TRIPASS XR تري باس

 Viral swab Viral conjunctivitis

Blood tests

Erythrocyte sedimentation rate, C-reactive protein Vasculitis, including giant cell arteritis

Antinuclear antibody Systemic lupus erythematosus

Rheumatoid factor Scleritis

Fasting glucose Diabetic retinopathy

Anti-acetylcholinesterase receptor antibody Myasthenia gravis

Quantiferon Uveitis

Serum angiotensin-converting enzyme Uveitis

Human immunodeficiency virus serology Vasculitis, uveitis

Syphilis serology Unexplained pathology and uveitis/vasculitis

Thyroid function tests Thyroid eye disease

Radiology

Chest X-ray Sarcoidosis/tuberculosis

Orbital ultrasound Incomplete fundal view

Optical coherence tomography Macular disease, glaucoma

Fundus fluorescein angiography Diabetic retinopathy, retinal vein occlusion

Computed tomography brain and sinuses Orbital cellulitis, thyroid eye disease, intracranial tumours, orbital compressive disease

Magnetic resonance imaging brain and orbits Pituitary tumour, compressive lesion

Carotid Doppler ultrasound Carotid artery stenosis in ocular ischaemic syndrome

Invasive tests

Lumbar puncture Idiopathic intracranial hypertension, inflammatory orbital neuropathies

Temporal artery biopsy Giant cell arteritis

OSCE example 1: Gradual visual loss

Mrs Johnson, 55 years old, presents with a gradual reduction of vision over the last 6 months in both eyes. She says that she also has distortion in

her vision when she is looking at straight lines. In addition, she feels constantly thirsty and is passing urine frequently.

Please examine this patient’s eyes

• Introduce yourself and clean your hands.

• Perform a general inspection, looking for any signs of squint. Check the bedside for any clues that the patient wears glasses.

• Assess visual acuity using a Snellen chart at the appropriate distance.

• Examine the eyes, looking for any conjunctival injection, chemosis or swelling.

• Dim the room lights.

• Test the pupillary light reflexes.

• Ideally, dilate the pupils at this stage.

• Test the red reflex in each eye.

• Dial the fundoscope to +10 and examine the anterior portion of the eye, including the lens.

• Dial the fundoscope back to 0 and examine the fundus, looking at the disc and superior, nasal, inferior and temporal fundus.

• Finally, inspect the macula.

• Thank the patient and clean your hands.

Summarise your findings

Visual acuity is reduced to 6/18 in both eyes, and fundoscopy reveals multiple retinal haemorrhages and exudates, some close to the macula.

Suggest a diagnosis

The most likely diagnosis is diabetic maculopathy.

Suggest initial investigations

Urine dipstick, fasting blood glucose and blood pressure.

Advanced level comments

Diabetic macular oedema is the most common cause of reduced vision in diabetic patients. It may result in distortion of vision, making straight lines

appear bent.

Investigations • 169

8

OSCE example 2: Double vision

Mr Penrose, 75 years old, presents with double vision that has increased rapidly over the last week. He says not only that objects appear side by side

but also that the two images are separated vertically. He feels that his eyelid is drooping on his left side. He constantly has to lift his eyelid to see out

of his left eye.

Please examine the patient’s eye movements

• Introduce yourself and clean your hands.

• Perform a general inspection: look for ptosis and squint, and examine the bedside for any spectacles that may contain a prism.

• Inspect visual acuity for each eye.

• Dim the room lights.

• Test pupillary light reflexes.

• Test all eye movements for ophthalmoplegia.

• Examine the optic nerve using an ophthalmoscope.

• Examine cranial nerves I, V, VI, VII, VIII, IX, X, XI and XII.

• Thank the patient and clean your hands.

Summarise your findings

The patient has a partial ptosis on the left with a dilated pupil. Eye movements are diminished with impaired adduction and elevation of the eyeball.

Double vision is confirmed on testing of eye movements.

Suggest a diagnosis

The most likely diagnosis is left incomplete III nerve palsy (complete palsy would cause total ptosis with relief of double vision).

Suggested investigations

Fasting glucose and cholesterol, blood pressure, erythrocyte sedimentation rate, and a magnetic resonance angiogram to check for an underlying

cerebral artery aneurysm.

Advanced level comments

Palsies of the III nerve result in ptosis and diplopia. Microvascular damage to the III nerve usually spares the pupil. Compressive lesions such as

aneurysm cause a dilated pupil, which responds poorly or is completely unresponsive to light.

Integrated examination sequence for ophthalmology

• Introduce yourself and clean your hands.

• Explain what you will be doing.

• Observe the patient as they walk into the room, looking for:

• Facial asymmetry.

• Proptosis.

• Gait (may indicate a possible cerebrovascular accident).

• Check visual acuity in each eye for distance and near vision.

• Undertake an assessment of the visual fields:

• Look for homonymous hemianopia, bitemporal hemianopia or any other obvious visual field defect.

• Check the pupils:

• Assess direct and consensual reflex.

