Chapter 4. Ear, nose and throat

Chapter



The ear



Anatomy of normal tympanic membrane



Cross-section of the ear

temporalis

muscle



auditory ossicles

malleus incus stapes



posterior

malleolar folds



semicircular

canal

vestibular

nerve

cochlea

nerve



external auditory canal



anterior mesotympanum



posterior



hypotympanum

pars tensa



lobule



lateral

process

anterior

malleolar attic

fold



cochlea



tympanic

cavity

tympanic

membrane



4



umbo



cone of

light



handle of

malleus



pars flaccida

eustachian

tube



Fig. 4.3 Anatomy of normal tympanic membrane.



Fig. 4.1 Cross-section of the whole structure of the ear.



Auditory ossicles

Pinna

helix



short

process



triangular

fossa



head



incus



antihelix



external

auditory

meatus



long

process

lateral

process



tragus



foot

plate



concha

lobule

(ear lobe)



crus head



malleus



manubrium

(handle)



stapes



Fig. 4.4 The auditory ossicles.



Fig. 4.2 The pinna.



part of hearing occurs within the cochlea, whereas the

neuro- part occurs within the eighth (VIII) nerve and

beyond.

The cochlea records the transmission of sound via hair

cells which convert the signal received into electrical

impulses. These are transmitted by the auditory (VIII)

nerve to the cerebral cortex.

The semicircular canals or balance organ form the

peripheral balance organ. There are three canals: the

superior, lateral and posterior. The organ is neurologically



connected to the eyes and cerebellum. The eyes,

proprioception and cerebellum, together with the cerebral

cortex, form the central balance control.



Symptoms of diseases of the ear

VISIBLE SYMPTOMS

Patients may present with symptoms of visible external

abnormalities. The conditions that may be seen usually

present because of concern about the cosmetic appearance

of the ear.

83



Chapter



4



Ear, nose and throat



•

•

•

•

•

•

•

•



Differential diagnosis



Questions to ask



Cosmetic presentations



Otalgia



Bat ears

Preauricular sinus

Accessory auricles

Anotia and microtia

Cauliflower ear (untreated haematoma)

Chondrodermatitis nodularis helicis

Basal cell carcinoma

Squamous cell carcinoma



•

•

•

•

•

•

•

•



Where is the pain and does it radiate?

How long has the pain been present?

Is the pain constant or intermittent?

Does anything provoke or relieve it?

Is there any swelling, discharge, deafness or vertigo?

Has anything been put in the ear?

Is there a past history of ear problems?

Is there a problem in other areas – teeth, pharynx,

cervical spine?



PAIN IN THE EAR (OTALGIA)

Pain in the ear may arise from the ear itself (usually

unilateral) but may arise from other sources. The cause

can usually be determined on history and clinical

examination. The possible causes of otalgia are summarised

in the differential diagnosis box.



Differential diagnosis

Otalgia



Pinna

External canal



Middle ear



Other sites



Perichondritis, cellulits

Neoplasm (basal cell or squamous cell)

Furuncle, furunculosis

Otitis externa

Impacted wax

Foreign body

Herpes zoster (Ramsay Hunt syndrome)

Neoplasm

Acute otitis media and its rare

sequelae (mastoiditis, meningitis and

cerebral abscess)

Secretory otitis media (glue ear)

Eustachian tube obstruction

Barotraumas

Neoplasm

Teeth, tongue, pharynx (including

tonsils and hypopharynx), sinuses,

temporomandibular joint, cervical

spine



To fully assess causes of otalgia it is necessary to

exclude causes of referred pain. The clinician should

directly question whether the patient has any problem

with other structures such as teeth, the pharynx or cervical

spine.

To assess aural causes of the symptom of otalgia, ask

about any associated swelling, discharge, deafness,

giddiness or vertigo. Any history of excessive contact with

water such as by swimming, bathing or showering is

relevant and it is wise to check that the patient has not

been putting anything into the external canal (cottonwool

buds, pins).

84



DISCHARGING EAR (OTORRHOEA)

The ear naturally discharges wax which is a mixture of

skin debris and apocrine gland secretion.

