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 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).

• 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 noise is heard in the

middle, or equally in both ears.

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. Fig. 9.8 Weber’s test.

A B

Fig. 9.9 Rinne’s test. A Testing bone conduction. B Testing air conduction.

178 • The ear, nose and throat

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

• 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 backwards 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 (Fig. 9.10B).

• Observe the eyes for nystagmus. If it is present, note

latency (time to onset), direction, duration and fatigue

(decrease on repeated manœuvres).

Repeat the test, turning the patient’s head to the other

side (Fig. 9.10C).

Normal patients have no nystagmus or symptoms of vertigo.

A positive Dix–Hallpike manœuvre 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 towards the lower ear (geotropic) occurs; this lasts for

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).

test is more sensitive and 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.

• 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

9.5 Tuning fork tests

Weber test Rinne test

Bilateral normal hearing Central AC>BC, bilateral

Bilateral symmetrical

sensorineural loss

Central AC>BC, bilateral

Unilateral or asymmetrical

sensorineural loss LEFT

Louder right AC>BC, bilaterala

Unilateral conductive loss LEFT Louder left BC>AC, left

AC>BC, right

Bilateral conductive loss

(worse on LEFT)

Louder left BC>AC, bilateral

a

Patients with a severe sensorineural loss may have BC>AC due to BC crossing

to the other better-hearing cochlea that is not being tested (false-negative

Rinne test).

AC, air conduction; BC, bone conduction.

A

120

degrees

B C

120

degrees

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.

Anatomy and physiology • 179

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).

Investigations

Initial investigations in ear disease are summarised in Box 9.6

and Figs 9.11–9.12.

• Hold the patient’s head, placing a hand on each side of it.

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.

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. 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.

9.6 Investigations in ear disease

Investigation Indication/comment

Swab from external auditory meatus Otorrhoea, such as in otitis externa or otitis media with a tympanic membrane perforation; microscopy and

culture can help guide treatment

Magnetic resonance imaging Acoustic neuroma (Fig. 9.11)

Asymmetrical sensorineural hearing loss or unilateral tinnitus

Audiometry 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 (Fig. 9.12)

Impedance audiometry (tympanometry) 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

Vestibular testing: Unilateral vestibular hypofunction

Caloric tests Water at 30°C and then 44°C is irrigated into the external ear canal. Electronystagmography records

nystagmus. The response is reduced in vestibular hypofunction

Posturography Reveals whether patients rely on vision or proprioception more than usual

Usually reserved for specialist balance clinics

Fig. 9.11 Magnetic resonance image showing a right acoustic

neuroma (arrow).

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 with bones of the face: the frontal bone, the ethmoid

bone and the maxilla. The nasal bones also attach to the nasal

septum and the 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 nose into two

nasal cavities that join posteriorly in the postnasal space. There

are three turbinates on each side of the nose, superior, middle and

inferior, which warm and moisten nasal airflow (Figs 9.13 and 9.14A).

One important function of the nose is olfaction. The olfactory

receptors are situated high in the nose in the olfactory cleft.

Olfactory fibres from the nasal mucosa pass through the cribriform

plate to the olfactory bulb in the anterior cranial fossa.

180 • The ear, nose and throat

trauma. Bilateral obstruction can be due to rhinitis (allergic or

non-allergic), or chronic rhinosinusitis with or without polyps.

Nasal discharge

Ask about:

unilateral or bilateral discharge (rhinorrhoea)

purulent or clear nature

anterior discharge or postnasal drip.

Clear, bilateral watery discharge suggests allergic or non-allergic

rhinitis. Purulent discharge can point to acute bacterial rhinosinusitis

or chronic rhinosinusitis. A unilateral, purulent discharge in a child

raises the possibility of a foreign body in the nose. Following a

head injury, unilateral clear rhinorrhoea suggests a possible CSF

leak secondary to an anterior skull-base fracture.

