Lecture Notes on Diseases of the Ear, Nose, and Throat PDF

Diseases of the Ear, Nose and Throat LECTURE NOTES ON Diseases of the Ear, Nose and Throat P.D. BULL MB, BCh, FRCS Consultant Otolaryngologist Royal Hallamshire Hospital and Sheffield Children’s Hospital Sheffield Honorary Senior Clinical Lecturer in Otolaryngology University o...

Diseases of the Ear, Nose and Throat LECTURE NOTES ON Diseases of the Ear, Nose and Throat P.D. BULL MB, BCh, FRCS Consultant Otolaryngologist Royal Hallamshire Hospital and Sheffield Children’s Hospital Sheffield Honorary Senior Clinical Lecturer in Otolaryngology University of Sheffield Ninth Edition Blackwell Science © 2002 by Blackwell Science Ltd a Blackwell Publishing Company Editorial Offices: Osney Mead, Oxford OX2 0EL, UK Tel: +44 (0)1865 206206 Blackwell Science Inc., 350 Main Street, Malden, MA 02148-5018, USA Tel: +1 781 388 8250 Blackwell Science Asia Pty, 54 University Street, Carlton,Victoria 3053, Australia Tel: +61 (0)3 9347 0300 Blackwell Wissenschafts Verlag, Kurfürstendamm 57, 10707 Berlin, Germany Tel: +49 (0)30 32 79 060 The right of the Author to be identified as the Author of this Work has been asserted in accordance with the Copyright, Designs and Patents Act 1988. All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted, in any form or by any means, electronic, mechanical, photocopying, recording or otherwise, except as permitted by the UK copyright, Designs and Patents Act 1988, without the prior permission of the publisher. First published 1961 Reprinted 1988, 1989 Reprinted 1962, 1965, 1967 Seventh edition 1991 Second edition 1968 Reprinted 1992, 1993, 1995 Reprinted 1970, 1971 Four Dragons edition 1991 Third edition 1972 Reprinted 1992, 1995 Reprinted 1975 Eighth edition 1996 Fourth edition 1976 International edition 1996 Reprinted 1978 Reprinted 1999 Fifth edition 1980 Ninth edition 2002 Sixth edition 1985 Library of Congress Cataloging-in-Publication Data Bull, P. D. Lecture notes on diseases of the ear, nose, and throat. — 9th ed. / P. D. Bull. p. cm. — (Lecture notes on) Includes index. ISBN 0-632-06506-0 (pbk.) 1. Otolaryngology. [DNLM: 1. Otorhinolaryngologic Diseases.WV 140 B935L 2002] I. Title: Diseases of the ear, nose, and throat. II. Title. III. Lecture notes series RF46.B954 2002 617.5¢1— dc21 2001007096 ISBN 0-632-06506-0 A catalogue record for this title is available from the British Library Set in 9/12 Gill Sans by SNP Best-set Typesetter Ltd., Hong Kong Printed and bound in India by Replika Press PVT Ltd For further information on Blackwell Publishing, visit our website: www.blackwell-science.com Contents Preface to the Ninth Edition, vii Preface to the First Edition, viii 1 The Ear: Some Applied Anatomy, 1 2 Clinical Examination of the Ear, 5 3 Testing the Hearing, 7 4 Deafness, 15 5 Conditions of the Pinna, 19 6 Conditions of the External Auditory Meatus, 25 7 Injury of the Tympanic Membrane, 33 8 Acute Otitis Media, 35 9 Chronic Otitis Media, 39 10 Complications of Middle-Ear Infection, 43 11 Otitis Media with Effusion, 51 12 Otosclerosis, 54 13 Earache (Otalgia), 57 14 Tinnitus, 59 15 Vertigo, 61 16 Facial Nerve Paralysis, 66 17 Clinical Examination of the Nose and Nasopharynx, 69 18 Foreign Body in the Nose, 71 19 Injuries of the Nose, 73 20 Epistaxis, 77 21 The Nasal Septum, 81 v vi Contents 22 Miscellaneous Nasal Infections, 86 23 Acute and Chronic Sinusitis, 88 24 Tumours of the Nose, Sinuses and Nasopharynx, 95 25 Allergic Rhinitis,Vasomotor Rhinitis and Nasal Polyps, 99 26 Choanal Atresia, 107 27 Adenoids, 109 28 The Tonsils and Oropharynx, 111 29 Tonsillectomy, 116 30 Retropharyngeal Abscess, 119 31 Examination of the Larynx, 121 32 Injuries of the Larynx and Trachea, 124 33 Acute Disorders of the Larynx, 126 34 Chronic Disorders of the Larynx, 129 35 Tumours of the Larynx, 131 36 Vocal Cord Paralysis, 135 37 Airway Obstruction in Infants and Children, 139 38 Conditions of the Hypopharynx, 148 39 Tracheostomy, 155 40 Diseases of the Salivary Glands, 163 Index, 173 Preface to the Ninth Edition This ninth edition of Lecture Notes on Diseases of the Ear, Nose and Throat again allows an updating of the text.We have been able to include on this oc- casion further colour photographs rather than line drawings which I hope will remain in the memory better and serve as reminders to the readers of the conditions that can occur within the upper aerodigestive tract. It is interesting in revising this little book every few years how much there is to change in fairly subtle ways as the specialty develops and technology im- proves.The trend in educational circles in the early part of the 21st century seems to be that students should learn less and less factual knowledge and there is far more concern with process and in a spirit of concordance with this (though not entire agreement), I have reduced the text of some of the chapters considerably and omitted quite a lot of details, particularly where it relates to surgical procedures. As before, I have avoided the cumbersome use of ‘he or she’, or ‘they’ as a singular pronoun and I hope that I will be forgiven again in the interest in avoiding prolixity for using ‘he’ to mean either gender without prejudice or favour. Acknowledgements I am pleased to acknowledge the invaluable help of the editorial and pro- duction departments of Blackwell Publishing who have encouraged the production of this new edition of Lecture Notes in Diseases of the Ear, Nose and Throat, and in particular to Fiona Goodgame and Alice Emmott. I am grateful to my clinical colleagues for advice willingly given and for help with the illustrations. I am indebted particularly to Mark Yardley, Tim Woolford, Charles Romanowski and Tim Hodgson. Without the skill and cooperation of the Department of Medical Illustration at the Royal Hallamshire Hospital, I would have had few images to include in this little book. I am grateful to Alun Bull for the cover images. P.D. Bull January 2002 vii Preface to the First Edition This book is intended for the undergraduate medical student and the house officer. It is hoped that, though elementary, it will also prove of use to the general practitioner. Many conditions encompassed within the so-called ‘specialist’ subjects are commonly seen in general practice, and the practitioner is therefore obliged to be familiar with them. He is not asked to perform complex aural operations, or even to be acquainted with their details, but he is expected to appreciate the significance of headache supervening in otitis media, to treat epitaxis, and to know the indications for tonsillectomy. Emphasis has therefore been laid on conditions that are important either because they are common or because they call for investigation or early treatment. Conversely, some are rare conditions and specialized techniques have received but scant attention, whilst others have been omitted, because the undergraduate should be protected from too much ‘small print’, which will clutter his mind and which belongs more properly to postgraduate studies. The study of past examination questions should be an integral part of the preparation for any examination, and students are strongly advised to ‘work-up’ the examination questions at the end of the book.Time spent in this occupation will certainly not be wasted, for the questions refer, in every case, to the fundamentals of the specialty. E.H. Miles Foxen ix  CHAPTER 1 The Ear: Some Applied Anatomy THE PINNA The external ear or pinna, is composed of cartilage with closely adherent perichondrium and skin. It is developed from six tubercles of the first branchial arch. Fistulae and accessory auricles result from failure of fusion of these tubercles. THE EXTERNAL AUDITORY MEATUS The external auditory meatus is about 25 mm in length, has a skeleton of cartilage in its outer third (where it contains hairs and ceruminous glands) and has bone in its inner two-thirds. The skin of the inner part is exceedingly thin, adherent and sensitive. At the medial end of the meatus there is the antero-inferior recess, in which wax, debris or foreign bodies may lodge. THE TYMPANIC MEMBRANE (F i g. 1. 1 ) The tympanic membrane is composed of three layer — skin, fibrous tissue and mucosa.The normal appearance of the membrane is pearly and opaque, with a well-defined light reflex due to its concave shape. THE TYMPANIC CAVITY Medial to the tympanic membrane, the tympanic cavity is an air-containing space 15 mm high and 15 mm antero-posteriorly, although only 2 mm deep in parts. The middle ear contains the ossicular chain of malleus, incus and stapes (Fig. 1.2) and its medial wall is crowded with structures closely relat- ed to one another: the facial nerve, the round and oval windows, the lateral semicircular canal and basal turn of the cochlea.The major reason for hav- ing an air-containing middle ear is to reduce the acoustic impedance that would be caused if a sound wave in air were to be applied directly to the cochlear fluids.Without this impedance matching, 99% of the sound energy would simply be reflected at an air/fluid interface. THE EUSTACHIAN TUBE The Eustachian tube connects the middle-ear cleft with the nasopharynx and is responsible for the aeration of the middle ear. The tube is more 1 2 Chapter 1: The Ear: Some Applied Anatomy Pars flaccida Handle of malleus Light reflex Pars tensa Fig. 1.1 The normal tympanic membrane (left). The shape of the incus is visible through the drum at 2o’clock. (Courtesy of MPJ Yardley.) RELATIONS OF EXTERNAL, MIDDLE AND INNER EAR Malleus Incus Stapes Semicircular canal Cochlea Carotid artery Facial nerve Eustachian tube Fig. 1.2 Diagram to show the relationship between the external, middle and inner ears.  