Pathological discharge from the ear varies in nature

from watery to foul-smelling or blood-stained. A

green-coloured discharge often indicates pseudomonas

infection, whereas a blackened discharge may indicate

fungal infection.

With foul-smelling discharge, or with the presence of

pseudomonas infection, middle ear disease (and therefore

a perforated tympanic membrane) should be suspected.

In the rare instance of a cerebrospinal fluid (CSF) leak,

due to trauma or surgery, the discharge will be watery. A

mucoid discharge is suggestive of middle ear disease.

Purulent discharge is commonly from infection of the

external canal.

A most common cause of a bloodstained discharge

is infection, but the rare instance of a squamous cell

carcinoma may present with this.

Discharge is often associated with otalgia and

the timing of the two symptoms will often indicate

the origin. Otalgia from middle ear disease is usually

relieved when the tympanic membrane ruptures

and discharges mucopus, whereas continuing pain

associated with discharge usually indicates external ear

inflammation.



Questions to ask

Otorrhoea



•

•

•

•

•

•



How long has it been present?

What is its relationship to pain?

Has it occurred previously?

What is its colour and consistency?

Is it blood-stained?

Is it offensive?



Chapter



The ear

Differential diagnosis

Discharging ear



Site

External ear

Middle ear



Inner ear



Diagnosis

Otitis externa – bacterial, fungal or

secondary to middle ear discharge

Acute suppurative otitis media, chronic

suppurative otitis media, mastoid

disease (rare), neoplasm (rare)

Fracture (CSF leak)



4



conduction and magnification of sound to the cochlea.

For sound to be conducted, the external canal must be

patent. It may be impeded by malformation, wax or

discharge. The tympanic membrane should be intact and

the middle ear aerated and free of discharge or adhesions.

The ossicular chain in the middle ear must be intact and

move freely. Testing of the integrity of middle ear function

is explained in the section on examination of the ear

(pages 90–92).



Sensorineural deafness

HEARING LOSS (DEAFNESS)

Hearing loss is recognised as being either conductive or

sensorineural. It varies in degree from minor to profound

and affects all age groups. Poor hearing is significant in

infants because of the association with slow or abnormal

development of speech. Assessment of hearing in infants

and young children is difficult (see p. 92). The clinician

should take careful note of parents’ concerns. Hearing

loss of old age is called presbyacusis. There are many

causes of hearing loss.

Conductive deafness

Conductive deafness is the term used to indicate that

hearing is being impaired by a malfunction in the



The sensory part of the ear is the cochlea, but for full

function the neural element is required. This comprises

the auditory nerve and cerebral cortex. To distinguish

between the sensory and neural element can be

difficult.

Hearing loss in the elderly (presbyacusis) is mainly due

to degeneration of the cochlea. The cochlea may be

damaged during life in other ways. This may be by

infection, vascular ischaemia, noise, drugs, surgery, or

Ménière’s disease.

The red flag symptom to alert the clinician is unilateral

deafness as this may indicate an acoustic neuroma. Early

treatment of this space-occupying lesion lessens morbidity

and mortality.



Differential diagnosis

Hearing loss



Age group

Infants

Young children



Adolescents



20–40 years



40–60 years



60+ years



Causes

Congenital

Secretory otitis media (glue ear)

Congenital

Secretory otitis media (glue ear)

Postinfective (meningitis, viral)

Congenital

Malingering

Postinfective (meningitis, viral)

Acoustic trauma or drugs

Postinfective (meningitis, viral)

Acoustic trauma or drugs

Otosclerosis

Acoustic neuroma

Ménière’s disease

Postoperative complications

Acoustic trauma or drugs

Otosclerosis

Acoustic neuroma

Ménière’s disease

Postoperative complications

Presbyacusis

Acoustic trauma or drugs

Acoustic neuroma

Postoperative complications



Type of loss

Conductive or

Conductive

Conductive or

Conductive

Sensorineural

Conductive or

—

Sensorineural

Sensorineural

Sensorineural

Sensorineural

Conductive

Sensorineural

Sensorineural

Conductive or

Sensorineural

Conductive

Sensorineural

Sensorineural

Conductive or

Sensorineural

Sensorineural

Sensorineural

Conductive or



sensorineural

sensorineural



sensorineural



sensorineural



sensorineural



sensorineural



85



Chapter



4



Ear, nose and throat

TINNITUS

Tinnitus is the symptom of noise in the ears. It is difficult

to investigate because it is a subjective symptom. It may

be heard as a continuous, pulsatile or episodic sound. The

sound may be difficult for the patient to describe but is

often noted as whistling, buzzing or crackling. The sounds

experienced are not complex auditory hallucinations as

found in certain psychoses.

