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EAR
Anatomy and physiology
The ear is the specialised sensory organ of hearing and
balance; it is divided anatomically into the external, middle and
inner ear.
External ear
The external ear consists of the cartilaginous pinna, the external
auditory canal (cartilage in the lateral one-third, bone in the
medial two-thirds), and the lateral surface of the tympanic
membrane (Fig. 9.1). Sound is collected and channelled by the
pinna and transmitted via the external auditory canal to the
tympanic membrane. The external auditory canal has an elongated S-shaped curve; hence it is important to retract the pinna
when examining the ear to see the tympanic membrane clearly.
The outer portion of the canal has hair and glands that produce
ear wax, which forms a protective barrier.
Middle ear
The middle ear is an air-filled space that contains the three bony,
articulated ossicles: the malleus, incus and stapes. The eustachian tube opens into the middle ear inferiorly and allows
equalisation of pressure and ventilation. Vibrations of the tympanic membrane are transmitted and amplified through the
ossicular chain and focus on to the smaller oval window on
which the stapes sits (see Fig. 9.1B). The malleus is attached to
the tympanic membrane and can be seen clearly on otoscopy
(Fig. 9.2). The long process of the incus can also be visible occasionally. The tympanic membrane has a flaccid upper part
(pars flaccida), and it is important to look carefully in this area as
this is where a cholesteatoma (an invasive collection of keratinising squamous epithelium) can form. The chorda tympani
nerve runs through the middle ear carrying taste fibres from the
anterior two-thirds of the tongue; these ‘hitch a ride’ with the
facial nerve, which runs through the mastoid bone in the wall of
the middle ear.
Inner ear
The inner ear contains the organs of hearing (cochlea) and balance (vestibular system). The vibration of the stapes footplate
stimulates fluid within the cochlea, resulting in the movement of
hair cells in the cochlea which are converted to electrical impulses along the vestibulocochlear nerve (VIII).
The vestibular system helps maintain balance, along with visual input and proprioception. The vestibular part of the inner ear
contains:
• The lateral, superior and posterior semicircular canals: these
lie at right angles to detect rotational motion of their fluid
(endolymph) in three planes.
• The utricle and the saccule: their hair cells are embedded in a
gel layer containing small crystals (otoliths), which are subject
to gravity and enable detection of head tilt and linear
acceleration.
Fig. 9.1 The ear. A The pinna. B Cross-section of the outer, middle and inner ear.
Helix
Triangular fossa
Antihelix
External
auditory meatus
Tragus
Concha
Earlobe
Pinna
Earlobe
B
Auditory ossicles
Malleus Incus Stapes
(on oval window)
Semicircular canal
Vestibular nerve
Cochlear nerve
Cochlea
Tympanic cavity
Tympanic membrane
Eustachian tube
External auditory
meatus
The history • 195
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9
A
B
Fig. 9.2 Structures seen on otoscopic examination of the right ear. A Main structures. B Normal tympanic membrane.
The history
Common presenting symptom s
Pain and itching
Ask about:
• quality of the pain
• preceding trauma, upper respiratory tract infection (URTI)
• associated symptoms: dysphagia/voice change (suggesting
possible referred pain from a throat lesion).
Otalgia (ear pain) associated with pruritus (itching) is often due
to otitis externa. Acute otitis media is common in children and
otalgia often follows an URTI. Other causes of otalgia are
described in Box 9.1.
Ear discharge
Ask about:
• purulent, mucoid or blood-stained discharge (otorrhoea)
• associated pain.
A purulent discharge can be caused by otitis externa or acute
otitis media with a perforation. A chronic offensive discharge may
be a sign of cholesteatoma.
Blood-stained discharge may suggest the presence of granulation tissue from infection or can be a result of trauma, with or
without an associated cerebrospinal fluid (CSF) leak.