The Ear 3 ANATOMY OF MIDDLE EAR AND MASTOID AIR CELLS Mastoid antrum Temporal lobe Attic Incus Malleus Lateral sinus Lateral semicircular canal Mastoid air cells Stapes Round-window niche Facial nerve Eustachian tube Fig. 1.3 Diagram to show the anatomy of the middle ear and mastoid air cells. horizontal in the infant than in the adult and secretions or vomit may enter the tympanic cavity more easily in the supine position. The tube is nor- mally closed and is opened by the palatal muscles on swallowing.This is im- paired by the presence of a palatal cleft. THE FACIAL NERVE The facial nerve is embedded in bone in its petrous part but exits at the sty- lomastoid foramen (Fig. 1.3). In infants, the mastoid process is undeveloped and the nerve very superficial. 4 Chapter 1: The Ear: Some Applied Anatomy THE LEFT TEMPORAL BONE Supra-meatal triangle Zygoma Tympanic ring Mastoid process Styloid process Fig. 1.4 The left temporal bone. Fig. 1.5 A preparation showing the bony inner ear of semicircular canals and cochlea (Preparation by Mr S Ell.) THE MASTOID CELLS The mastoid cells form a honeycomb within the temporal bone, acting as a reservoir of air to limit pressure changes within the middle ear.The extent of pneumatization is very variable and is usually reduced in chronic middle- ear disease. CHAPTER 2 Clinical Examination of the Ear The examination of the ear includes close inspection of the pinna, the ex- ternal auditory canal and the tympanic membrane. Scars from any previous surgery may be inconspicuous and easily missed. The ear is most conveniently examined with an auriscope (Fig. 2.1). Modern auriscopes have distal illumination via a fibre-optic cone giving a bright, even light. Because interpretation of the appearance depends to a Fig. 2.1 Auriscope with halogen bulb lighting via a fibreoptic cone. 5 6 Chapter 2: Clinical Examination of the Ear large extent on colour, it is essential that the battery should be in good con- dition to give a white light. A common error in examination of the tympanic membrane is to use too small a speculum; the largest that can be inserted easily should be used. Good auriscopes are expensive but are a worthwhile investment. Impor- tant points in the examination of the ear are listed in Box 2.1. EXAMINATION OF THE EAR 1 Look for any previous scars. 2 Examine the pinna and outer meatus by head-mirror or room lighting. 3 Remove any wax or debris by syringing, or by instruments if you are practised in this. 4 Pull the pinna gently backwards and upwards (downwards and backwards in infants) to straighten out the meatus. 5 Insert the auriscope gently into the meatus and see where you are going by looking through the instrument. If you cannot get a good view, either the speculum is the wrong size or the angulation is wrong. 6 Inspect the external canal. 7 Inspect all parts of the tympanic membrane by varying the angle of the speculum. 8 Do not be satisfied until you have seen the membrane completely. 9 The normal appearance of the membrane varies and can only be learnt by practice. Such practice will lead to the recognition of subtle abnormalities as well as the more obvious ones. Box 2.1 Examination of the ear.  CHAPTER 3 Testing the Hearing There are three stages to testing the hearing and all are important. Audiograms can be wrong. 1 Clinical assessment of the degree of deafness. 2 Tuning fork tests. 3 Audiometry. CLINICAL ASSESSMENT OF THE DEGREE OF DEAFNESS By talking to the patient, the examiner quickly appreciates how well a patient can hear and this assessment continues throughout the interview. A more formal assessment is then made by asking the patient to repeat words spoken by the examiner at different intensities and distances in each ear in turn. The result is recorded as, for example, whispered voice (WV) at 150 cm in a patient with slight deafness, or conversational voice (CV) at 15 cm in a deafer individual. If profound unilateral deafness is suspected, the good ear should be masked with a Barany noise box and the deaf ear tested by shouting into it. The limitations of voice and whisper tests must be borne in mind; they are approximations but with practice can be a good guide to the level of hearing and will confirm the audiometric findings. TUNING FORK TESTS Before considering tuning fork tests it is necessary to have a basic concept of classification of deafness. Almost every form of deafness (and there are many) may be classified under one of these headings: conductive deafness; sensorineural deafness; mixed conductive and sensorineural deafness. Conductive deafness (Fig. 3.1) Conductive deafness results from mechanical attenuation of the sound waves in the outer or middle ear, preventing sound energy from reaching 7 8 Chapter 3:Testing the Hearing CONDUCTIVE DEAFNESS Fig. 3.1 Conductive deafness is caused by an abnormality of the external or middle ear (shaded). the cochlear fluids. It may be remediable by surgery and so it is important it is recognized.The hearing by bone conduction will be normal in pure con- ductive deafness. Sensorineural deafness (Fig. 3.2) Sensorineural deafness results from defective function of the cochlea or of the auditory nerve, and prevents neural impulses from being transmitted to the auditory cortex of the brain. Mixed deafness Mixed deafness is the term used to describe a combination of conductive and sensorineural deafness in the same ear. RINNE’S TEST This test compares the relative effectiveness of sound transmission through the middle ear by air conduction (AC), and bypassing the middle ear by bone conduction (BC). It is usually performed as follows: a tuning fork of 512 Hz (cycles per second) is struck and held close to the patient’s ear; it is then  Testing the Hearing 9 SENSORINEURAL DEAFNESS Fig. 3.2 Sensorineural deafness is caused by an abnormality of the cochlea or the auditory nerve (shaded). placed firmly on the mastoid process and the patient is asked to state whether it is heard better by BC or AC. Interpretation of Rinne’s test If AC>BC–called Rinne positive–the middle and outer ears are functioning normally. If BC > AC – called Rinne negative – there is defective function of the outer or middle ear. Rinne’s test tells you little or nothing about cochlear function. It is a test of middle-ear function. WEBER’S TEST This test is useful in determining the type of deafness a patient may have and in deciding which ear has the better-functioning cochlea. The base of a vibrating tuning fork is held on the vertex of the head and the patient is asked whether the sound is heard centrally or is referred to one or other ear. In conductive deafness the sound is heard in the deafer ear. In sensorineural deafness the sound is heard in the better-hearing ear (Figs 3.3–3.5) 10 Chapter 3:Testing the Hearing SYMMETRICAL HEARING IN BOTH EARS Fig. 3.3 Tuning fork tests showing a positive Rinne in each ear and the Weber test referred equally to AC>BC AC>BC each ear, indicating symmetrical hearing in both ears with normal middle-ear function. AUDIOMETRY PURE TONE AUDIOMETRY Pure tone audiometry provides a measurement of hearing levels by AC and BC and depends on the cooperation of the subject.The test should be car- ried out in a sound-proofed room. The audiometer is an instrument that generates pure tone signals ranging from 125 to 12 000 Hz (12 kHz) at vari- able intensities.The signal is fed to the patient through ear phones (for AC) or a small vibrator applied to the mastoid process (for BC). Signals of in- creasing intensity at each frequency are fed to the patient, who indicates when the test tone can be heard.The threshold of hearing at each frequen- cy is charted in the form of an audiogram (Figs 3.6–3.8), with hearing loss expressed in decibels (dB). Decibels are logarithmic units of relative inten- sity of sound energy.When testing hearing by BC, it is essential to mask the opposite ear with narrow-band noise to avoid cross-transmission of the signal to the other ear.  Testing the Hearing 11 SENSORINEURAL DEAFNESS IN RIGHT EAR Fig. 3.4 Sensorineural deafness in the right ear. The Rinne test is positive AC>BC AC>BC on both sides and the Weber test is referred to the left ear. SPEECH AUDIOMETRY Speech audiometry is employed to measure the ability of each ear to dis- criminate the spoken word at different intensities. A recorded word list is supplied to the patient through the audiometer at increasing loudness levels, and the score is plotted on a graph. In some disorders, the in- telligibility of speech may fall off above a certain intensity level. It usually implies the presence of loudness recruitment — an abnormal growth of loud- ness perception. Above a critical threshold, sounds are suddenly perceived as having become excessively loud.This is indicative of cochlear disorder. IMPEDANCE TYMPANOMETRY Impedance tympanometry measures not hearing but, indirectly, the com- pliance of the middle-ear structures. A pure tone signal of known intensity is fed into the external auditory canal and a microphone in the ear probe measures reflected sound levels.Thus, the sound admitted to the ear can be measured. Most sound is absorbed when the compliance is maximal, and, by altering the pressure in the external canal, a measure can be made of the 12 Chapter 3:Testing the Hearing CONDUCTIVE DEAFNESS IN RIGHT EAR Fig. 3.5 Conductive deafness in the right ear. BC>AC AC>BC The Rinne test is negative on the right, positive on the left and the Weber test is referred to the right ear. NORMAL PURE TONE AUDIOGRAM Right -20 -10 X X 0 X X X X 10 Hearing loss (dB ISO) 20 30 40 50 60 70 80 90 100 110 120 125 250 500 1000 2000 4000 8000 Fig. 3.6 A normal pure Frequency (Hz) tone audiogram. o–o–o, right ear; x–x–x, left ear.  