The most common cause of tinnitus is the onset of

sensorineural deafness associated with degeneration of

the cochlea. However, anything which interferes with the

hearing mechanism (even wax) may produce tinnitus. All

the possible causes of hearing loss should be considered

when tinnitus is present. It is one of the triad of symptoms

that are observed in Ménière’s disease, the others being

vertigo and loss of hearing. Tinnitus may arise from the

Eustachian tube, which is also the site of the rare condition

of palatal myoclonus.

In present day usage it is unusual to see tinnitus caused

by drugs, but it may be seen in the treatment of rheumatic

fever by high dose aspirin and is a recognised side-effect

of aminoglycosides. High doses of nonsteroidal antiinflammatory drugs may also induce tinnitus. This form

of drug-induced tinnitus is usually reversible on stopping

the medication.

A red flag sign is when the tinnitus is unilateral. As

with unilateral deafness, an acoustic neuroma must be

considered and investigated.

VERTIGO (DIZZINESS)

Vertigo is a symptom of imagined spinning or unsteadiness.

The patient feels they or their surroundings are moving.

This is true vertigo and is caused by inner ear, vestibular,

dysfunction. Vertigo arising from the vestibular mechanism

is known as peripheral vertigo.

Acute labyrinthine dysfunction

Acute labyrinthine dysfunction is the term used for severe

episodic vertigo of sudden onset. Its cause includes

diagnoses such as viral, idiopathic or vascular labyrinthitis.

The disorder may last for days and may be prolonged in

benign positional vertigo.

Benign positional vertigo

Benign positional vertigo is recognised by the shortlasting onset of vertigo with movement of the head. It

may be one of the sequelae of acute labyrinthine

dysfunction. Other causes are trauma or idiopathic.

Central causes of vertigo

Other manifestations of giddiness arise from different

sites. The vestibular (inner ear) cause of vertigo is

known as peripheral vertigo and that arising from other

sites is termed central vertigo. Inputs from the eyes,

proprioception, cerebellum, brainstem, cerebrum and

reticular formation all have a function in balance. The loss

of balance in central vertigo is not of the rotational type

86



but is manifest by a feeling of unsteadiness and is not

usually associated with nausea or vomiting. One possible

cause of this is a hypotensive state, perhaps caused by

drugs in the management of hypertension. Vertigo of

vestibular (peripheral) origin is almost always accompanied

by nausea and/or vomiting, whereas this is less common

in central vertigo. Another distinguishing feature is that

peripheral vertigo is usually intermittent and is not

progressive. Giddiness of central origin is often constant

and progressive.

The red flag sign in vertigo, requiring urgent

investigation or referral, is the possibility of a transient

ischaemic attack (TIA) or vertebrobasilar ischaemia. The

other associated signs suggesting these conditions as

a possible cause are raised blood pressure, dysarthria,

visual disturbance, neck problems and loss of

coordination.

Questions to ask

Vertigo



•

•

•

•

•

•

•

•

•



How would you describe the giddiness?

How long has it been present?

Is it intermittent?

How long does it last?

What precipitates it (e.g. change of posture or head

movement)?

Are you on any medication (ototoxic or lowering

blood pressure)?

Do you have any nausea or vomiting?

Have you ever had ear problems or surgery?

Do you have any deafness or tinnitus?