Hearing loss
Ask about:
• sudden or gradual onset
9.1 Causes and features of earache (otalgia)
Cause Clinical features
Otological
Acute otitis externa Pain worsens on touching outer ear, tragus
Acute otitis media Severe pain, red, bulging tympanic
Perichondritis Erythematous, swollen pinna
Trauma Pinna haematoma, pinna laceration,
Herpes zoster (Ramsay
Hunt syndrome)
Malignancy Mass in ear canal or on pinna
Non-otological
Tonsillitis
Peritonsillar abscess
Temporomandibular
joint dysfunction
Dental disease Toothache, e.g. due to dental abscess
Cervical spine disease Neck pain/tenderness
Cancer of the pharynx
or larynx
• precipitating factors: trauma, URTI, noise exposure,
antibiotics
• impact of the hearing loss on the patient’s function.
Hearing loss can be a result of disruption in the conduction
mechanism or may have sensorineural causes such as failure of
Swelling of ear canal
Purulent discharge and itching
membrane, purulent discharge if tympanic
membrane perforation present
haemotympanum (blood behind tympanic
membrane); cerebrospinal fluid leak or facial
nerve palsy may be present
Vesicles in ear canal, facial nerve palsy may
be present; vertigo is common
Sore throat, tonsil inflammation
Trismus, soft-palate swelling in peritonsillar
abscess
Tenderness, clicking of joint on jaw opening
Associated sore throat, hoarseness,
dysphagia, weight loss, neck lump
196 • THEEAR,NOSEANDTHROAT
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the VIII nerve or cochlea (Box 9.2). Profound loss before speech
acquisition affects speech development and quality.
Tinnitus
Tinnitus is an awareness of a noise in the absence of an external
stimulus.
Ask about:
• quality of tinnitus: high-pitched, ringing, pulsatile
• intermittent or constant nature
• whether it is unilateral or bilateral
• associated hearing loss or other ear symptoms.
Tinnitus is usually associated with hearing loss. An acoustic
neuroma (a tumour of the vestibulocochlear nerve, cranial nerve
VIII) needs to be considered in unilateral tinnitus or tinnitus with
an asymmetrical sensorineural hearing loss.
Vertigo
Vertigo is a sensation of movement relative to one’s surroundings. Rotational movements are most common, and patients
often have associated nausea, vomiting, and postural or gait
instability. Vertigo can originate peripherally or, less often, centrally (brainstem, cerebellum). Patients will often say they are
‘dizzy’ when describing the illusion of movement that is vertigo. It
is very important to clarify exactly what they mean by this.
Lightheadedness is not a vestibular symptom, but unsteadiness
may be.
Ask about:
• duration and frequency of episodes
• aggravating or provoking factors (position, head movement)
9.2 Causes of hearing loss
Conductive
• Wax
• Otitis externa
• Middle ear effusion
• Trauma to the tympanic
Sensorineural
• Genetic, e.g. Alport’s
• Prenatal infection, e.g.
• Birth injury
• Infection:
a
Disruption to the mechanical transfer of sound in the outer ear,
eardrum or ossicles.
b
Cochlear or central damage.
a
membrane/ossicles
syndrome
rubella
• Meningitis
• Measles
• Mumps
b
• Otosclerosis
• Chronic middle ear infection
• Tumours of the middle ear
• Trauma
• Ménière’s disease
• Degenerative (presbyacusis)
• Occupation- or other noise-induced
• Acoustic neuroma
• Idiopathic
• associated ‘fullness in the ear’ during the episode (Ménière’s
disease)
• associated focal neurology (cerebrovascular event)
• fluctuating hearing loss or tinnitus
• associated headaches, nausea or aura (migraine)
• previous significant head injury; previous URTI.
• The most common causes of vertigo include benign parox-
ysmal positional vertigo (attributed to debris within the posterior semicircular canal), vestibular neuritis (also known as
vestibular neuronitis, a viral or postviral inflammatory disorder)
and Ménière’s disease (caused by excess endolymphatic
fluid pressure). Other causes include migraine, cerebral
ischaemia, drugs and head trauma. Discriminating features
are described in Box 9.3.
Nystagmus
Nystagmus is an involuntary rhythmic oscillation of the eyes,
which can be horizontal, vertical, rotatory or multidirectional. It
may be continuous, paroxysmal, or evoked by manoeuvres such
as gaze or head position. The most common form, ‘jerk
nystagmus’, consists of alternating phases of a slow drift in one
direction with a corrective saccadic ‘jerk’ in the opposite direction. The direction of the fast jerk is used to define the direction of
nystagmus (Box 9.4). Pendular nystagmus, in which there is a
sinusoidal oscillation without a fast phase, is less common.