Testing the Hearing 13 SENSORINEURAL DEAFNESS AUDIOGRAM Right -20 -10 0 10 X Hearing loss (dB ISO) 20 X 30 X 40 50 X X 60 70 80 90 100 Fig. 3.7 A pure tone 110 audiogram showing 120 sensorineural deafness 125 250 500 1000 2000 4000 8000 maximal at 4 kHz typical Frequency (Hz) of noise-induced deafness. compliance at different pressures. Impedance testing is widely used as a screening method for otitis media with effusion (OME) in children. If there is fluid in the middle ear, the compliance curve is flattened. ELECTRIC RESPONSE AUDIOMETRY Electric response audiometry is a collective term for various investigations whereby action potentials at various points within the long and complex auditory pathway can be recorded. The action potential (AP) is evoked by a sound stimulus applied to the ear either through headphones or free field, and the resulting AP is collected in a computer store. Although each AP is tiny, it occurs at the same time interval after the stimulus (usually a click of very short duration) and so a train of stimuli will produce an easily detectable response, while the averaging ability of the computer will average out the more random electrical activity, such as the EEG. By making the computer look at different time windows, responses at various sites in the auditory pathway can be investigated. As the response travels from the cochlea to the auditory cortex, the latency increases from about 1-4 to 300 ms. 14 Chapter 3:Testing the Hearing CONDUCTIVE DEAFNESS -20 -10 0 10 [ [ [ [ Hearing loss (dB ISO) 20 [ 30 40 50 60 70 Fig. 3.8 A pure tone 80 audiogram showing 90 conductive deafness. The 100 bone conduction is normal 110 but the air conduction 120 curve is impaired. A case 125 250 500 1000 2000 4000 8000 of otosclerosis. [---[---[, Frequency (Hz) bone conduction; o–o–o, air conduction. There are three main responses used in clinical audiology. 1 Electrocochleogram (E Coch G), which is recorded from an electrode inserted through the ear drum onto the promontory and can be recorded under anaesthetic. 2 Brain-stem responses, recorded from external electrodes (BSER). 3 Slow vertex or cortical responses, again recorded from external electrodes (SVR or CERA). Electric response audiometry has the unique advantage of being an objec- tive measure of hearing requiring no cooperation from the subject. It is of value in assessing hearing thresholds in babies and small children and in cases of dispute such as litigation for industrial deafness. Oto-acoustic emissions (OAE) When the cochlea is subjected to a sound wave it is stimulated to produce itself an emission of sound generated within the cochlea. This can be de- tected and recorded and has been used as a screening test of hearing in new- born babies. It is now in routine clinical use in testing those babies who are particularly at risk of hearing problems, such as premature or hypoxic neonates, and is likely to play a part in universal screening for hearing loss.  CHAPTER 4 Deafness Attention has already been drawn to the two major categories of deafness — conductive and sensorineural. The distinction is easily made by tuning fork tests, which should never be omitted. CAUSES There is no strict order in the list featured in Table 4.1, because the fre- quency with which various causes of deafness occur varies from one com- munity to another and from one age group to another. Nevertheless, some indication is given by division into ‘more common’ and ‘less common’ groups. Always try to make a diagnosis of the cause of deafness and start by deciding whether it is conductive or sensorineural. MANAGEMENT The management of a number of specific conditions will be dealt with in subsequent chapters but some general comments are appropriate. The deaf child Early diagnosis of deafness in the infant is essential if irretrievable develop- mental delay is to be avoided.The health visitor should screen all babies at about 8 months of age and those failing a routine test must be referred to a specialist audiological centre without delay for more thorough investiga- tion. Some babies are ‘at risk’ of deafness and are tested as soon after birth as possible.They include those affected by: 1 prematurity and low birth-weight; 2 perinatal hypoxia; 3 Rhesus disease; 4 family history of hereditary deafness; 5 intrauterine exposure to viruses such as rubella, cytomegalovirus and HIV. The testing of babies suspected or at risk of being deaf is very specialized. The mother’s assessment is very important and should always be taken se- riously. She is likely to be right if she thinks her child’s hearing is not normal. Testing of ‘at risk’ babies in the neonatal period is now carried out in many centres by the recording of otoacoustic emissions (see Chapter 3). 15 16 Chapter 4: Deafness Conductive Sensorineural More common Wax Presbycusis (deafness of old age) Acute otitis media Noise-induced (prolonged exposure to high noise level, industrial deafness, chronic otitis media disco music) Barotrauma Congenital (maternal rubella, cytomegalovirus, Otosclerosis toxoplasmosis, hereditary deafness, anoxia, jaundice, congenital syphilis) Injury of the tympanic membrane Drug-induced (aminoglycoside antibiotics, aspirin, quinine, some diuretics, some beta blockers) Menière’s disease Late otosclerosis Infections (CSOM, mumps, herpes zoster, meningitis, syphilis) Less common Traumatic ossicular dislocation Acoustic neuroma Congenital atresia of the external Head injury canal Agenesis of the middle ear CNS disease (multiple sclerosis, metastases) Tumours of the middle ear Metabolic (diabetes, hypothyroidism, Paget’s disease of bone) Psychogenic Unknown aetiology Table 4.1 Causes of deafness. Sudden sensorineural deafness Sudden sensorineural deafness is an otological emergency and should be treated as seriously as would be sudden blindness. Immediate admission to hospital should be arranged, as delay may mean permanent deafness. Sudden deafness may be unilateral or bilateral and most cases are re- garded as being viral or vascular in origin. Investigation may fail to show a cause and treatment is usually with low-molecular-weight dextran, steroids and inhaled carbon dioxide. Bilateral profound deafness, especially if of sud- den onset, is a devastating blow and for this reason various organizations exist to give advice and support. Vestibular Schwannoma (Acoustic neuroma) Vestibular Schwannoma is a benign tumour of the superior vestibular nerve in the internal auditory meatus or cerebello-pontine (CP) angle. It is usually unilateral, except in familial neurofibromatosis (NF2), when it may be bilat-  Deafness 17 Fig. 4.1 An MR scan after gadolinium contrast showing an acoustic neuroma. eral. In its early stages, it causes a progressive hearing loss and some imbal- ance. As it enlarges, it may encroach on the trigeminal nerve in the CP angle, causing loss of corneal sensation. In its advanced stage, there is raised in- tracranial pressure and brain stem displacement. Early diagnosis reduces the morbidity and mortality of operations. Unilateral sensorineural deaf- ness should always be investigated to exclude a neuroma. Audiometry will confirm the hearing loss. MR scanning will identify even small tumours with certainty (Fig. 4.1). Hearing aids In cochlear forms of sensorineural deafness, loudness recruitment is often a marked feature. This results in an intolerance of noise above a certain threshold, and makes the provision of amplification very difficult. The choice of hearing aids is now large. Most are worn behind the ear with a mould fitting into the meatus. If the mould does not fit well, oscilla- tory feedback will occur and the patient will not wear the aid. More sophis- ticated (and expensive) are the ‘all-in-the-ear’ aids, where the electronics are built into a mould made to fit the patient’s ear. They give good direc- tional hearing and, because they are individually built, the output can be 18 Chapter 4: Deafness matched to the patient’s deafness. The current generation of hearing aids are digital, allowing more refinement in the sound processing and more control of the aid. A recent development has been the bone-anchored hearing aid (BAHA). A titanium screw is threaded into the temporal bone and allowed to fuse to the bone (osseo-integration). A transcutaneous abutment then allows the attachment of a special hearing aid that transmits sound directly by bone conduction to the cochlea.The main application of BAHA is to pa- tients with no ear canal, or chronic ear disease, who are unable to wear a conventional aid and is much more effective than the old-fashioned bone conductor aid. Cochlear implants Much research has been done, both in the USA and Europe, on the implan- tation of electrodes into the cochlea to stimulate the auditory nerve. The apparatus consists of a microphone, an electronic sound processor and a single or multichannel electrode implanted into the cochlea. Cochlear im- plantation is only appropriate for the profoundly deaf. Results, particularly with an intracochlear multichannel device, can be spectacular, with some patients able to converse easily. Most patients obtain a significant improve- ment in their ability to