audiometry 17–19

children 18impedance 19, 82pure-tone 17speech discrimination 18

Auditory brain stem response(ABR) 18

Auriscope 2, 5, 7, 81

Balance tests 20–24Barany box 12Barium swallow 232, 233, 234Barotrauma 7, 91, 137Basal cell carcinoma see

CarcinomaBat ears 49–51Behçet's syndrome 175Bell's palsy 8, 97, 98Benign migratory glossitis 176Benign paroxysmal positional

vertigo 22–23Bing (occlusion) test 12Blom–Singer valve 222–223Blue drum 84, 91Blue sclerae 92Brain abscess 139Branchial cyst 249Bullae, hemorrhagic 175Burn scars 58

Calculusparotid gland 175, 244submandibular gland238–240

Caldwell-Luc operation 143Caloric test 24Canal paresis 24Candida albicans 69, 200Candidiasis, oral 200–202

AIDS-related 200, 202Carbenoxolone 174Carcinoma 97

adenoid cystic 171, 238, 241basal cell 60, 106, 107, 158

treatment 107, 158esophageal 236external auditory meatus 70

laryngeal 220–221, 223subglottic 220supraglottic 220vocal cord 220, 221

nasal 106, 156–160antrum 157columella 132, 160septum 160vestibule 160

palate 190pinna 60postnasal space 162–163pyriform fossa 236sinuses

ethmoid 157maxillary 156

squamous cell 106, 160,182, 220tongue 180, 182tonsil 190

Catarrh 135Cellulitis

cervical 235, 245columella 133orbital 139

Cerebral ischaemia 20Cervical cellulitis 235, 245Cervical osteoarthritis 24, 233Chalk patches 72, 83Chancre 181Chemodectoma 191, 249Children

hearing assessmentaudiometry 18, 19otoacoustic

emissions 20laryngeal examination 37nasal examination 29nasal glioma 102snoring in 109, 186see also Specificconditions

Chloramphenicol 66Choanal atresia 100, 101Cholesteatoma 6, 76, 77–78,

97Chondrodermatitis nodularis

helicis chronicis 61Chorda tympani nerve 7, 8Chowes 58Ciliary dyskinesia 144Circumvallate papillae 36Cocaine-related vestibulitis

131, 132Cochlear implant 15Columella

carcinoma 132, 160cellulitis 133furuncle 133retraction 118

Common cold 134Conductive hearing loss see

Hearing lossCor pulmonale 189Cranio-facial resection 156Cricopharyngeal spasm 232,

233Cricothyrotomy

cannula with trocar 229site of 230

Cystic fibrosis 144Cystic hygroma 249Cysts

branchial 249

Index

A B

C


Index 253

dental 34dermoid 104, 248nasoalveolar 103postnasal (Thornvaldts)

35retention 194sebaceous 56, 243thyroglossal 247–248

Darwin's tubercle 44Dental cysts 34Dental sinusitis 139Dermoid 104, 248Diabetes mellitus 66Diplacusis 25Disseminated lupus

erythematosus 136Down's syndrome 189Drop attacks 24

Earbleeding from 91cauliflower ear 56examination 4–9

auriscopy 5, 7, 81microscopy 9pinna retraction 4pneumatic otoscopy

6–7foreign body 65ossicles, injury to 91prominent 49–51prosthetic 46referred pain 8, 190syringing 64–65

after mastoidectomy80

see also External auditory meatus; Middle ear; Pinna;

Tympanic membraneEardrum see Tympanic

membraneEarrings 52–54Eczema 53, 66, 132

see also Nasal vestibulitisElectrocochleography (ECoG)

18Electrogustometry 41, 98Electronystagmography 24Endaural incision 81Endoscopy

ear 7flexible 3laryngeal 38, 211nasal 30, 31, 126postnasal space 31, 35, 163rigid 3

sinuses 34–35surgery 143

Epiglottis 37laryngomalacia and 214

Epiglottitis 209Epistaxis 150–155

control of 151cautery 152

with enlarged adenoids 109

with hereditary nasal telangiectasia 153–154

with nasal carcinoma 159with septal hemangioma

155with septal perforation

127Epley maneuver 22, 23Epstein–Barr virus 202Erysipelas 58Erythema multiforme 175Esophageal reflux 233Esophagus 38

carcinoma 236foreign body 235perforation 235

Ethmoid sinus 139carcinoma 157CT scan 33, 142sinusitis 136, 137, 139,

140Eustachian tube

dysfunction 78, 84obstruction 82, 87patulous 87

Examinationear 4–9instruments 2, 3larynx 37–38lighting 3nose 29–35pharynx 36postnasal space 31, 35sinuses 33–35