Epistaxis (bleeding from inside the nose)

Ask about:

unilateral or bilateral bleeding

frequency and duration of episodes

The paranasal sinuses are air-filled spaces in the skull. There

are paired frontal, sphenoid, maxillary and anterior and posterior

ethmoid sinuses. The anterior nasal sinuses (frontal, maxillary

and anterior ethmoid) drain into the middle meatus (between

the middle turbinate and lateral wall of the nose). The posterior

ethmoid and sphenoid sinuses drain into the sphenoethmoidal

recess (between the superior turbinate and nasal septum).

The history

Common presenting symptoms

Nasal obstruction

Ask about:

unilateral or bilateral obstruction

associated symptoms (bleeding, swelling, pain).

Unilateral nasal obstruction may be caused by anatomical

blockage, such as a deviated septum possibly secondary to

A Frequency in hertz (Hz) Hearing level in decibels (dB)

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Frequency in hertz (Hz)

Hearing level in decibels (dB)

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B Frequency in hertz (Hz) Hearing level in decibels (dB)

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C Frequency in hertz (Hz) Hearing level in decibels (dB)

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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)

The history • 181

9

If bleeding is unilateral and associated with nasal obstruction

and pain, the possibility of sinonasal malignancy should be

considered. In adolescent males with unilateral nasal obstruction

and epistaxis, the rare diagnosis of juvenile angiofibroma should

be excluded on nasendoscopy by an ear, nose and throat

specialist.

Sneezing

Ask about:

associated itchy, red eyes

whether symptoms occur all year round, only during

certain seasons, or during contact with allergens.

Sneezing is a protective sudden expulsive effort triggered by

local irritants in the nose and is most commonly due to allergy

or viral URTIs.

Disturbance of smell

Ask about:

complete loss of smell (anosmia)

reduced sense of smell (hyposmia)

unpleasant smells (cacosmia)

associated nasal symptoms such as obstruction

and rhinorrhoea, which may suggest rhinitis or nasal

polyps

recent head injury

recent URTI.

A sudden onset of anosmia can occur following a significant

head injury or viral URTI due to damage to the olfactory

epithelium. Inflammation and swelling in the nasal mucosa as

a result of rhinitis, chronic rhinosinusitis or nasal polyps usually

cause hyposmia. Cacosmia is usually caused by infection in the

nose or sinuses, or occasionally by a foreign body in the nose.

Phantosmia describes olfactory hallucinations, which may occur

in temporal lobe epilepsy.

Nasal and facial pain

Nasal pain is rare, except following trauma. Facial pain can

be caused by a number of problems but is often incorrectly

attributed to sinusitis. The key to identifying the cause of facial

pain is an accurate history.

provoking factors such as trauma, sneezing, or blowing or

picking nose

bleeding from the front or back of the nose.

The nasal septum has a very rich blood supply, particularly in

Little’s area (anterior septum), which is a common site for bleeding.

Tip

Tip

Ala nasi Ala nasi

Anterior nares Anterior nares

Vestibule

Columella

Pituitary

fossa

Columella

Cranial cavity

Bony portion of

nasal septum

Sphenoid sinus

Septal cartilage

Little’s area

Hard palate

Hard palate

Nasopharynx

Cranial cavity

Frontal sinus

Frontal sinus

Superior turbinate

Inferior turbinate

Middle turbinate

Vestibule

Sphenoid sinus

Bridge

Inferior view of nose

Nasal septum

Lateral wall of nose

External nose

Fig. 9.13 The nose and paranasal sinuses.

$ % &

Fig. 9.14 Nasal abnormalities. A Turbinate hypertrophy. B Nasal septum perforation post-surgery. C Nasal polyps.

182 • The ear, nose and throat

Drug history

Ask about:

use of anticoagulants, including warfarin, apixaban or

rivaroxaban

use of antiplatelet drugs (aspirin, clopidogrel).

Intranasal cocaine use can cause septal perforation, epistaxis,

crusting and whistling.

Family history

A family history of atopy is relevant in rhinitis. In patients with

epistaxis it is important to establish a family history of hereditary

haemorrhagic telangiectasia or inherited bleeding disorders.