communicate and implantation has been extended for use in children. It is no longer an experimental procedure but a valuable therapeutic technique. Lip-reading Instruction in lip-reading is carried out much better while usable hearing persists and should always be advised to those at risk of total or profound deafness. Electronic aids for the deaf Amplifying telephones are easily available to the deaf and telephone compa- nies usually provide willing advice. Many modern hearing aids are fitted with a loop inductance system to make the use of telephones easier. Various computerized voice analysers that give a rapid visual display are also available, but these require the services of a skilled operator and are still in the developmental phase. Automatic voice recognition machines may take over this role in the foreseeable future. CHAPTER 5 Conditions of the Pinna CONGENITAL Protruding ears Sometimes unkindly known as ‘bat ears’, the terms protruding or promi- nent should be used. The underlying deformity is the absence of the ante- helical fold in the auricular cartilage. Afflicted children are often teased mercilessly and surgical correction can be carried out after the age of four. Operation consists of exposing the lateral aspect of the cartilage from behind the pinna and scoring it to produce a rounded fold (Fig. 5.1). Accessory auricles Accessory auricles are small tags, often containing cartilage, on a line between the angle of the mouth and the tragus (Fig. 5.2). They may be multiple. Pre-auricular sinus Pre-auricular sinus is a small blind pit that occurs commonly anterior to the root of the helix; it is sometimes bilateral and may be familial. Recurrent in- fection requires excision (Fig. 5.3). Microtia Microtia, or failure of development of the pinna, may be associated with atresia of the ear canal (Fig. 5.2). Absence or severe malformation of the ex- ternal ear, as in Treacher Collins syndrome, may be remedied by the fitting of prosthetic ears attached by bone-anchored titanium screws (see BAHA, Chapter 4, page 18). A bone-anchored hearing aid can be fitted at the same time, although it is often fitted at a much earlier age than prosthetic ears in order to allow speech development. 19 20 Chapter 5: Conditions of the Pinna Fig. 5.1 A child with protruding ears. TRAUMA Haematoma Subperichondrial haematoma of the pinna usually occurs as a result of a shearing blow (Fig. 5.4). The pinna is ballooned and the outline of the cartilage is lost. Left untreated, severe deformity will result — a cauliflower ear. Treatment consists of evacuation of the clot and the reapposition of cartilage and perichondrium by pressure dressings or vacuum drain. AVULSION Very rarely, avulsion of the pinna may occur. If the avulsed ear is preserved, reattachment may be possible.  The Pinna 21 Fig. 5.2 Right ear showing congenital meatal atresia, an accessory auricle and deformity of the pinna. INFLAMMATION Acute dermatitis Acute dermatitis of the pinna may occur as an extension of meatal infection in otitis externa: it is commonly caused by a sensitivity reaction to topically applied antibiotics, especially chloramphenicol or neomycin (Fig. 5.5). TREATMENT 1 The ear canal should be adequately treated (q.v). 2 If there is any suspicion of a sensitivity reaction, topical treatment with antibiotics should be withdrawn. 3 The ear may be treated with glycerine and ichthammol, or steroid oint- ment may be applied sparingly. 4 Severe cases may require admission to hospital.  22 Chapter 5: Conditions of the Pinna Fig. 5.3 Pre-auricular sinus. (a) (b) Fig. 5.4 Auricular haematoma before and after drainage.  The Pinna 23 Fig. 5.5 Severe otitis externa and perichondritis of the pinna. Dictum If otitis externa gets worse on treatment, it is probably due to drug sensitiv- ity. Stop the treatment. Perichondritis Perichondritis may follow injury to the cartilage and may be very destruc- tive. It may follow mastoid surgery or may follow ear piercing, particularly with the modern trend for multiple perforations that may go through the cartilage.Treatment must be vigorous, with parenteral antibiotics and inci- sion if necessary. It goes without saying that if it is due to piercing the ear, the stud should be removed. 24 Chapter 5: Conditions of the Pinna WEDGE EXCISION Fig. 5.6 Wedge excision of carcinoma of the pinna. The defect is repaired by direct closure. Chondrodermatitis chronicis helicis Chondrodermatitis chronicis helicis occurs in the elderly as a painful ulcer- ated lesion on the rim of the helix. It resembles a neoplasm and should be removed for histology. TUMOURS Squamous cell and basal cell carcinomas These tumours occur usually on the upper edge of the pinna, and when small are easily treated by wedge excision (Fig. 5.6). Large tumours of the pinna or outer meatus will require more radical treatment, often with skin flap repair. CHAPTER 6 Conditions of the External Auditory Meatus CONGENITAL Congenital atresia (Greek: a — negative; tretos — bored through) may be of variable severity; there may be a shallow blind pit or no cavity at all. There may be associated absence of the pinna (microtia) and there may be absence or abnormality of the middle or inner ear (Fig. 5.2). In bilateral cases the cochlear function needs to be measured carefully. If it is good, surgery may be considered. Previously an attempt would have been made to fashion an external auditory canal but better hearing results are obtained by the provision of a BAHA (see Chapter 4, page 18). At the same time any malformation of the pinna can be corrected by a prosthesis attached to a similar osseo-integrated titanium implant. Until such surgery is possible (at about age 3–4) the child with bilateral atresia of the external auditory canal will need to wear a bone conductor hearing aid held on by pressure from some sort of headband. In unilateral cases, it is of prime importance to assess the hearing in the unaffected ear. If it is good, operation on the affected side is unnecessary. External ears can be constructed by a plastic procedure or can be replaced by prostheses anchored to the ear by adhesive or by titanium implants in the skull bone. FOREIGN BODY Small children often put beads, pips, paper and other objects into their own ears, but they will usually blame someone else! Adults may get a foreign body stuck in an attempt to clean the ear, e.g. with match sticks, or cotton buds. Although the management is straightforward, several points arise. 1 Syringing is usually successful in removing a foreign body. 2 The chief danger lies in clumsy attempts to remove the foreign body and rupture of the tympanic membrane may result. Do not attempt to remove a foreign body unless you have already developed some skill with instruments. 25 26 Chapter 6: Conditions of the External Auditory Meatus 3 If the child (or adult) is uncooperative, do not persevere but resort in- stead to general anaesthesia. This does not need to be done as an urgent case but can be added to a routine list. INSECTS Live insects, such as moths or flies, in the outer meatus produce dramatic ‘tinnitus’. Peace is restored by the instillation of spirit or olive oil and the corpse can then be syringed out. WAX WAX IN AN EAR IS NORMAL Wax or cerumen is produced by the ceruminous glands in the outer meatus and migrates laterally along the meatus. Some people produce large amounts of wax but many cases of impacted wax are due to the use of cot- ton wool buds in a misguided attempt to clean the ears. Impacted wax may cause some deafness or irritation of the meatal skin and is most easily removed by syringing. Ear syringing is a procedure that almost any doctor or nurse is expected to carry out with skill and that the general practitioner should perform with a flawless technique. Attention must be paid to the points listed in Box 6.1. EAR SYRINGING PROCEDURE: 1 History. Has the patient had a discharging ear? If any possibility of a dry perforation, do not syringe. 2 Inspection. If wax seems very hard, always soften over a period of one week by using warm olive oil drops nightly. In the case of exceedingly stubborn wax, the patient may be advised to use sodium bicarbonate ear drops (BPC), and there are several ‘quick- acting’ ceruminolytic agents on the market. Occasionally, a patient reacts badly to the use of the latter and develops otitis externa. They should certainly not be employed in the case of a patient who is known to suffer from recurrent infections of the meatal canal. 3 Towels. Protect the patient well with towels and waterproofs. He will not be amused by having his clothing soaked. 4 Lighting. Use a mirror or lamp. 5 Solution. Sodium bicarbonate, 4–5 g to 500 mL, or normal saline are ideal. Tapwater is satisfactory. 6 Solution temperature. This is vital. It should be 38°C (100°F). Any departure of more than a few degrees may precipitate the patient onto the floor with vertigo. 7 Tools. Metal syringes and Bacon syringes are capable of applying high pressures and the nozzle may also do damage. The preferred instrument is an electrically driven water Continued  External Auditory Meatus 27 pump with a small hand-held nozzle and a foot operated control (Fig. 6.1). It provides an elegant means of ear syringing. 8 Direction. Direct stream of solution along roof of auditory canal (Fig. 6.2). 9 Inspection. After removal of wax, inspect thoroughly to make sure none remains. This advice might seem superfluous, but is frequently ignored. 