Nystagmus may be caused by disorders of the vestibular, visual
or cerebellar pathway.
Past medical history
Ask about:
• previous ear surgery, trauma
• recurrent ear infections
• systemic conditions associated with hearing loss (such as
granulomatosis with polyangiitis)
• any significant previous illnesses, such as meningitis, which
can result in sensorineural hearing loss.
Drug history
The aminoglycoside antibiotics (such as gentamicin), aspirin,
furosemide and some chemotherapy agents (cisplatin) are
ototoxic.
Family history
Some causes of sensorineural hearing loss and otosclerosis are
congenital. Otosclerosis causes a conductive hearing loss due to
fixation of the stapes footplate.
Social history
The patient’s occupation should be noted, as well as any significant previous exposure to loud noise.
9.3 Diagnosing vertigo
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The physical examination • 197
Benign paroxysmal
positional vertigo Vestibular neuritis Ménière’s disease
Duration Seconds Days Hours Hours–migraine
Hearing
loss
Tinnitus À À þþ À
Aural
fullness
Episodic Yes Rarely Recurrent vertigo; persistent tinnitus and
Triggers Lying on affected ear Possible presence of upper
MS, Multiple sclerosis.
À À þþ À
À À þþ À
progressive sensorineural deafness
None Drugs (e.g., aminoglycosides)
respiratory symptoms
Central vertigo (migraine, MS,
brainstem ischaemia, drugs)
Days and weeks – MS
Migraine–recurs
Central nervous system damage–usually
some recovery but often persistent
cardiovascular disease
9.4 Characteristics of nystagmus
Nystagmus type Clinical pathology Characteristics
Fast phase Maximal on looking
Jerk:
Peripheral Semicircular canal, vestibular nerve Unidirectional
Central Brainstem, cerebellum Bidirectional (changes with direction of gaze)
Dysconjugate (ataxic) Interconnections of III, IV and VI
nerves (medial longitudinal bundle)
Pendular Eyes, e.g., congenital blindness No fast phase Straight ahead
Not suppressed by optic fixation
Patient too dizzy to walk
Dix–Hallpike fatigues on repetition
Suppressed by optic fixation
Patient can walk (even with nystagmus)
Dix–Hallpike persists
Typically affects the abducting eye To either side
Away from affected side
To either side
9
The physical examination
Examination sequence (Video 18)
Inspection
• Pinna skin, shape, size, position, scars from previous sur-
gery/trauma, deformity
Palpation
• Gently pull on the pinna and push on the tragus to check for
pain.
• Gently palpate over the mastoid bone behind the ear to
assess for pain or swelling.
Otoscopy
• Use the largest otoscope speculum that will comfortably fit
the meatus.
• Explain to the patient what you are going to do.
• Hold the otoscope in your right hand for examining the right
ear (left hand to examine left ear). Rest the ulnar border of
your hand against the patient’s cheek to enable better control
and to avoid trauma if the patient moves (Fig. 9.3).
• Gently pull the pinna upwards and backwards to straighten
the cartilaginous external auditory canal. Use the left hand to
retract the right pinna (see Fig. 9.3).
• Inspect the external auditory canal through the speculum,
noting wax, foreign bodies or discharge. You should identify
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Fig. 9.3 Examination of the ear using an otoscope.
the tympanic membrane and the light reflex anteroinferiorly
(see Fig. 9.2).
Tympanic membrane perforations can be central or marginal,
and the position and size of the perforation should be noted as a
percentage (Fig. 9.6A). A severe retraction pocket of the pars
tensa can mimic a perforation (see Fig. 9.6B). A retraction of the
pars flaccida can contain a cholesteatoma, which may cause an
offensive discharge and erode the bony ossicles, resulting in a
conductive hearing loss (see Fig. 9.5C). Fluid behind the tympanic membrane is called otitis media with effusion (OME, or
‘glue ear’, Fig. 9.7A), and a fluid level may be seen (see
Fig. 9.7B). This commonly affects children and can be treated
surgically with insertion of a ventilation tube or grommet (see
Fig. 9.6C). If persistent OME is seen in adults, the postnasal
space needs to be examined by a specialist to exclude a lesion in
that site. Acute otitis media presents with pain; the tympanic
membrane can become inflamed (see Fig. 9.7C), and may bulge
and eventually perforate.