Social history

Occupation is relevant because exposure to inhaled allergens,

occupational dusts and chemicals may exacerbate rhinitis.

Exposure to hardwood dust is associated with an increased

risk of sinonasal cancers. Atopic patients should be asked

about pets.

Heavy alcohol intake, leading to liver disease, can affect

coagulation and is relevant for epistaxis. Smoking impedes

mucociliary clearance and can contribute to nasal problems.

The physical examination

Examination sequence

• Assess the external appearance of the nose, noting

swelling, bruising, skin changes and deformity.

• Stand above the seated patient to assess any external

deviation.

• Ask the patient to look straight ahead. Elevate the tip of

their nose using your non-dominant thumb to align the

nostrils with the rest of the nasal cavity.

• Look into each nostril and assess the anterior nasal

septum (Fig. 9.16); note the mucosal covering, visible

vessels in Little’s area, crusting, ulceration and septal

perforation. In trauma, a septal haematoma should be

excluded.

Using an otoscope with a large speculum in an adult,

assess the inferior turbinates. Note any hypertrophy and

swelling of the turbinate mucosa.

• You may see large polyps on anterior rhinoscopy. To

distinguish between hypertrophied inferior turbinates and

nasal polyps, you can lightly touch the swelling with a

cotton bud (polyps lack sensation).

• Palpate the nasal bones to assess for bony or

cartilaginous deformity.

• In trauma, palpate the infraorbital ridges to exclude a step

deformity and also to check infraorbital sensation. Eye

movements should be assessed to rule out restriction of

movement related to ‘orbital blowout’.

• Place a metal spatula under the nostrils and look for

condensation marks to assess airway patency.

• Palpate for cervical lymphadenopathy (p. 32).

• Note that rigid nasendoscopy and tests of olfaction are

confined to specialist clinics.

Ask about:

quality of pain: for example, throbbing, aching, sharp,

stabbing, tight-band

location of pain: unilateral or bilateral

duration and frequency of pain

associated nasal symptoms

associated nausea, photophobia or aura (migraine)

relieving and exacerbating factors.

The differential diagnosis of facial pain includes temporomandibular joint dysfunction, migraine, dental disease, chronic

rhinosinusitis, trigeminal neuralgia (severe, sharp pain in a

trigeminal distribution), tension headache (band-like, tight pain)

and cluster headaches (unilateral nasal discharge, eye watering).

Nasal deformity

The most common cause of nasal deformity is trauma, resulting

in swelling, bruising and deviation of the nose. The swelling

following trauma will settle over a couple of weeks but residual

deviation may remain if the nasal bones were fractured and

displaced. It is important to establish the impact of the nasal

injury on function (nasal breathing, sense of smell) and cosmetic

appearance.

Nasal septal destruction or perforation can result in ‘saddle

deformity’ of the nasal bridge. Causes include granulomatosis

with polyangiitis, trauma, cocaine abuse, congenital syphilis and

iatrogenic factors (septal surgery, Fig. 9.14B).

The nose can appear widened in acromegaly or with advanced

nasal polyposis (Fig. 9.14C). Rhinophyma can also result from

chronic acne rosacea of the nasal skin (Fig. 9.15).

Past medical history

Ask about:

history of atopy

asthma (around one-third of patients with allergic rhinitis

have asthma)

prior nasal trauma or surgery

history of bronchial infection (cystic fibrosis or ciliary

disorders may affect the nose and lower airways).

For patients with epistaxis it is important to identify any history

of bleeding diathesis or hypertension.

Fig. 9.15 Rhinophyma as a complication of rosacea.

Investigations • 183

9

A B

Fig. 9.16 Nasal examination. A Elevation of the tip of the nose to give a clear view of the anterior nares. B Anterior rhinoscopy using an otoscope

with a large speculum.

9.7 Investigations in nasal disease

Investigation Indication/comment

Plain X-ray Not indicated for nasal bone fracture

Only required if associated facial fracture is suspected

Nasal endoscopy Inflammatory sinus disease, malignancy

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