10 Drying. Mop excess solution from meatal canal. Stagnation predisposes to otitis externa. Box 6.1 Ear syringing procedure. OTITIS EXTERNA Otitis externa is a diffuse inflammation of the skin lining the external audi- tory meatus. It may be bacterial or fungal (otomycosis), and is characterized by irritation, desquamation, scanty discharge and tendency to relapse.The treatment is simple, but success is absolutely dependent upon patience, care and meticulous attention to detail. CAUSES Some people are particularly prone to otitis externa, often because of a narrow or tortuous external canal. Most people can allow water into their Fig. 6.1 An electric pulse pump used for ear syringing. 28 Chapter 6: Conditions of the External Auditory Meatus SYRINGING AN EAR Fig. 6.2 The stream of solution when syringing an ear should be directed along the roof of the external auditory canal. ears with impunity but in others otitis externa is the inevitable result. Swim- ming baths are a common source of otitis externa. Poking the ear with a fin- ger or towel further traumatizes the skin and introduces new organisms. Further irritation occurs, leading to further interference with the ear, so causing more trauma. A vicious circle is set up. Otitis externa may occur after staying in hotter climates than usual, where increased sweating and bathing are predisposing factors. Underlying skin disease, such as eczema or psoriasis, may occur in the ear canal and produce very refractory otitis externa. Ear syringing, especially if it causes trauma, may result in otitis externa. PATHOLOGY A mixed infection of varying organisms is not infrequent, the most com- monly found types being: Staphylococcus pyogenes; Pseudomonas pyocyanea; diphtheroids;  External Auditory Meatus 29 Fig. 6.3 Fungal otitis externa showing the spores of Aspergillus niger. (Courtesy of MPJ Yardley.) Proteus vulgaris; Escherichia coli; Streptococcus faecalis; Aspergillus niger (Fig. 6.3); Candida albicans. SYMPTOMS 1 Irritation. 2 Discharge (scanty). 3 Pain (usually moderate, sometimes severe, increased by jaw movement). 4 Deafness. SIGNS 1 Meatal tenderness, especially on movement of the pinna or compres- sion of the tragus. 2 Moist debris, often smelly and keratotic, the removal of which reveals red desquamated skin and oedema of the meatal walls and often the tym- panic membrane. MANAGEMENT Scrupulous aural toilet is the key to successful treatment of otitis externa. No medication will be effective if the ear is full of debris and pus. Investigation Investigation of the offending microorganism is essential. A swab should be sent for culture and it is prudent to mention the possibility of fungal 30 Chapter 6: Conditions of the External Auditory Meatus infection in your request, especially if the patient has already had topical antibiotic treatment. Aural toilet Aural toilet must be performed and can be done most conveniently by dry mopping. Fluffed-up cotton wool about the size of a postage stamp is ap- plied to the Jobson Horn probe and, under direct vision, the ear is cleaned with a gentle rotatory action. Once the cotton wool is soiled it is replaced. Pay particular attention to the antero-inferior recess, which may be difficult to clean. Gentle syringing is also permissible to clear the debris. Dressings If the otitis externa is severe, a length of 1 cm ribbon gauze, impregnated with appropriate medication, should be inserted gently into the meatus, and renewed daily until the meatus has returned to normal. If it does not do so within 7–10 days, think again!. The following medications are of value on the dressing: 1 8% aluminium acetate; 2 10% ichthammol in glycerine; 3 ointment of gramicidin, neomycin, nystatin and triamcinolone (Tri-Adcortyl); 4 other medication may be used as dictated by the result of culture. If fungal otitis externa is present, dressings of 3% amphotericin, miconazole or nystatin may be used. If the otitis externa is less severe and there is little meatal swelling, it may respond to a combination of antibiotic and steroid ear drops. The antibiotics are usually those that are not given systemically. The antibiotics most commonly used are neomycin, gramicidin and framycetin. Remember that prolonged use may result in fungal infection or in sensitivity dermatitis. Prevention of recurrence Prevention of recurrence is not always possible; the patient should be ad- vised to keep the ears dry, especially when washing the hair or showering. A large piece of cotton wool coated inVaseline and placed in the concha is ad- visable, and if the patient is very keen to swim it is worthwhile investing in custom-made silicone rubber earplugs. The use of a proprietory prepara- tion of spirit and acetic acid prophylactically after swimming is useful in re- ducing otitis externa. Equally important is the avoidance of scratching and poking the ears. Itching may be controlled with antihistamines given orally, especially at bedtime. If meatal stenosis predisposes to recurrent infection, meatoplasty (surgical enlargement of meatus) may be advisable.  External Auditory Meatus 31 NB. Do not make a diagnosis of otitis externa until you have satisfied your- self that the tympanic membrane is intact. If the ear fails to settle, look again and again to make sure that you are not dealing with a case of otitis media with a discharging perforation. FURUNCULOSIS Furunculosis of the external canal results from infection of a hair follicle and so must occur in the lateral part of the meatus. The organism is usually Staphylococcus; the pain is often out of proportion to the visible lesion. SYMPTOMS Pain Pain is as severe as that of renal colic and the patient may need pethidine. The pain is made much worse by movement of the pinna or pressure on the tragus. Deafness Deafness is usually slight and due to meatal occlusion by the furuncle. Signs There is often no visible lesion but the introduction of an aural speculum causes intense pain. If the furuncle is larger, it will be seen as a red swelling in the outer meatus and there may be more than one furuncle present. At a more advanced stage, the furuncle will be seen to be pointing or may pre- sent as a fluctuant abscess. TREATMENT The insertion of a wick soaked in 10% ichthammol in glycerine (Glyc & Ic) is painful at the time but provides rapid relief. Flucloxacillin should be given parenterally for 24 h, followed by oral medication. Analgesics are necessary; the patient will often need pethidine and is not fit for work. Recurrent cases are not common — exclude diabetes and take a nasal swab in case the patient is a Staphylococcus carrier. EXOSTOSES Exostoses or small osteomata of the external auditory meatus are fairly common and usually bilateral.They are much more common in those who swim a lot in cold water, although the reason is not known. 32 Chapter 6: Conditions of the External Auditory Meatus There may be 2 or 3 little tumours arising in each bony meatus.They are sessile, hard, smooth, covered with very thin skin and when gently probed are often exquisitely sensitive. Their rate of growth is extremely slow and they may give rise to no symptoms, but if wax or debris accumulates be- tween the tympanic membrane and the exostoses, its removal may tax the patience of the most skilled manipulator. In such cases, surgical removal of the exostoses may be indicated and is carried out with the aid of the oper- ating microscope and drill. MALIGNANT DISEASE Malignant disease of the auditory meatus is rare and usually occurs in the elderly. If confined to the outer meatus, it behaves like skin cancer and can be treated by wide excision and skin grafting. If it spreads to invade the mid- dle ear, facial nerve and temporomandibular joint, it is a relentless and terri- ble affliction. Pain becomes intractable and intolerable and there is a blood-stained discharge from the ear. Treatment then is by radiotherapy, radical surgery or a combination of the two.Treatment is not possible in some cases, and the outlook is poor in the extreme. CHAPTER 7 Injury of the Tympanic Membrane The tympanic membrane, being deeply placed, is well protected from injury. Damage does occur, however, and may be direct or indirect. Direct trauma is caused by poking in the ear with sharp implements, such as hair grips, in an attempt to clean the ear; it is caused by syringing or unskilled attempts to remove wax or foreign bodies. Indirect trauma is usually caused by pressure from a slap with an open hand or from blast injury; it may occur from temporal bone fracture (Fig. 7.1). Welding sparks may cause severe damage to the tympanic membrane. Fig. 7.1 Operative picture showing fracture of the temporal bone (which had caused facial nerve damage). 33 34 Chapter 7: Injury of the Tympanic Membrane TEAR IN THE TYMPANIC MEMBRANE Fig. 7.2 Traumatic perforation of the tympanic membrane, showing a ragged perforation with blood in the external auditory canal. SYMPTOMS 1 Pain, acute at time of rupture, usually transient. 2 Deafness, not usually severe, conductive in type. Cochlear damage may occur from excessive movement of the stapes. 3 Tinnitus, may be persistent — this is cochlear damage. 4 Vertigo, rarely. SIGNS 1 Bleeding from the ear. 2 Blood clot in the meatus. 3 A visible tear in the tympanic membrane (Fig. 7.2). TREATMENT — leave it alone 1 Do not clean out the ear. 2 Do not put in drops. 3 Do not syringe. If the injury has been caused by direct trauma, treat with prophylactic antibiotics. In other cases, give antibiotics if there is evidence of infection supervening. In virtually every case, the tear in the tympanic membrane will close rapidly. Do not regard the ear as healed until the hearing has returned to normal.  