Testing hearing (Video 19)
Whispered voice test
Congenital deformities of the pinna, like microtia (Fig. 9.4A)or
low-set ears, can be associated with other conditions such as
hearing loss and Down’s syndrome. Children can also have
protruding ears that occasionally require corrective surgery
(pinnaplasty). Trauma can result in a pinna haematoma (see
Fig. 9.4B) and subsequent ‘cauliflower ear’ due to cartilage ne-
crosis if untreated. Trauma may also cause mastoid bruising
(‘Battle’s sign’), suggesting a possible skull-base fracture. Lesions on the pinna are relatively common and can be related to
sun exposure; they include actinic keratosis, and basal cell and
squamous cell cancers (see Fig. 9.4C).
If discharge is noted on otoscopy and the tympanic membrane is intact, otitis externa is the likely cause (Fig. 9.5A). The
canal can reveal exostoses, abnormal bone growth due to cold
water exposure, often seen in surfers (see Fig. 9.5B).
Scarring on the tympanic membrane (tympanosclerosis) can
be caused by previous grommet insertion or infections.
Examination sequence (Video 19A)
• Stand behind the patient.
• Start testing with your mouth about 15 cm from the ear you
are assessing.
• Mask hearing in the patient’s other ear by rubbing the tragus
(‘masking’).
• Ask the patient to repeat a combination of numbers and
letters (e.g. 3-B-7). Start with a normal speaking voice to
confirm that the patient understands the test. Then, lower
your voice to a clear whisper.
• Repeat the test but this time at arm’s length from the pa-
tient’s ear. People with normal hearing can repeat the
sequence correctly when whispered at 60 cm.
• If the patient responds incorrectly, the test is repeated using a
different number/letter combination.
• If 50% or more of the items in the two triplets are incorrect,
the test is abnormal.
ABC
Fig. 9.4 The pinna. A Microtia. B Haematoma. C Squamous cancer (arrow).
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ABC
Fig. 9.5 Auditory canal abnormalities. A Otitis externa. B Exostosis of the external auditory meatus. C Cholesteatoma.
9
ABC
Fig. 9.6 Tympanic membrane abnormalities. A Tympanic membrane perforation (arrow). B Retraction pocket of the pars tensa (arrow). C Grommet
in situ.
A
Fig. 9.7 Otitis media. A With effusion. B Fluid level behind the tympanic membrane (arrow). C Acute otitis media.
B
C
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Fig. 9.8 Weber’s test.
Tuning fork tests
A 512-Hz tuning fork can be used to help differentiate between
conductive and sensorineural hearing loss.
Weber’s test
Examination sequence (Video 19B)
• Strike the prongs of the tuning fork against a padded surface
to make it vibrate.
• Place the base of the vibrating tuning fork in the middle of the
patient’s forehead (Fig. 9.8).
• Ask the patient, ‘Where do you hear the sound?’
• Record which side Weber’s test lateralises to if not central.
In a patient with normal hearing, the sound would be expected
to be heard in the middle, or equally in both ears; however, up to
40% of people with normal hearing will lateralise on Weber’s test.
Therefore, Weber’s test should only be interpreted in patients
with hearing loss.
In conductive hearing loss, the sound is heard louder in the
affected ear. In unilateral sensorineural hearing loss, it is heard
louder in the unaffected ear. If there is symmetrical hearing loss, it
will be heard in the middle.
Rinne’s test
Examination sequence (Video 19C)
• Strike the prongs of the tuning fork against a padded surface
to make it vibrate.
• Place the vibrating tuning fork on the mastoid process
(Fig. 9.9A) and ask, ‘Can you hear this?’ Then ask the patient
to ‘tell me when you hear it stop’.