External auditory meatusenlargement after

mastoidectomy 80examination 4furunculosis 67osteoma 71otitis externa 62, 66–70skin migration 62–63stenosis 67syringing 64–65wax impaction 62, 64

Facial palsy 59, 97–98bilateral 97tests of facial nerve

involvement 98Fine needle aspiration (FNA)

242Fistula

oroantral 137, 139perilymph 6, 91

Fistula test 6Fluconazole 202Foliate linguae 36Forceps, angled 2Foreign body

ear 65esophagus 235nose 129–130

removal 130Frenzel glasses 20Frontal sinus 139

CT scan 142mucocele 140–141sinusitis 137, 139, 140

Fungiform papillae 41Furuncle 4, 47–48, 66

columella 133Furunculosis 4, 67

Gait abnormalities 21Gentamycin 25Geographic tongue 176Glioma, nasal 102Globus pharyngeus 232–233Glomus jugulare tumor 28, 90,

183Glossitis 168

benign migratory 176median rhomboid 181

Glue ear 82–86impedance testing 19, 82see also Otitis media

Gonococcus 195Gouty tophi 61Granulation tissue

aural 79laryngeal 220malignant otitis externa

69nasal 132, 156

Granuloma 53, 88, 132, 156larynx 216

intubation 216, 221pyogenic 166Wegener's 135, 136

Grommets 86, 88insertion 85–86occlusion 88–89

Gumma 180

D

E

F

G


254 Index

Hairy leukoplakia 202Halitosis 192Hay fever 134Head mirror 3, 4Headache

cluster 138sinusitis and 137, 140

Headlight, fiberoptic/electric 3Hearing aids 13–15

bone-anchored 14, 46cochlear implant 15digital 13, 14

Hearing loss 10–12audiometry 17–19conductive 10–13, 19

audiogram 17deep otitis externa

and 68otitis media and 89otosclerosis and 92Paget's disease and

95glue ear 84–85otoacoustic emissions 20psychosomatic 18radiology 16sensorineural 10–11, 13,

19acoustic neuroma

and 16audiogram 17in Ménière's disease

25tests 11–12tinnitus and 28total 12

in one ear 12Heel–toe walking 21Hemangioma 101

lip 166nose 101septal 155tongue 177vocal cord 217

Hematomanasal 111

septal 113, 114, 117, 118

pinna 56vocal cord nodule 213

Hemolytic streptococcus 195Hemotympanum 84Hereditary nasal telangiectasia

153–154Herpes, geniculate 59Herpes simplex, lip 167Herpes zoster 59

otitis externa and 70Hiatus hernia 233, 234Hillocks 44

HIV infectionmouth ulcers 202oral candidiasis 202see also AIDS

Hoarseness 211, 212, 224children 212, 213laryngitis 210see also Larynx; Vocal

cordsHodgkin's disease 249Horner's syndrome 251Human papilloma virus 213Hydrocortisone 171Hyperemia

laryngeal mucous membrane 210, 218

pharyngeal mucous membrane 203

tonsil 195vocal cords 217, 231

Hypertelorism 100Hypertension 24Hyperventilation 20Hypoglossal nerve paralysis

183Hypoglycemia 20Hypotension, orthostatic 20Hysterical aphonia 224Hysterical dysphonia 224