CHAPTER 8 Acute Otitis Media Acute otitis media, i.e. acute inflammation of the middle-ear cavity, is a com- mon condition and is frequently bilateral. It occurs most commonly in chil- dren and it is important that it is managed with care to prevent subsequent complications. It most commonly follows an acute upper respiratory tract infection and may be viral or bacterial. Unless the ear discharges pus from which an organism is cultured it is impossible to decide one way or the other. PATHOLOGY Acute otitis media is an infection of the mucous membrane of the whole of the middle-ear cleft — Eustachian tube, tympanic cavity, attic, aditus, mastoid antrum and air cells. The bacteria responsible for acute otitis media are: Streptococcus pneu- moniae 35%, Haemophilus influenzae 25%, Moraxella catarrhalis 15%. Group A streptococci and Staphylococcus aureus may also be responsible. The sequence of events in acute otitis media is as follows: 1 organisms invade the mucous membrane causing inflammation, oedema, exudate and later, pus; 2 oedema closes the Eustachian tube, preventing aeration and drainage; 3 pressure from the pus rises, causing the drum to bulge; 4 necrosis of the tympanic membrane results in perforation; 5 the ear continues to drain until the infection resolves. CAUSES OF ACUTE OTITIS MEDIA More common Less common Common cold Sinusitis Acute tonsillitis Haemotympanum Influenza Trauma to the tympanic Coryza of measles, scarlet fever, membrane whooping cough Barotrauma (air flight) Diving Temporal bone fracture Box 8.1 Causes of acute otitis media. 35 36 Chapter 8: Acute Otitis Media SYMPTOMS Earache Earache may be slight in a mild case, but more usually it is throbbing and severe.The child may cry and scream inconsolably until the ear perforates, the pain is relieved and peace is restored. Deafness Deafness is always present in acute otitis media. It is conductive in nature and may be accompanied by tinnitus. In an adult, the deafness or tinnitus may be the first complaint. SIGNS Pyrexia The child is flushed and ill.The temperature may be as high as 40°C. Tenderness There is usually some tenderness to pressure on the mastoid antrum. The tympanic membrane The tympanic membrane varies in appearance according to the stage of the infection. 1 Loss of lustre and break-up of the light reflex. 2 Injection of the small vessels around the periphery and along the handle of the malleus. 3 Redness and fullness of the drum; the malleus handle becomes more vertical. 4 Bulging, with loss of landmarks. Purple colour. Outer layer may desqua- mate, causing blood-stained serous discharge. Early necrosis may be recog- nized, heralding imminent perforation. 5 Perforation with otorrhoea, which will often be blood-stained. Profuse and mucoid at first, later becoming thick and yellow. Mucoid discharge Mucoid discharge from an ear must mean that there is a perforation of the tympanic membrane.There are no mucous glands in the external canal. TREATMENT The treatment depends on the stage reached by the infection.The following stages may be considered: early, bulging and discharging.  Acute Otitis Media 37 Early Antibiotics Penicillin remains the drug of choice in most cases, and ideally should be given initially by injection followed by oral medication. In children under 5 years, when Haemophilus influenzae is likely to be present, amoxycillin will be more effective, and should always be considered if there is not a rapid response to penicillin. Co-amoxiclav is useful in Moraxella infections. Be guided by sensitivity reports from the laboratory. Analgesics Simple analgesics, such as aspirin or paracetamol, should suffice. Avoid the use of aspirin in children because of the risk of Reye’s syndrome. Nasal vasoconstrictors The role of 0.5% ephedrine nasal drops is traditional but its value is uncer- tain in the presence of acute inflammation of the middle ear. Ear drops Ear drops are of no value in acute otitis media with an intact drum. Especial- ly illogical is the use of drops containing local anaesthetics, which can have no effect on the middle-ear mucosa yet may cause a sensitivity reaction in the meatal skin. Bulging Myringotomy is necessary when bulging of the tympanic membrane per- sists, despite adequate antibiotic therapy. It should be carried out under general anaesthesia in theatre and a large incision in the membrane should be made to allow the ear to drain. Pus should be sent for bacteriological assessment. Following myringotomy, the ear will discharge and the outer meatus should be dry-mopped regularly. Discharging — nature’s myringotomy If the ear is already discharging when the patient is first seen, a swab should be sent for culture of the organism. Antibiotic therapy should be started but modified if necessary when the result of the sensitivities is known. Regular aural toilet will be necessary. FURTHER MANAGEMENT Do not consider acute otitis media to be cured until the hearing and the ap- pearance of the membrane have returned to normal. 38 Chapter 8: Acute Otitis Media If resolution does not occur, suspect: 1 the nose, sinuses or nasopharynx? Infection may be present; 2 the choice or dose of antibiotic; 3 low-grade infection in the mastoid cells. RECURRENT ACUTE OTITIS MEDIA (AOM) Some children are susceptible to repeated attacks of AOM. There may be an underlying immunological deficit such as IgA deficiency or hypogamma- globulinaemia that will need to be investigated. Long-term treatment with half-dose cotrimoxazole may be beneficial. If the attacks persist, grommet insertion may prevent further attacks but may result in purulent discharge. CHAPTER 9 Chronic Otitis Media If an attack of acute otitis media fails to heal, the perforation and discharge may in some cases persist.This leads to mixed infection and further damage to the middle-ear structures, with worsening conductive deafness.The pre- disposing factors in the development of chronic suppurative otitis media (CSOM) are listed in Box 9.1. CAUSES OF CHRONIC OTITIS MEDIA: 1 Late treatment of acute otitis media. 2 Inadequate or inappropriate antibiotic therapy. 3 Upper airway sepsis. 4 Lowered resistance, e.g. malnutrition, anaemia, immunological impairment. 5 Particularly virulent infection, e.g. measles. There are two major types of CSOM. 1 Mucosal disease with tympanic membrane perforation (tubo-tympanic disease, relatively safe). 2 Bony: (a) osteitis; (b) cholesteatoma — dangerous (attico-antral disease). Box 9.1 Causes of chronic otitis media. Mucosal infection In these cases there may be underlying nasal or pharyngeal sepsis that will require attention if the ear is to heal. The ear will discharge, usually copiously, and the discharge is mucoid. Remember — mucoid discharge from an ear must mean that there is a perforation present, even if you cannot identify it. The perforation is in the pars tensa, and may be large or very small and difficult to see (Fig. 9.1). Serious complications are very rare but if left untreated the condition may result in permanent deafness. 39 40 Chapter 9: Chronic Otitis Media Long process Handle of of incus Malleus Fig. 9.1 A large central perforation of the tympanic membrane. The handle of the malleus and the long process of the incus are visible. (Courtesy of MPJ Yardley.) The ear may become quiescent from time to time, a feature less likely to happen with bony CSOM, and the perforation may heal. If healing does not occur, surgical repair may be necessary. TREATMENT OF MUCOSAL-TYPE CSOM Ear discharge When the ear is discharging, a swab should be sent for bacteriological analy- sis. The mainstay of treatment is thorough and regular aural toilet. Appro- priate (as determined by the culture report) antibiotic therapy is instituted and in most cases the ear will rapidly become dry.The perforation may heal, especially if it is small. If the ear does not rapidly become dry, admission to hospital for regular aural toilet is often effective. If infection persists, look for chronic nasal or pharyngeal infection. Dry perforation When there is a dry perforation, surgery may be considered but is not mandatory.Myringoplasty is the repair of a tympanic membrane perforation; the tympanic membrane is exposed by an external incision, the rim of the perforation is stripped of epithelium and a graft is applied, usually on the medial aspect of the membrane. Various tissues have been used for graft material but that in most common use is autologous temporalis fascia, which is readily available at the operation site. Success rates for this pro- cedure are very high; repair of the tympanic membrane may be combined with ossicular reconstruction, if necessary, in order to restore hearing — the operation is then referred to as a tympanoplasty.  Chronic Otitis Media 41 Fig. 9.2 Crusting of the pars flaccida suggestive of underlying cholesteatoma. (Courtesy of MPJ Yardley.) Fig. 9.3 Erosion of the attic bone to reveal cholesteatoma. (Courtesy of MPJ Yardley.) BONY OR ATTICO-ANTRAL TYPE OF CSOM The bone affected by this type of CSOM comprises the tympanic ring, the ossicles, the mastoid air cells and the bony walls of the attic, aditus and antrum.The perforation is postero-superior (Fig. 9.2) or in the pars flaccida (Schrapnell’s membrane) (Fig. 9.3) and involves the bony annulus. The discharge is often scanty but usually persistent, and is often foul smelling. There are other features of this type of CSOM. 1 Granulations as a result of osteitis — bright red and bleed on touch. 