Differential diagnosis

Central and peripheral vertigo



Diagnosis

Acute labyrinthine dysfunction

Benign positional vertigo

Ménière’s disease

Multiple sclerosis

Transient ischaemic attack (TIA)

Vertebrobasilar ischaemia

Head injury



Site

Peripheral

Peripheral

Peripheral

Central

Central

Central

Central or peripheral



Examination of the ear

THE AUROSCOPE

Use the largest aural speculum that fits in the external

canal comfortably. Hold the auroscope at its point of

balance (centre of gravity). Balance it lightly in the hand.

Do not grab it like a screwdriver! Use the same hand as

the ear (left hand for left ear) (see Fig. 4.5). When inserting



Chapter



The ear



4



Preauricular sinus



preauricular

sinus



tragus



Fig. 4.5 How to hold the auroscope.



the auroscope retract the pinna posteriorly with the free

hand (right hand for left ear). This opens the canal for

easier inspection. Always examine the pinna before

examining the external canal.

Do not rush to insert the auroscope and, when inserting

it, look at the canal throughout its whole length. Observe

for any anatomical abnormality and note the external

appearance of any discharge or eczema. The appearance

of discharge, if mucoid, may indicate middle ear disease

rather than otitis externa, whereas evidence of eczematous

skin in the pinna (or psoriasis) may indicate that otitis

externa will be found in the canal.

Look also for scars of mastoid surgery (pre- or postauricular) because passing the auroscope too hastily into

the ear may result in a large posterior mastoid cavity

being overlooked.



Fig. 4.6 Site of preauricular sinus.



Accessory auricles



tragus



accessory

auricle(s)



EXTERNAL EAR

Pinna

Minor congenital abnormalities Bat ears is the term

given to ears which do not lie flat against the head but

protrude outwards. They occur in about 2% of the

population and if to be surgically corrected this is best left

until after six years of age.

Pre-auricular sinus is a defect in embryological

development and usually occurs antero-superiorly to the

tragus (Fig. 4.6).

Accessory auricles occur anterior to the tragus (Fig.

4.7) and are another embryonic fault.

Gross congenital deformities are rare and include

anotia (complete absence of the pinna). The conditions

can occur with normal or abnormal development of the

middle and inner ear.

Skin changes Eczema or psoriasis are common conditions

which may involve the pinna and external canal. Like

any skin condition, secondary infection is a possible

complication and is more likely to occur in the external

ear because of the accumulation of debris.

Infection/inflammation can be severe with pain,

redness and swelling. The infection may be an extension

of infection from the external canal but even if localised



Fig. 4.7 Site of accessory auricles.



to the pinna should be treated with systemic antibiotics.

Infections of the pinna include cellulitis and perichondritis,

where the underlying cartilage is infected.

Cauliflower ears are the result of previous untreated

traumatic haematoma of the pinna. Early surgical

treatment of the initial haematoma may prevent lasting

deformity.

Chondrodermatitis nodularis helicis is a benign

nodular condition usually of the helix of the ear. The

aetiology is unknown but, as it occurs in later life, may

be related to sun damage. It can only be differentiated

from malignant conditions by biopsy.

Basal cell carcinomata and squamous cell carcinomata

are tumours most commonly seen on the pinna and

require appropriate surgical treatment.

Chondromata arise from cartilage, which forms the

outer one-third of the canal. They may vary in size

from being quite small to obstructing the whole canal.

87



Chapter



4



Ear, nose and throat

They rarely need attention but may make it difficult to

remove wax and observe the inner part of the canal

and the tympanic membrane. To the inexperienced eye

chondromata may appear alarming and arouse concern

about malignancy. They are swellings that are covered by

normal epithelium and vary greatly in size from minor

swellings to those obstructing most of the external

canal.

External canal

The diameter of the canal is very variable and even in

some adults may be very narrow. In a child the canal is

straight and the tympanic membrane is easily seen. In

adults the distal part of the canal, close to the tympanic

membrane, narrows (the isthmus) in its final third and

deflects downwards. This results in a recess inferiorly

with an acute angle being formed between canal and

tympanic membrane. It is thus more difficult to see the

whole tympanic membrane and debris or foreign bodies

are more easily concealed from the clinician in the recess

(see Fig. 4.1).