Impedance testing 19, 82Implants

cochlear 15osseo-integrated 46

Incus 7squamous epithelium on

76Infectious mononucleosis

198–200in patients without tonsils

200Insect in ear 65Internal carotid aneurysm 191Iodoform sensitivity 58Ischaemia

cerebral 20vertebro-basilar 24

Jobson–Horne probe 2

Keloids 52–53, 243Keratosis 168

obturans 62pharyngeus 193, 194

Ketoconazole 202Kiesselbach's plexus 150

Lacrimation test 98Laryngeal mirror 2, 37Laryngeal nodules 212–213

with hematoma 213Laryngeal web 211Laryngectomy 222–223

partial 222total 222

Laryngitis 210acute 210, 217chronic 210, 216, 218,

219, 220laryngeal nodules

212prolapse of the

ventricular mucous membrane 219

hypertrophy of the ventricular bands 218

Laryngocele 250Laryngomalacia 214Laryngoscopy

fiberoptic 37indirect 37

Larynxcarcinoma 220–221, 223

subglottic 220supraglottic 220

examination 37–38children 37endoscopy 38, 211

granuloma 216intubation 216, 221

inflammation 210microsurgery 227papilloma 213–214polyp at the anterior

commissure 216subglottic stenosis 231

children 231see also Hoarseness; Vocal

cordsLaser surgery 181, 221Leukoplakia 182, 219, 220

hairy 202Lingual thyroid 179Lingual tonsil 189, 193Lip

hemangioma 166herpes simplex 167mucocele 166ulcers 166–167

Lipoma 249Little's area 29, 150–152Ludwig's angina 245Lupus vulgaris 161Lyme disease 97Lymph node

abscess 239

H L

I

J

K


Index 255

enlargement 191, 239Lymphoma 109Lymphosarcoma 162, 190

Magnetic resonance imaging(MRI) 16

Malingering 18, 40Malleus fixation 6Mandibular

underdevelopment 124Masseter muscle, congenital

hypertrophy 241Mastoidectomy 80–81, 90

meatus enlargement 80Mastoiditis 89Maxillary sinus

acute sinusitis 136–139, 142

antral washout 138surgical treatment

139chronic sinusitis 140, 142CT scan 33, 142endoscopy 34–35radiographs 142transillumination 34

Maxillectomy 156Mediastinitis 235Melanoma 60, 70

malignant 156Melkersson–Rosenthal's

syndrome 97Ménière's disease 24, 25–27Meningitis 12, 139Mentoplasty 123Metronidazole 197Microtia 45–46Middle ear

aural granulation 79aural polyp 79cholesteatoma 77–78fluid 6, 19, 87mastoid abscess 80surgery 93–96

middle-ear operatingmicroscope 96

see also Otitis mediaMigrainous neuralgia 138Mirror

head 3, 4laryngeal 2, 37postnasal 2, 31

Monilla 200Mucocele

frontal sinus 140–141lip 166ranula 179

Multiple sclerosis 20Mumps 12, 239, 242Myringitis

bullous 70granular 68, 69, 79

Myringoplasty 75Myringotomy 85–86

excess bleeding 88, 89Myxoedema 210

Nasal adhesion 133Nasal allergy 134Nasal fracture 111

complications 112–113Nasal glioma 102Nasal hemangioma 101

septal 155Nasal hematoma 111

septal 113, 114, 117, 118Nasal obstruction 101, 113,

125–126, 127adenoids 109–110rhinitis 135rhinometry 32sinusitis 137, 140snoring and 185synechiae 133vestibulitis 131see also Nasal polyps

Nasal papilloma 105, 156excision 105pedunculated 29

Nasal polyps 144–147, 149, 156

antrochoanal 147, 149oropharynx 147recurrent 144

Nasal saddling 113, 114–117, 132, 135

childhood 117grafts 115–116plastic surgery 118

Nasal septum 29abscess 118carcinoma 160deviation 125–127

childhood 127septoplasty 125, 126,

132submucous resection

(SMR) 125vestibulitis and 131,

132hemangioma 155hematoma 113, 114, 117,

118perforation 125, 127–128,

131spur 125, 126

Nasal tumors 156–163see also Specific tumors

Nasal vestibule 29carcinoma 160

papilloma 29ulceration 161

Nasal vestibulitis 128–129, 131–132, 200

children 132Nasoalveolar cysts 103Nasopharynx see Postnasal

spaceNeck

radiography 38swellings 245–251

Neomycin 58, 66Neoplasms see Specific

neoplasmsNeuralgia, migrainous 138Neuroblastoma 249Neurofibroma 191, 249Nickel sensitivity 53Noise trauma 17Nose

deformities 100–102bifid nose 100congenital atresia

100–101saddling 113,

114–117, 132, 135examination 29–35

children 29endoscopy 30, 31,

126rhinometry 32speculum 29–30

foreign body 129–130removal 130

inflammation, chronic 161

Nose bleeds see EpistaxisNystagmus 20, 22, 24Nystatin 200, 202

Occlusion (Bing) test 12Orbit

lateral displacement with mucocele 140–141

surgical emphysema of112

Orbital abscess 139Orbital cellulitis 139Oroantral fistula 137, 139Oropharynx

candidiasis 200, 201nasal polyps 147scleroma 204

Osseo-integrated implants 46Osteoarthritis, cervical 24, 233Osteogenesis imperfecta tarda

