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)

associated ‘fullness in the ear’ during the episode

(Ménière’s disease)

associated focal neurology (cerebrovascular event)

fluctuating hearing loss or tinnitus

9.3 Diagnosing vertigo

Benign paroxysmal

positional vertigo Vestibular neuritis Ménière’s disease

Central vertigo (migraine, MS,

brainstem ischaemia, drugs)

Duration Seconds Days Hours Hours – migraine

Days and weeks – MS

Long-term – cerebrovascular accident

Hearing loss – – ++ –

Tinnitus – – ++ –

Aural fullness – – ++ –

Episodic Yes Rarely Recurrent vertigo; persistent

tinnitus and progressive

sensorineural deafness

Migraine – recurs

Central nervous system damage – usually

some recovery but often persistent

Triggers Lying on affected ear Possible presence of upper

respiratory symptoms

None Drugs (e.g. aminoglycosides)

Cardiovascular disease

MS, multiple sclerosis.

9.4 Characteristics of nystagmus

Nystagmus type Clinical pathology Characteristics

Fast phase Maximal on looking

Jerk:

Peripheral Semicircular canal, vestibular nerve Unidirectional

Not suppressed by optic fixation

Patient too dizzy to walk

Dix–Hallpike fatigues on repetition

Away from affected side

Central Brainstem, cerebellum Bidirectional (changes with direction of gaze)

Suppressed by optic fixation

Patient can walk (even with nystagmus)

Dix–Hallpike persists

To either side

Dysconjugate (ataxic) Interconnections of III, IV and VI nerves

(medial longitudinal bundle)

Typically affects the abducting eye To either side

Pendular Eyes, e.g. congenital blindness No fast phase Straight ahead

The physical examination • 175

9

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 (Fig. 9.3).

• Inspect the external auditory canal through the speculum,

noting wax, foreign bodies or discharge. You should

identify the tympanic membrane and the light reflex

anteroinferiorly (see Fig. 9.2).

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 (Fig.

9.4B) and subsequent ‘cauliflower ear’ due to cartilage necrosis

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 (Fig. 9.4C).

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 significant 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.

The physical examination

Examination sequence

Inspection

• Pinna skin, shape, size, position, scars from previous

surgery/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. Fig. 9.3 Examination of the ear using an otoscope.

$ % &

Fig. 9.4 The pinna. A Microtia. B Haematoma. C Squamous cancer (arrow).

176 • The ear, nose and throat

an offensive discharge and erode the bony ossicles, resulting in

a conductive hearing loss (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 (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 (Fig. 9.7C), and may bulge and eventually

perforate.

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 (Fig. 9.5B).

Scarring on the tympanic membrane (tympanosclerosis)

can be caused by previous grommet insertion or infections.

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 (Fig. 9.6B). A retraction of the

pars flaccida can contain a cholesteatoma, which may cause

$ % &

Fig. 9.5 Auditory canal abnormalities. A Otitis externa. B Exostosis of the external auditory meatus. C Cholesteatoma.

$ % &

Fig. 9.6 Tympanic membrane abnormalities. A Tympanic membrane perforation (arrow). B Retraction pocket of the pars tensa (arrow). C Grommet

in situ.

$ % &

Fig. 9.7 Otitis media. A With effusion. B Fluid level behind the tympanic membrane (arrow). C Acute otitis media.

The physical examination • 177

9

Rinne’s test

Examination sequence

• Strike the prongs of the tuning fork against a hard surface

to make it vibrate.

• Place the vibrating tuning fork on the mastoid process

(Fig. 9.9A).

• Now place the still-vibrating base at the external auditory

meatus and ask, ‘Is it louder in front of your ear or

behind?’ (Fig. 9.9B).

With normal hearing, the sound is heard louder 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 the sound is heard louder when

the tuning fork is on the mastoid process (‘Rinne-negative’).

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

Testing hearing

Whispered voice test

Examination sequence

• 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 multisyllable

numbers and words. Start with a normal speaking voice to

confirm that the patient understands the test. Lower your

voice to a clear whisper.

Repeat the test but this time at arm’s length from the

patient’s ear. People with normal hearing can repeat

words whispered at 60 cm.

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

• Strike the prongs of the tuning fork against a hard surface

to make it vibrate.

• Place the base of the vibrating tuning fork in the middle of

the patient’s forehead (Fig. 9.8).

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