Wax Wax is the natural accumulation of skin debris and

secreted oil from the apocrine glands of the external canal

and unless causing symptoms does not need to be

removed. Before full examination of the external canal

can be complete, the ear should be cleaned of wax. Wax,

impacted or otherwise, is one of the commonest

conditions of the ear dealt with by the general physician.

It may present with a difficulty in hearing or even with

pain.

The production and accumulation of wax (rather than

its natural expulsion) is dependent on occupational and

genetic factors (gene on chromosome 16). The removal

of impacted wax gives the greatest relief (in both hearing

and discomfort) to an afflicted patient.

The most common method used to clear wax is by

syringing or the now more acceptable irrigation (by an

electrical pulsed pump). There are contraindications to

syringing.



a Jobson Horne probe (tipped with cotton wool) to dry

the outer part of the external canal. In addition to the

Jobson Horne probe, useful instruments for removing

wax include a wax hook, crocodile forceps and aural

forceps (Fig. 4.8).

Water used to irrigate wax should be at 37°C (hand

temperature). Variation in this temperature may stimulate

the labyrinth, causing temporary giddiness.

The ENT specialist will have access to microsuction,

which is light suction applied by an aural cannula under

operating-microscope vision.

Whatever method is used to clean the external canal,

this must be done before any external canal or middle ear

disease can be diagnosed.

Otitis externa

Otitis externa is an infection of the external canal. Infections

include furuncle or generalised furunculosis and otitis

externa, bacterial or fungal. Otitis externa causes discharge,

irritation and often pain. The colour of the discharge is

discussed in the section on symptoms (see p. 83) but when

observing the discharge the possible presence of the spores

of a fungal growth should be noted.



Review



Furunculosis



Contraindications to syringing



A single furuncle or generalised furunculosis of the

external canal is usually painful and may be extremely so.

Furuncles can be recognised as a small boil in the external

canal. The lesion may be quite distal and it may be easily

missed if the auroscope is inserted too deeply without

observing the whole length of the canal. Furunculosis is

recognised by the appearance of multiple boils or

abscesses in the canal and is associated with severe

pain and swelling of the external canal which may be

completely occluded.



• Previous ear surgery – mastoid, tympanoplasty,

stapedectomy

• Previous otitis externa

• Perforation

• Tinnitus

• Labyrinthine disturbance



Water in the ears is a common trigger for otitis externa

and it is important that the ears are fully cleaned if

possible so that no water is trapped behind any remaining

wax. The ears should be carefully dried after syringing

and it is useful to have an operator trained in the use of

88



Fig. 4.8 Instruments useful in the removal of wax. From left to

right: Jobson Horne probe, wax hook, crocodile forceps, aural

forceps, aural speculum, aural sucker.



Myringitis bullosa

This is a manifestation of viral otitis externa where blisters

are to be seen on the epithelial surface of the tympanic

membrane.



Chapter



The ear



4



Suppurative acute otitis media

Suppurative otitis media is one of the possible sequelae

of acute otitis media. With this the tympanic membrane

ruptures and releases the mucopus formed by the acute

otitis media infection. Again this condition usually

resolves spontaneously because of the release of the

mucopus.

Chronic suppurative otitis media

This can be defined as a continuing discharging tympanic

membrane perforation. The tympanic perforation of acute

suppurative otitis media may remain, together with the

discharge and become chronic. Referral to an ENT

specialist is then indicated so that the possible extension

of the infection into the mastoid and beyond (meninges

and brain) can be assessed.

Fig. 4.9 Normal tympanic membrane.



THE MIDDLE EAR

Tympanic membrane

The whole circumference of the membrane should be

visualised. In its normal state the membrane appears grey

and shiny and through it the handle of the malleus

is visible with its inferior pole (the umbo) pointing

posteriorly. Inferior to the umbo, an arc of light reflects

back to the observer. This arc is directed antero-inferiorly

(Fig. 4.9).

Any vascular infiltration should be noted and this may

occur either along the handle of the malleus or involve

the tympanic membrane as a whole.