92Osteoma 71

swimmer's 71Otitis externa 62, 66–70

M

N

O


256 Index

bullous 70Otitis externa chronic 67

deep 68eardrum perforation and

69eczematous 66fungal 69malignant 69with herpes zoster 70

Otitis media 17, 72acute 89–90, 109children 82–86, 89, 109eardrum perforation and

75, 76with effusion 78, 82–86,

89, 109chronic 87–88myringotomy 85

Otoacoustic emissions 20Otorrhea

cholesteatoma and 77eardrum perforation and

75, 89Otosclerosis 17, 92–93

Paget's disease 95Palate

carcinoma 190trauma 208

following tonsillectomy 207

Papillaecircumvallate 36fungiform 41

Papillomalaryngeal 213–214nasal 105, 156

excision 105pedunculated 29

tongue 178tonsil 187uvula 187

Papillomatosis, recurrent respiratory 213–214

management 214Parotid gland

calculus 175, 244sialectasis 244tumors 191, 240–241

adenolymphoma 241pleomorphic

adenoma 240Parotitis see MumpsPatterson–Brown–Kelly

syndrome 168Paul–Bunnell test 198Pemphigus 175Penicillin 58, 89, 133, 195, 197,

245

Periadenitis mucosa necroticarecurrens 174

Perichondritis 54, 57septal 128

Perilymph fistula 6, 91Pharyngeal pouch 234Pharyngitis 195

chronic 203Pharynx, examination 36Phonosurgery 224Pinna 44–61

abscess 54basal cell carcinoma 60burn scars 58deformities

Darwin's tubercle 44hillocks 44microtia 45–46preauricular sinuses

46–48prominent ears

49–51earrings and 52–54gouty tophi 61granuloma 53hematoma 56iodoform sensitivity 58keloids 52–53nickel sensitivity 53perichondritis 54, 57relapsing polychondritis

57retraction 4sebaceous cyst 56solar keratoses 60trauma 54, 55, 56ulceration 60, 61

Pleomorphic adenoma 171,238, 240, 241

Plummer–Vinson syndrome168

Pneumatic otoscope 6, 9Polyarteritis nodosa 132Polychondritis, relapsing 57Polyp

anterior commissure ofthe larynx 216

aural 79nasal 144–147, 149, 156

antrochoanal 147, 149oropharynx 147recurrent 144

vocal cord 215Postaural incision 81Postnasal mirror 2, 31Postnasal space

carcinoma 162–163examination 31

endoscopy 31, 35, 163

Thornvaldts cyst 35Preauricular sinuses 46–47

excision 48Prednisolone 97Presbycousis 17Prochlorperazine 25Pseudomonas pyocyanea 57,

68Pyocele 141Pyolaryngocele 250Pyriform fossa, carcinoma 236

Quinsy 190, 191, 197–198, 204bleeding 197tonsillectomy 197, 204

Radiographyadenoids 110, 189esophageal foreign bodies

235hearing loss assessment

16nasal fracture 112neck 38sinuses 33

maxillary 142tonsils 189

Radiotherapycarcinoma

maxillary 156nasal 158, 159postnasal space 162

glomus jugulare tumor 90

Ramsay–Hunt syndrome 59Ranula 179Reinke's edema 218Relapsing polychondritis 57Retention cysts 194Rhabdomyosarcoma 139Rhinitis

acute 134atrophic 136chronic 135granular 132medicamentosa 135

Rhinolith 130Rhinometry 32

acoustic 32Rhinophyma 106Rhinoplasty 119–124, 146

external 122nasal tip 121with mandibular

advancement 124with mentoplasty 123

Rhinorrhoea 134, 137, 140with enlarged adenoids

109Rhinoscleroma 136, 204

P

Q

R


Index 257

Rinne test 11, 12Romberg test 21

Salivary glandscalculus 175, 238–240see also Parotid gland;

Submandibular glandSarcoidosis 97, 132, 161Scarring

burn scars, pinna 58scar revision 108scleroma and 204tympanic membrane

72–73, 86Schirmer's test 98Schwannoma 16Scleroma 204Screamer's nodules 212, 213Sebaceous cyst 243

pinna 56Sensorineural hearing loss see

Hearing lossSeptoplasty 125, 126, 132Sialectasis 244Sialogram 244Singer's nodules 212Sinuses

cavernous sinus thrombosis 138

endoscopic surgery 143examination 33–35

CT scan 33, 142endoscopy 34–35radiography 33, 142transillumination 34

nasal 122preauricular 46–47

excision 48submental 246see also Ethmoid sinus;