• Now place the tuning fork at the external auditory meatus and
ask, ‘Can you still hear it’ (see Fig. 9.9B). In a patient with
normal hearing, they will still hear it.
To maximise the sound for the patient, the "U" of the tuning
fork should face forward.
Alternative technique: loudness comparison
• Strike the prongs of the tuning fork against a padded surface
to make it vibrate.
• Place the vibrating tuning fork on the mastoid process for
about 2 seconds.
• Now place the still-vibrating tuning fork at the external audi-
tory meatus and ask, ‘Is it louder in front of your ear or
behind?’
With normal hearing, sound is heard louder or longer when the
tuning fork is at the external auditory meatus. That is, air conduction (AC) is better than bone conduction (BC), recorded as
AC>BC. This normal result is recorded as ‘Rinne-positive’.
In conductive hearing loss, bone conduction is better than air
conduction (BC>AC); thus, sound is heard louder when the
tuning fork is on the mastoid process (‘Rinne-negative’). This
finding is associated with a high likelihood that the patient has a
AB
Fig. 9.9 Rinne’s test. A Testing bone conduction. B Testing air conduction.
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conductive hearing loss of at least 20 dB. A false-negative
Rinne’s test may occur if there is profound hearing loss on one
side. This is due to sound being conducted through the bone of
the skull to the other ‘good’ ear. Weber’s test can detect a
hearing loss of just 5 dB; therefore, the tuning fork will lateralise
to the affected ear in conductive hearing loss before Rinne’s test
becomes abnormal (negative). In sensorineural hearing loss,
Rinne’s test will be positive, as air conduction is better than bone
conduction.
Tuning fork test findings are summarised in Box 9.5.
Testing vestibular function
Testing for nystagmus
Examination sequence
• Patients should be tested with spectacles or contact lenses
for best corrected vision.
9.5 Tuning fork tests
Weber’s test Rinne’s test
Bilateral normal hearing Central AC>BC, bilateral
Bilateral symmetrical
sensorineural loss
Unilateral or asymmetrical
sensorineural loss LEFT
Unilateral conductive loss LEFT Louder left BC>AC, left
Bilateral conductive loss
(worse on LEFT)
a
Patients with a severe sensorineural loss may have BC > AC due to
BC crossing to the o ther better-hearing cochlea that is not being
tested (false-negative Rinne’s test).
AC, Air conduction; BC, bone conduction.
Central AC>BC, bilateral
Louder right AC>BC, bilateral
AC>BC, right
Louder left BC>AC, bilateral
a
• With the patient seated, ask them to fixate on a stationary
target in a neutral gaze position and observe for spontaneous
nystagmus.
• Hold your finger an arm’s length away, level with the patient’s
eye, and ask the patient to focus on and follow the tip of your
finger. Slowly move your finger from side to side and up and
down and observe the eyes for any oscillations, avoiding
extremes of gaze where physiological nystagmus may occur.
This assesses for gaze nystagmus and smooth pursuit.
• If any oscillations are present, note:
• whether they are horizontal, vertical or rotatory
• which direction of gaze causes the most marked nystagmus
• in which direction the fast phase of jerk nystagmus occurs
Discriminating characteristics of nystagmus are detailed in
Box 9.4.
Dix–Hallpike positional test
Examination sequence (Video 19D)
• Ask the patient to sit upright, close to the end of the couch.
• Turn the patient’s head 45 degrees to one side (Fig. 9.10A).
• Rapidly lower the patient backward so that their head is now
30 degrees below the horizontal. Keep supporting the head
and ask the patient to keep their eyes open, even if they feel
dizzy (see Fig. 9.10B).
• Observe the eyes for nystagmus. If it is present, note latency
(time to onset), direction, duration and fatigue (decrease on
repeated manoeuvres).
• Repeat the test, turning the patient’s head to the other side
(see Fig. 9.10C).