Superior to the handle of the malleus is the pars

flaccida. This is the part of the tympanic membrane that

is mobile and will move either by instigating a Valsalva

manoeuvre or by using an auroscope with pneumatic

attachment. Demonstration of the mobility of the pars

flaccida will assure the clinician of aeration of the middle

ear and therefore of patency of the Eustachian tube. The

main area of the tympanic membrane is called the pars

tensa and comprises the largest part of the membrane. It

is in this part that a perforation may be noted. Here also

chalk patches (tympanosclerosis) may be seen.

Acute otitis media

This is the most common middle ear infection and is

particularly common in childhood. The presenting

symptoms are fever and otalgia. In infancy, otalgia is

recognised by the child being restless and crying. The

onset is rapid and is usually associated with an upper

respiratory tract virus infection.

On clinical examination of the ear, the tympanic

membrane is inflamed and the epithelium of the

membrane is often distorted (‘pavement’ epithelium) or

bulging. The condition normally resolves with or without

treatment.



Acute mastoiditis, meningitis and cerebral abscess

Though rare, these are all possible sequelae of acute otitis

media and should be considered when there is continuing

fever, otorrhoea, otalgia and any suspicion of cerebral

signs present. Acute mastoiditis may be detected by

examination of the mastoid bone for swelling, redness or

tenderness.

It should be noted that these conditions may progress

very rapidly from an attack of acute otitis media.

Eustachian tube dysfunction

This may present with otalgia, reduced or distorted

hearing, or with tinnitus. As the condition advances,

vascular infiltration of the tympanic membrane along the

handle of the malleus develops and the malleus becomes

more prominent as the increasing negative pressure

in the middle ear causes retraction of the tympanic

membrane.

As a result of the negative pressure in the middle ear,

and blockage of the Eustachian tube, the mobility of the

pars flaccida is lost. This can be demonstrated by asking

the patient to perform the Valsalva manoeuvre and

observing for movement (or lack of) in the pars flaccida.

This can be replicated by use of the puffer with a

pneumatic auroscope. Graphical demonstration of

Eustachian tube dysfunction can be obtained using

tympanometry.

Tympanometry Tympanometry (Figs 4.10, 4.11) provides

a good method for detecting middle ear effusion. A

flat trace on the tympanogram indicates an immobile

tympanic membrane suggestive of middle ear effusion.

Secretory otitis media (glue ear)

This is a condition of mucoid secretions in the middle ear

which results primarily in reduction in hearing. It occurs

as a result of poor aeration of the middle ear caused by

Eustachian tube dysfunction. It is mainly a disease of

children in whom adenoidal obstruction of the Eustachian

tube is a prominent feature. However it can occur in

adults whose nasal airway is compromised.

89



Chapter



4



Ear, nose and throat



Fig. 4.10 Tympanometer in use.



1.5



left ear



Fig. 4.12 Ventilation tube (grommet) in situ.



1.0

1



Uea (+200)



Yd (mmhO)



2



0.5

0

0

–400



– 200

0

pressure (daPa)



+200



Fig. 4.11 Normal tympanogram showing tympanic membrane

response to pressure.



Clinical diagnosis is made in several ways. Bubbles of

mucous may be seen on examination of the tympanic

membrane. Otherwise all the clinical aspects of Eustachian

tube dysfunction may be elicited (see above).

The importance of this condition is for children in

whom speech, language or educational development

may be delayed due to reduction in hearing. If there is

evidence of such delay in development, or if there is

a persistent (longer than three months) reduction of

hearing, referral to an ENT specialist is advisable for

consideration of grommet insertion (Fig. 4.12) and

adenoidectomy.

Dry perforation

This may occur due to trauma or as a result of a previous

middle ear infection and may be of varying size from very

small to involving the vast majority of the tympanic

membrane and exposing structures in the middle ear

(Fig. 4.13).

THE INNER EAR

Information about inner ear disease is mainly obtained

from the history of the condition that the patient gives,

whether it is deafness, tinnitus or giddiness. The inner

ear cannot be examined directly and information on its

function is obtained by various methods and tests.

90



Fig. 4.13 Large tympanic membrane perforation. Incudostapedial

joint just visible posterosuperiorly; round window visible posteriorly.