Frontal sinus; Maxillary

sinus; Sphenoid sinusSinusitis 34, 125, 134, 144

acute 136–139maxillary 136–139,

142chronic 140, 142dental 139

Sleep apnea 186obstructive, tonsillitis and

189Sleep studies 186Smell, testing 39, 40Snoring 185–186

assessment 186in children 109, 186treatment 184, 185–186,

187uvula and 184

Soft palatescleroma 204ulcers 173, 203uvulopalatoplasty 184,

185–186see also Palate

Solar keratoses 60Specula 3

aural 2nasal 2, 29–30Siegle's 9

Speech discriminationaudiometry 18

Sphenoid sinus 139CT scan 142sinusitis 137

Squamous cell carcinoma seeCarcinoma

Stapedectomy 93–95Stapedial reflex 98Stapes 92

fixation 92injury 91prosthesis 93–95

Stomatitis, angular 168Streptococcus, hemolytic 195Stridor 213, 214, 228, 245Stroboscopy 224–225Subglottic stenosis 231Submandibular gland

calculus 238–240enlarged 238excision 240

Submental sinus 246Supratonsillar cleft 192Swabs 2Synechiae 133Syphilis

secondary 175, 203tertiary 182tongue ulceration 181

Systemic lupus erythematosus132

Taste buds 41Taste, testing 39, 41, 98Telangiectasia 153–154Thrush, oral 200–202Thyroglossal cyst 247–248Thyroid, lingual 179Tinnitus 28

in Ménière's disease 25maskers 28

Tongue 176–183black hairy 176carcinoma 180, 182circumvallate papillae 36depressor 2, 36

tonsil size and 188examination 36

foliate linguae 36fungiform papillae 41geographic 176hemangiomas 177hypoglossal nerveparalysis 183leukoplakia 182lingual thyroid 179papilloma 178taste testing 39, 41tie 176ulceration 173, 180–182

Tonsil 205carcinoma 190enlargement 109, 188

simulated 191unilateral 190

examination 36exudate 192, 194, 195hyperemia 195keratosis pharyngeus

193, 194lingual 189, 193meeting in the mid-line

188, 189papillomas 187retention cysts 194size 188ulcers 203

Tonsillar fossae 205blood clot following

tonsillitis 206, 207Tonsillary lymph node

enlargement 239Tonsillectomy 192, 197,

204–208guillotine tonsillectomy

208palatal trauma 207

Tonsillitis 189, 204acute 195–196, 204secondary infection 206,

207see also Quinsy

Torus mandibularis 169–170Torus palatinus 169Trachea 38Tracheostome 222–223

stomal stud 222Tracheostomy 228–230

site of 230Transillumination 34Treacher-Collins syndrome 45Triamcinolone 52, 171Trichloroacetic acid 152Tuberculosis 180

cervical abscesses 246Tuning fork 2

hearing tests 11, 12Tympanic membrane 72–77

barotrauma 7blue drum 84, 91

S

T


258 Index

Tympanic membranechalk patches 72, 83deep otitis externa 68examination 4–9mobility 6, 9, 82–83normal appearance 6–7otitis media with effusion

and 82–83, 87perforation 72

attic 77central 75healing 75marginal 76otitis externa and 69otitis media and 75,

76, 89safe 75traumatic 74–75unsafe 76

retracted 73, 78scarring 72–73, 86vesicle 83

Tympanoplasty, intact canalwall 81

Tympanosclerosis 6, 72, 86Tympanotomy 90

Ulcersaphthous 171–175, 180contact ulcers of the

larynx 216lip 166–167nasal vestibule 161pinna 60, 61soft palate 173, 203tongue 173, 180–182tonsil 203with HIV infection 202

Uvula 184bifid 184papillomas 187

Uvulopalatoplasty 184,185–186

Ventricular bands, hypertrophy218

Vertebral angiogram 24Vertebro-basilar ischaemia 24Vertigo 20–24

benign paroxysmalpositional vertigo 22–23in Ménière's disease 25

Vestibulitis see Nasalvestibulitis

Vocal cords 210carcinoma 220, 221edema 218hemangiomas 217

nodules 212–213with hematoma 213

paralysis 224, 226pedunculated polyp 215see also Hoarseness;

Larynx

Warthin's tumor 241Wax impaction 62, 64Weber test 11, 12Wegener's granuloma 135,

136

U

V

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