TRIPASS XR تري باس

 

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