Deafness

Tuning fork tests Tuning forks are the first and an

important tool to investigate deafness (Fig. 4.14). A

tuning fork with a frequency of 256 Hz (C256, middle C

on the piano) can be used to undertake the Rinne and

Weber tests (see below) with which it should be relatively

easy for the clinician to differentiate conductive from

sensorineural deafness.

It is also most helpful to have a high-tone tuning fork

of about 4096 Hz. In deafness of old age (presbyacusis)

it is the high tones that the patient first loses the ability

to hear. Holding a sounding tuning fork of 4096 Hz a few

centimetres away from the entrance of the external ear

will ascertain whether there is a degree of high-tone

hearing loss.

• Weber test. This test is performed by placing a tuning

fork (C256) on the midline of the skull, usually on the



Chapter



The ear



4



mastoid bone. It will be heard less well than if the

tuning fork is placed close to the external canal. If it is

heard louder on the mastoid bone, the test is negative

and indicates that the ossicular chain is not magnifying

the sound for some reason.

A false negative Rinne test may occur if the ear has a

profound sensorineural deafness. With an ear conducting

normally the test should be positive, but the bone

conduction (the tuning fork placed on the mastoid bone)

sound may be picked up by the opposite ear and therefore

thought by the patient to be louder than air conduction;

whereas such profound deafness in the tested ear negates

the test for conduction (false negative Rinne). This finding

will be supported by the fact that the Weber test will be

referred to the other (less deaf) ear.

As already explained, in conductive deafness there

is an interruption of sound, and/or sound magnification,

in the external or middle ear. Sensorineural deafness

indicates a problem with the cochlea or auditory nervous

system.



Fig. 4.14 Tuning forks: left, 4096 Hz; right, 256 Hz.



Weber test

Differential diagnosis

Rinne negative (conductive deafness)



Obstruction of

external canal



L



R



L



R



Middle ear pathology



Fig. 4.15 Weber test.



forehead (Fig. 4.15). With normal hearing the sound of

the tuning fork is heard centrally (equally in both ears).

If it is referred to one side, that side either has a

conductive deafness or has a better sensorineural

hearing than the other side.



Differential diagnosis

Weber test



Conductive deafness

Sensorineural deafness



Weber referred to side of

conductive deafness

Weber referred to better ear



• Rinne test. This test clarifies whether or not there is

conductive deafness (Fig. 4.16). It tests the efficiency of

the ossicular chain. In a normal ear the Rinne test will

be positive. A tuning fork (C256) is first placed on the



Impacted wax

Exostosis

Debris (otitis externa)

Foreign body

Canal atresia

Perforation of tympanic

membrane

Ossicular chain problem

– congenital

– otosclerosis

– trauma

– post-infective adhesions

– Eustachian tube dysfunction



Audiometry The definitive test for hearing acuity is by

audiometry. There may be subjective errors in the tuning

fork tests. There may also be subjective anomalies in

audiometric testing but these are less likely. Audiometric

testing shows in graphic form both bone and air

conduction (Fig. 4.17).

The normal annotation used when producing an

audiogram is as follows:

•

•

•

•



X

O

⊃

⊂



refers to air conduction in the left ear

refers to air conduction in the right ear

refers to bone conduction in the left ear

refers to bone conduction in the right ear



The horizontal axis indicates the frequency of the sound

in Hz and the vertical axis indicates the hearing level in

decibels (dB). Levels of hearing recorded between zero

and 20 dB are considered to be within normal limits.

91



Chapter



4



Ear, nose and throat



Rinne‘s test

a



c



b



d



Fig. 4.16 Rinne test: (a) bone conduction, (b) air conduction, (c) perceptive deafness, (d) conductive deafness.

air conduction



right



left



bone conduction



unmasked B



–10



–10



0

10



20



20

hearing level (dB)



0

10



30

40

50

60

70



30

40

50

60

70



80



80



90



90



100



100



110



110



120



left



nominal masking levels

–20



–20



hearing level (dB)



right



masked



125



250



500



1000



2000



4000



8000



frequency (Hz)



120



125



250



500



1000



2000



4000



8000



frequency (Hz)



Fig. 4.17 A blank audiogram.