• Test for a relative afferent pupillary defect. Note that the pupils should be checked only after visual acuity and visual field assessment has been

undertaken, as the lights used to examine the pupils may dazzle the patient and interfere with accurate visual field and acuity assessment.

• Dilate both pupils using tropicamide 1% eye drops.

• Examine each eye using the direct ophthalmoscope:

• Assess the ocular surface.

• Look at the red reflex (opacity may indicate either a cataract or vitreous opacities such as debris or haemorrhage).

• Focus on the optic disc: look at colour, shape and cupping, as well as swelling.

• Examine the blood vessel arcades in each quadrant.

• Examine the macula.

• Ask patient to look up, down, right and left so that you can examine the peripheral retina.

• Examine extraocular movements if the patient presents with diplopia or if it is clinically indicated.

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9

The ear, nose and throat

Iain Hathorn

Ear 172

Anatomy and physiology 172

External ear 172

Middle ear 172

Inner ear 173

The history 173

Common presenting symptoms 173

Past medical history 175

Drug history 175

Family history 175

Social history 175

The physical examination 175

Testing hearing 177

Testing vestibular function 178

Investigations 179

Nose and sinuses 179

Anatomy and physiology 179

The history 180

Common presenting symptoms 180

Past medical history 182

Drug history 182

Family history 182

Social history 182

The physical examination 182

Investigations 183

Mouth, throat and neck 184

Anatomy and physiology 184

Mouth 184

Throat 184

Teeth 184

Neck 184

The history 184

Common presenting symptoms 184

Past medical history 187

Drug history 187

Social and family history 187

The physical examination 187

Mouth and throat 187

Neck 189

Investigations 190

OSCE example 1: Hoarseness 190

OSCE example 2: Neck lump 191

Integrated examination sequence for ear, nose and throat disease 191

172 • The ear, nose and throat

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 focused on to the smaller oval window on which the

stapes sits (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

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

Semicircular canal

Vestibular nerve

Cochlear nerve

Cochlea

Eustachian tube

Auditory ossicles

Malleus Incus Stapes

(on oval window)

Tympanic cavity

Tympanic membrane

External auditory

meatus

Pinna

Earlobe

A

Triangular fossa

Helix

External

auditory meatus

Tragus

Earlobe

Concha

Antihelix

B

Fig. 9.1 The ear. A The pinna. B Cross-section of the outer, middle and inner ear.

A B

Fig. 9.2 Structures seen on otoscopic examination of the right ear. A Main structures. B Normal tympanic membrane.

EAR

The history • 173

9

of 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.

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. This results 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.

The history

Common presenting symptoms

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

• precipitating factors: trauma, URTI, noise exposure,

antibiotics

• impact of the hearing loss on the patient’s function.

Hearing loss can be due to disruption in the conduction

mechanism or may have sensorineural causes, such as failure

9.1 Causes and features of earache (otalgia)

Cause Clinical features

Otological

Acute otitis externa Pain worse on touching outer ear, tragus

Swelling of ear canal

Purulent discharge and itching

Acute otitis media Severe pain, red, bulging tympanic

membrane, purulent discharge if tympanic

membrane perforation present

Perichondritis Erythematous, swollen pinna

Trauma Pinna haematoma, pinna laceration,

haemotympanum (blood behind tympanic

membrane); cerebrospinal fluid leak or

facial nerve palsy may be present

Herpes zoster (Ramsay

Hunt syndrome)

Vesicles in ear canal, facial nerve palsy

may be present; vertigo is common

Malignancy Mass in ear canal or on pinna

Non-otological

Tonsillitis

Peritonsillar abscess

Sore throat, tonsil inflammation

Trismus, soft-palate swelling in peritonsillar

abscess

Temporomandibular

joint dysfunction

Tenderness, clicking of joint on jaw opening

Dental disease Toothache, e.g. due to dental abscess

Cervical spine disease Neck pain/tenderness

Cancer of the pharynx

or larynx

Associated sore throat, hoarseness,

dysphagia, weight loss, neck lump

9.2 Causes of hearing loss

Conductivea

• Wax

• Otitis externa

• Middle ear effusion

• Trauma to the tympanic

membrane/ossicles

• Otosclerosis

• Chronic middle ear infection

• Tumours of the middle ear

Sensorineuralb

• Genetic, e.g. Alport’s

syndrome

• Prenatal infection, e.g. rubella

• Birth injury

• Infection:

• Meningitis

• Measles

• Mumps

• Trauma

• Ménière’s disease

• Degenerative (presbyacusis)

• Occupation- or other

noise-induced

• Acoustic neuroma

• Idiopathic

a

Disruption to the mechanical transfer of sound in the outer ear, eardrum or

ossicles. b

Cochlear or central damage.

174 • The ear, nose and throat

• associated headaches, nausea or aura (migraine)

• previous significant head injury; previous URTI.

The most common causes of vertigo include benign paroxysmal

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 or paroxysmal, or evoked by manœuvres

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.

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)

• 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).

• 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

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