2 Aural polyps — formed of granulation tissue, which may fill the meatus and present at its outer end. 42 Chapter 9: Chronic Otitis Media MODIFIED RADICAL MASTOIDECTOMY Fig. 9.4 Modified radical mastoidectomy; note the shape of the cavity, the facial nerve ridge and the bulge caused by the lateral semicircular canal. 3 Cholesteatoma.This is formed by squamous epithelium within the mid- dle-ear cleft, starting as a retraction pocket in the tympanic membrane. It results in accumulation of keratotic debris. This will be visible through the perforation as keratin flakes, which are white and smelly. The cholesteatoma expands and damages vital structures, such as dura, lateral sinus, facial nerve and lateral semicircular canal. Cholesteatoma is potentially lethal if untreated. TREATMENT OF BONY-TYPE CSOM 1 Regular aural toilet in early cases of annular osteitis may be adequate to prevent progression, but such a case should be watched closely. 2 Suction toilet under the microscope may evacuate a small pocket of cholesteatoma, and a dry ear may result. 3 Mastoidectomy is nearly always necessary in established cholesteatoma and takes several forms, depending on the extent of the disease (Fig. 9.4).  CHAPTER 10 Complications of Middle-Ear Infection Acute mastoiditis Acute mastoiditis is the result of extension of acute otitis media into the mastoid air cells with suppuration and bone necrosis. Common in the preantibiotic era, it is now rare in the Western world (Fig. 10.1). SYMPTOMS 1 Pain — persistent and throbbing. 2 Otorrhoea — usually creamy and profuse. 3 Increasing deafness. SIGNS 1 Pyrexia. 2 General state — the patient is obviously ill. 3 Tenderness is marked over the mastoid antrum. 4 Swelling in the postauricular region, with obliteration of the sulcus.The pinna is pushed down and forward (Fig. 10.2). 5 Sagging of the meatal roof or posterior wall. 6 The tympanic membrane is either perforated and the ear discharging, or it is red and bulging. If the tympanic membrane is normal, the patient does not have acute mastoiditis. INVESTIGATIONS 1 White blood count — raised neutrophil count. 2 CT scanning shows opacity and air cell coalescence. OCCASIONAL FEATURES OF ACUTE MASTOIDITIS 1 Subperiosteal abscess over the mastoid process. 2 Bezold’s abscess — pus breaks through the mastoid tip and forms an abscess in the neck. 3 Zygomatic mastoiditis — results in swelling over the zygoma. 43 44 Chapter 10: Complications of Middle-Ear Infection CHRONIC OTITIS MEDIA 4 2 5 4 3 6 1 7 9 8 Fig. 10.1 Complications of chronic otitis media. 1, Acute mastoiditis; 2, Meningitis; 3, Extradural abscess; 4, Brain abscess (temporal lobe and cerebellum); 5, Subdural abscess; 6, Labyrinthitis; 7, Lateral sinus thrombosis; 8, Facial nerve paralysis; 9, Petrositis. TREATMENT When the diagnosis of acute mastoiditis has been made, do not delay. The patient should be admitted to hospital. 1 Antibiotics should be administered intravenously (i.v).The choice of an- tibiotic, as always, depends on the sensitivity of the organism. If the organ- ism is not known and there is no pus to culture, start amoxycillin and metronidazole immediately. 2 Cortical mastoidectomy. If there is a subperiosteal abscess or if the re- sponse to antibiotics is not rapid and complete, cortical mastoidectomy must be performed.The mastoid is exposed by a postaural incision and the cortex is removed by drilling. All mastoid air cells are then opened, remov- ing pus and granulations. The incision is closed with drainage. The object of this operation is to drain the mastoid antrum and air cells but leave the middle ear, the ossicles and the external meatus untouched.  Middle-Ear Infection 45 Fig. 10.2 Acute mastoiditis. Meningitis CLINICAL FEATURES 1 The patient is unwell. 2 Pyrexia — may only be slight. 3 Neck rigidity. 4 Positive Kernig’s sign. 5 Photophobia. 6 Cerebrospinal fluid (CSF) — lumbar puncture essential unless there is raised intracranial pressure (q.v). (a) Often cloudy. (b) Pressure raised. (c) White cells raised. (d) Protein raised. (e) Chloride lowered. (f) Glucose lowered. (g) Organisms present on culture and Gram stain. 46 Chapter 10: Complications of Middle-Ear Infection TREATMENT 1 Do not give antibiotic until CSF has been obtained for culture and con- firmation of diagnosis.Then start penicillin parenterally and intrathecally. 2 Mastoidectomy is necessary if meningitis results from mastoiditis and should not be delayed.The type of operation will be dictated by the extent and nature of the ear disease. Extradural abscess An abscess formed by direct extension either above the tegmen or around the lateral sinus (perisinus abscess). The features of mastoiditis are present and often accentuated. Severe pain is common.The condition may only be recognized at operation. In addition to antibiotics, mastoid surgery is essential to treat the un- derlying ear disease and drain the abscess. Brain abscess Otogenic brain abscess may occur in the cerebellum or in the temporal lobe of the cerebrum.The two routes by which infection reaches the brain are by direct spread via bone and meninges or via blood vessels, i.e. thrombophlebitis. A brain abscess may develop with great speed or may develop more gradually over a period of months.The effects are produced by: 1 systemic effects of infection, i.e. malaise, pyrexia — which may be absent; 2 raised intracranial pressure, i.e. headache, drowsiness, confusion, im- paired consciousness, papilloedema; 3 localizing signs. TEMPORAL LOBE ABSCESS Localizing signs (Fig. 10.3): 1 dysphasia — more common with left-sided abscesses; 2 contralateral upper quadrantic homonymous hemianopia; 3 paralysis — contralateral face and arm, rarely leg; 4 hallucinations of taste and smell. CEREBELLAR ABSCESS Localizing signs: 1 neck stiffness; 2 weakness and loss of tone on same side; 3 ataxia — falling to same side; 4 intention tremor with past-pointing;  Middle-Ear Infection 47 Fig. 10.3 CT scan with contrast showing temporal lobe abscess resulting from chronic middle ear disease. (Courtesy of Dr T. Hodgson.) 5 dysdiadokokinesis; 6 nystagmus — coarse and slow; 7 vertigo — sometimes. DIAGNOSIS OF INTRACRANIAL SEPSIS: 1 Any patient with chronic ear disease who develops pain or headache should be suspected of having intracranial extension. 2 Any patient who has otogenic meningitis, labyrinthitis or lateral sinus thrombosis may also have a brain abscess. 3 Lumbar puncture may be dangerous owing to pressure coning. 4 Neurosurgical advice should be sought at an early stage if intracranial suppuration is suspected. 5 Confirmation and localization of the abscess will require further investigation. Computerized tomography (CT) scanning will demonstrate intracra- nial abscesses reliably and should always be performed when it is suspected. Magnetic resonance (MR) imaging shows soft-tissue lesions with more de- tail than CT but gives no bone detail. If in doubt what to do, discuss the problem with a radiologist. 48 Chapter 10: Complications of Middle-Ear Infection TREATMENT It is the brain abscess that will kill the patient, and it is this that must take sur- gical priority.The abscess should be drained through a burr hole, or excised via a craniotomy and then, if the patient’s condition permits, mastoidecto- my should be performed under the same anaesthetic. After pus has been obtained for culture, aggressive therapy with antibiotics is essential, to be amended as necessary when the sensitivity is known. PROGNOSIS The prognosis of brain abscess has improved with the use of antibiotics and modern diagnostic methods but still carries a high mortality; the outlook is better for cerebral abscesses than cerebellar, in which the mortality rate may be 70%. Left untreated, death from brain abscess occurs from pressure coning, rupture into a ventricle or spreading encephalitis. Subdural abscess Subdural abscess more commonly occurs in the frontal region from sinusitis, but may result from ear disease. Focal epilepsy may develop from cortical damage.The prognosis is poor. Labyrinthitis Infection may reach the labyrinth by erosion of a fistula by cholesteatoma. It may rarely arise in acute otitis media. CLINICAL FEATURES 1 Vertigo may be mild in serous labyrinthitis or overwhelming in purulent labyrinthitis. 2 Nausea and vomiting. 3 Nystagmus towards the opposite side. 4 There may be a positive fistula test — pressure on the tragus causes vertigo or eye deviation by inducing movement of the perilymph. 5 There will be profound sensorineural deafness in purulent labyrinthitis. TREATMENT 1 Antibiotics. 2 Mastoidectomy for chronic ear disease. 3 Occasionally, labyrinthine drainage.  Middle-Ear Infection 49 Lateral sinus thrombosis A perisinus abscess from mastoiditis causes thrombosis of the lateral sinus and ascending cortical thrombo-phlebitis. Septic emboli are given off and metastatic abscesses may occur. The prognosis is poor but improved by early diagnosis and treatment. CLINICAL FEATURES 1 Swinging pyrexia — up to 40 °C. 2 Rigors. 3 Polymorph leucocytosis. 4 Positive Tobey–Ayer test — sometimes. Compression of contralateral internal jugular vein Æ rise in CSF pressure. Compression of ipsilateral internal jugular vein Æ no rise. 5 Meningeal signs — sometimes. 6 Positive blood cultures, especially if taken during a rigor. 7 Papilloedema — sometimes. 8 Metastatic abscesses — prognosis poor. 9 Cortical signs — facial weakness, hemiparesis. TREATMENT 1 Antibiotics. 