Oto-acoustic emissions test (to screen for deafness

in infancy)

This is a screening test for neonates. It is non-invasive

and relies on a sound transmitted to a baby’s ear

producing an auto-acoustic emission or echo. This echo

can be measured by computer. A negative response may

indicate infant hearing impairment, but the test can give

false readings. The infant can then be referred for the

more accurate auditory brain-stem response test.

Labyrinthine dysfunction

Nystagmus occurs with stimulation of the vestibular

system. The direction of the nystagmus indicates the side

affected. The direction of the fast element is away from

92



the affected side, although the nystagmus is named to

the side of the fast element. Thus nystagmus (fast) to the

right indicates an affected left labyrinth.

The caloric test is carried out by irrigating the ear canal

with cold or warm water. This induces nystagmus. Lack

of response indicates no function in the labyrinth of the

side tested. This finding may be indicative of Ménière’s

disease.

Benign positional vertigo

Hallpike (Dix–Hallpike) test This is a definitive test for

benign positional vertigo. If vertigo is induced by the

manoeuvre, the test is deemed positive. The manoeuvre

is performed by sitting the patient on a couch with their



Chapter



The nose

legs extended. The clinician turns the head 45° to one

side and lays the patient fully on their back and slightly

extends the neck. The test is positive if nystagmus is

provoked by this. The cause of the vertigo can then be

established as peripheral (in the labyrinth) as opposed to

central.



4



The nose and paranasal sinuses

external nose



inferior view of nose

tip

ala nasi



bridge



Red flag – urgent referral

The ear



•

•

•

•

•



Sudden onset of unilateral deafness

Unilateral deafness even if not of sudden onset

Persistent unilateral tinnitus

Unresolving ear discharge

Acute and unremitting otalgia not responding to

treatment

• Vertigo if TIA or vertebrobasilar ischaemia a

possibility



vestibule



anterior

naris



tip



ala nasi

columella



columella

nasal septum



sphenoid

sinus



cranial

cavity



pituitary

fossa



The nose

vomer



Structure of the nose and sinuses



hard palate



frontal sinus

bony portion

of nasal

septum



septal

cartilage



nasopharynx

lateral wall of nose



Diagrams of the nose and paranasal sinuses are shown

in Figure 4.18.



sphenoid

sinus



cranial

cavity



superior

turbinate



EXTERNAL NOSE

The external appearance of the nose (before it may be

distorted by injury or disease) is variable due to genetic

factors. It is dependent on the shape of the cartilage and

bone structure.

The external structure of the nose consists of skin

overlying a bone and cartilaginous support. This skin

continues into the anterior nares (the vestibule). The skin

of the nose contains many sebaceous glands and within

the vestibule the skin contains both hair and sebaceous

cells. The proximal one-third of the nose is constructed

of bone while the distal two-thirds is cartilage.

NASAL CAVITY

The interior structure is called the nasal cavity. After the

vestibule, the surface is lined with ciliated columnar

epithelium except in its upper part, which is lined with

olfactory epithelium. The ciliated columnar epithelium

lines the whole respiratory tract, indicating the importance

of the nose in this system. The sinuses are also lined with

ciliated columnar epithelium.

The central pillar at the entrance to the nose is the

columella from which the nasal septum extends posteriorly. This is cartilaginous in its outer structure, becoming

bony after about half its length. The bony part is formed

by perpendicular plate of the ethmoid and inferiorly by

the vomer, which is an extension of the maxillary crest.

The septum is often not straight in its development.



frontal sinus



middle

turbinate

vestibule

hard palate



inferior

turbinate



coronal section of nasal cavity and sinuses

ethmoidal air

cells



orbit

middle

meatus



middle

turbinate



inferior

meatus



inferior

turbinate



maxillary

sinus

(antrum)



Fig. 4.18 Diagrams of nose and paranasal sinuses.



Turbinates extend from the lateral wall of the nasal

cavity and act as air-warming processes. These are the

inferior, middle and superior turbinates. The inferior

turbinate is easily seen through the vestibule by elevating

the tip of the nose. Drainage of the nasolacrimal duct

occurs under the inferior turbinate; of the maxillary,

anterior ethmoid and frontal sinuses from under the

93