Normal patients have no nystagmus or symptoms of vertigo. A
positive Dix–Hallpike manoeuvre is diagnostic for benign paroxysmal positional vertigo. There is a delay of 5–20 seconds before
the patient experiences vertigo and before rotatory jerk
nystagmus toward the lower ear (geotropic) occurs; this lasts for
9
A
Fig. 9.10 Dix–Hallpike position test. The examiner looks for nystagmus (usually accompanied by vertigo). Both nystagmus and vertigo typically decrease
(fatigue) on repeat testing. See text for details.
120
degrees
BC
120
degrees
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9.6 Investigations in ear disease
Investigation Indication/comment
Swab from external auditory
meatus
Magnetic resonance imaging Acoustic neuroma (see Fig. 9.11)
Audiometry
Impedance audiometry
(tympanometry)
Vestibular testing
Caloric tests
Posturography
Otorrhoea, such as in otitis externa or otitis media with a tympanic membrane perforation; microscopy and culture can
help guide treatment
Asymmetrical sensorineural hearing loss or unilateral tinnitus
Hearing loss
A single-frequency tone at different noise levels is presented to each ear in turn through headphones in a soundproof
booth. The intensity of sound is reduced in 10-decibel steps until patients can no longer hear it. The hearing threshold
is the quietest sound they can hear. Audiograms display air and bone conduction thresholds, and conductive and
sensorineural hearing loss can therefore be differentiated (see Fig. 9.12)
Conductive hearing loss (e.g., otitis media with effusion, ossicular discontinuity, otosclerosis)
Eustachian tube dysfunction
The compliance of the tympanic membrane is measured during changes in pressure in the ear canal; compliance
should be maximal at atmospheric pressure
Unilateral vestibular hypofunction
Water at 30
response is reduced in vestibular hypofunction
Reveals whether patients rely on vision or proprioception more than usual
Usually reserved for specialist balance clinics
C and then 44C is irrigated into the external ear canal. Electronystagmography records nystagmus. The
• Rapidly turn the patient’s head to one side in the horizontal
plane (roughly 15 degrees) and watch for any corrective
movement of the eyes. Repeat, turning the head towards the
other side. The eyes remain fixed on the examiner’s nose in a
normal test. When the head is turned towards the affected
side, the eyes move with the head, and there is then a
corrective saccade.
Fig. 9.11 Magnetic resonance image showing a right acoustic neu-
roma (arrow).
less than 30 seconds. The response fatigues on repeated testing
due to adaptation. Immediate nystagmus without adaptation,
and not necessarily with associated vertigo, can be caused by
central pathology.
Head impulse test (or head thrust test)
Examination sequence
• Sit opposite the patient and ask them to focus on a target
(usually your nose).
• Hold the patient’s head, placing a hand on each side
of it.
This is a test of the vestibulo-ocular reflex. The presence of a
corrective saccade is a positive test and indicates a deficiency in
the vestibulo-ocular reflex. It is useful to identify unilateral peripheral vestibular hypofunction. You must be careful when
performing this test in patients with neck problems because of
the rapid movements of the head.
Unterberger’s test
Examination sequence
• Ask the patient to march on the spot with their eyes closed
and their arms outstretched in front of them. The patient will
rotate to the side of the damaged labyrinth.
Fistula test
Examination sequence
• Compress the tragus repeatedly against the external auditory
meatus to occlude it.
Anatomy and physiology • 203
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Fig. 9.12 Hearing test (audiogram). A Normal-hearing right and left ears. B Right sensorineural loss. C Right conductive hearing loss. ( Right air
conduction,
Left air conduction, Bone conduction)
9
If imbalance or vertigo with nystagmus is induced, it suggests
an abnormal communication between the middle ear and
vestibular system (such as erosion due to cholesteatoma).
NOSE AND SINUSES
Anatomy and physiology
The external nose consists of two nasal bones that provide
support and stability to the nose. The nasal bones articulate with
each other and the bones of the face: the frontal bone, the
Investigations
Initial investigations in ear disease are summarised in Box 9.6
and Figs 9.11 and 9.12.
ethmoid bone and the maxilla. The nasal bones also attach to the
nasal septum and paired upper lateral cartilages of the nose.
There are two further paired cartilages, the lower lateral cartilages, which form the nasal tip. Internally the nasal septum,
which is bone posteriorly and cartilage anteriorly, separates the
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