2 Mastoidectomy with wide exposure of the lateral sinus and even removal of infected thrombus. Facial paralysis Facial paralysis can result from both acute and chronic otitis media. 1 Acute otitis media — especially in children and especially if the facial nerve canal in the middle ear is dehiscent. It is, however, uncommon. 2 Chronic otitis media — cholesteatoma may erode the bone around the horizontal and vertical parts of the facial nerve, and infection and granula- tions cause facial paralysis. In the early stages, the patient will complain of dribbling from the corner of the mouth. Clinical examination confirms the diagnosis — it may be difficult to detect if the weakness is minimal. TREATMENT If due to acute otitis media, a full recovery with antibiotic therapy is to be expected. If due to CSOM, mastoidectomy is mandatory, with clearance of dis- ease from around the facial nerve. 50 Chapter 10: Complications of Middle-Ear Infection Remember — a facial palsy occurring in the presence of chronic ear disease is not Bell’s palsy and active treatment is needed if the palsy is not to become permanent. Do not give steroids. Petrositis Very rarely, infection may spread to the petrous apex and involve the VIth cranial nerve. CLINICAL FEATURES (GRADENIGO’S SYNDROME): 1 Diplopia from lateral rectus palsy. 2 Trigeminal pain. 3 Evidence of middle-ear infection. TREATMENT 1 Antibiotics. 2 Mastoidectomy with drainage of the apical cells.  CHAPTER 11 Otitis Media with Effusion Otitis media with effusion (OME), or ‘glue ear’, is a present-day epidemic af- fecting up to one-third of all children at some time in their lives.The condi- tion is due to the accumulation of fluid, either serous or viscous, within the middle-ear cleft, resulting in conductive deafness. It is commonest in small children and those of primary school age and may cause significant deafness. It is essential that general practitioners are able to recognize the condition. It may be responsible for developmental and educational impairment, and if untreated may result in permanent middle-ear changes. It occurs in adults, usually as a serous effusion and may rarely be a sign of nasopharyngeal malignancy. SYMPTOMS 1 Deafness may be the only symptom. 2 Discomfort in the ear — rarely severe. 3 Occasionally, tinnitus or unsteadiness. CAUSES OF OME 1 Nasopharyngeal obstruction, e.g. large adenoids or tumour resulting in Eustachian tube dysfunction. The condition may be associated with recurrent attacks of acute otitis media. 2 Acute otitis media, untreated, will often give rise to a spontaneous perforation and drainage of the middle ear. Such a result will be prevented by treatment with an antibiotic and, if treatment is inadequate, middle-ear effusion may occur. 3 Allergic rhinitis, often missed in children, will predispose to middle-ear effusions. 4 Parental smoking has been shown to predispose to OME in children. 5 OME is commoner in winter months. 6 Otitic barotrauma — most commonly caused by descent in an aircraft, especially if the subject has a cold. Failure of middle-ear ventilation results in middle-ear effusion, sometimes blood-stained. Also occurs in scuba divers. 7 In many cases of secretory otitis media, no cause is apparent. Box 11.1 Causes of otitis media with effusion. 51 52 Chapter 11: Otitis Media with Effusion Fig. 11.1 Otitis media with effusion. Note the yellow discoloration of the tympanic membrane. (Courtesy of MPJ Yardley.) SIGNS 1 Fluid in the middle ear — a variable appearance that may be difficult to recognize. 2 Dull appearance with radial vessels visible on the tympanic membrane and handle of the malleus. 3 Retraction of the tympanic membrane. 4 Yellow/orange tinge to tympanic membrane (Fig. 11.1) or 5 Dark blue or grey colour of tympanic membrane. 6 Hair lines or bubbles — rarely seen. 7 Tuning fork tests show conductive deafness, i.e. bone conduction > air conduction 8 Flat impedance curve. TREATMENT In children 1 Many cases will resolve spontaneously, and the child should usually be observed for 3 months before embarking on surgery. 2 The use of antihistamines and mucolytics is of no proven benefit. Antibiotic therapy may help in the short term. Surgery is indicated if hearing loss persists for 3 months or if there is recurring pain. 3 Surgical treatment. Adenoidectomy It has been shown that adenoidectomy is beneficial in the long-term resolu- tion of OME. The maximum benefit occurs between the ages of 4 and 8 years.  Otitis Media with Effusion 53 Fig. 11.2 Right tympanic membrane with grommet in place. (Courtesy of MPJ Yardley.) Myringotomy and grommet insertion (Fig. 11.2) Myringotomy and grommet insertion is now the most commonly per- formed operation in the UK and USA. Under general anaesthetic, the tym- panic membrane is incised antero-inferiorly. The glue is aspirated and a grommet inserted into the incision.The function of the grommet is to ven- tilate the middle ear and not to drain the fluid; most surgeons now allow swimming after grommet insertion, but not diving or swimming under water. The grommet will extrude after a variable period, the average time being 6 months. Repeated insertion is sometimes necessary if the effusion recurs. In adults Examination of the nasopharynx to exclude tumour is essential, especially if the effusion is unilateral. Under the same anaesthetic, a grommet may be inserted. Secretory otitis media in adults not due to tumour usually follows a cold. Resolution is usually spontaneous, but may take up to 6 weeks. CHAPTER 12 Otosclerosis Otosclerosis, usually an hereditary disorder, causes abnormal bone to be formed around the stapes footplate, preventing its normal movement. Conductive deafness then results. More rarely, the bone of the cochlea is affected and results in sensorineural deafness. CLINICAL FEATURES OF OTOSCLEROSIS 1 Usual onset in second and third decades. 2 Two-thirds give a family history. 3 Two-thirds are female. The gene is not sex-linked but pregnancy may make the deafness worse. Not many men get pregnant, so more females present for treatment! 4 Deafness may be unilateral or bilateral. 5 Paracusis is often present — the patient is able to hear better in noisy surroundings. 6 Tinnitus is often present — it may not be relieved by operation. 7 The tympanic membranes are normal. 8 Tuning fork tests show the deafness to be conductive. 9 Cochlear impairment may be present. 10 Audiometry. Air conduction impaired. Bone conduction initially normal but deteriorates as the disease progresses. Box 12.1 Clinical features of otosclerosis. TREATMENT Stapedectomy First performed in 1956, stapedectomy is an elegant solution to the prob- lem.The middle ear is exposed (Fig. 12.1), the stapes superstructure is re- moved and the footplate perforated. A prosthesis of stainless steel orTeflon in place of the stapes is attached to the long process of the incus with its dis- tal end in the oval window (Fig. 12.2). The patient is usually discharged the following day and should refrain from strenuous activity for at least a month. Stapedectomy may result in total loss of hearing in the operated ear, and patients should be made aware of such risk before operation. 54  Otosclerosis 55 STAPEDECTOMY: MIDDLE EAR EXPOSED Long process of incus Facial nerve Round window Chorda tympani Stapes footplate Fig. 12.1 The surgical approach to stapedectomy, showing the tympano- meatal flap elevated. STAPEDECTOMY: INSERTING PROSTHETIC PISTON Fig. 12.2 Stapedectomy. The superstructure of the stapes has been removed, the footplate opened and covered with a vein before inserting a prosthetic piston. 56 Chapter 12: Otosclerosis Hearing aids and lip-reading Modern hearing aids are of great benefit to patients with conductive deaf- ness and have the advantage of causing no risk to the patient’s hearing. A hearing aid should always be offered to a patient as an alternative to surgery. If the disease is progressing rapidly and profound deafness seems likely, instruction in lip-reading should never be neglected at a stage when the patient still has usable hearing.  CHAPTER 13 Earache (Otalgia) Earache may be due to ear disease, or may be referred from disease elsewhere. It is referred earache that so often causes difficulty in diagnosis. Aural causes Earache may be caused by any disease of the external ear or middle-ear cleft and the diagnosis is obvious on examination of the ear.The most common causes are acute otitis media, acute otitis externa, furunculosis and, very rarely, acute mastoiditis. Malignant disease of the ear will cause intractable earache. If the ear is not convincingly abnormal, look for a source of referred otalgia; you will nearly always find it. Referred earache Pain may be referred to the ear via the following nerves: 1 the auriculo-temporal branch of the trigeminal nerve from, for example, carious teeth, impacted molar teeth, the temporomandibular joint or the tongue; 2 tympanic branch of the glossopharyngeal nerve from, for example, tonsillectomy, tonsillitis/quinsy, carcinoma of base of tongue or tonsil or glosso-pharyngeal neuralgia; 3 sensory branch of the facial nerve from, for example, herpes zoster; 4 auricular branch of the vagus nerve from, for example, carcinoma of larynx, carcinoma of piriform fossa or postcricoid carcinoma; 5 great auricular nerve (C2–3) and lesser occipital nerve (C2) from, for example, cervical spondylosis. Some causes of referred otalgia merit special mention on account of their frequency or diagnostic importance. POST-TONSILLECTOMY EARACHE Post-tonsillectomy earache is usual, but do not forget to examine the ear. Otitis media may be present.