When patients present with a change in vision, ask:

Did the change in vision start suddenly or gradually?

How is the vision affected (loss of vision, cloudy vision,

floaters, distortion)?

Is it one or both eyes that are affected?

Is the whole or only part of the visual field affected?

If partial, which part of the visual field is affected?

Pain

Ask:

when the pain began

whether anything started the pain

about the character of the pain

how severe the pain is

if the pain is exacerbated or relieved by any factors

whether the pain is associated with any other symptoms.

The cornea is one of the most highly innervated regions of the

body. When the corneal nerves are activated, this leads to pain,

the sensation of foreign body, reflex watering and photophobia.

There are, however, many other causes of a painful eye. Box

8.3 summarises the history and examination findings associated

with these.

156 • The visual system

8.1 Common causes of an acute change in vision

Cause Clinical features Cause Clinical features

Unilateral

Giant cell

arteritis

• Painless loss of vision

• Age >50 years

• Weight loss

• Loss of appetite, fatigue

• Jaw or tongue claudication

• Temporal headache

• Pale or swollen optic disc

• RAPD

Vitreous

haemorrhage

• Painless loss of vision

• Risk in proliferative diabetic retinopathy

• History of flashing lights or floaters may precede

haemorrhage in posterior vitreous detachment

• Poor fundus view on examination

• Reduction or loss of the red reflex

• Usually no RAPD if retina is intact

Central

retinal vein

occlusion

• Acute, painless loss of vision

• May have RAPD if severe

• Greater risk if hypertensive

• Haemorrhages, exudates and tortuous retinal veins

(Fig. 8.7A)

Wet

age-related

macular

degeneration

• Sudden painless loss of central vision

• Age >55 years

• Increased risk in smokers

• Haemorrhage at the macula (Fig. 8.7E)

Retinal

detachment

• Painless loss of vision

• Association with flashing lights or floaters

• History of a curtain coming across vision

• Myopic patients at greater risk

• RAPD if macula is involved

• Pale raised retina usually with a retinal tear (Fig. 8.7B)

Anterior

ischaemic optic

neuropathy

• Painless loss of upper or lower visual field

• Increased risk in vasculopaths

• Examination may reveal optic disc swelling

Central

retinal arterial

occlusion

• Acute, painless loss of vision

• Carotid bruit may be heard

• RAPD

• Increased risk in vasculopaths

• Examination: pale retina with a cherry red spot at the

fovea (Fig. 8.7C)

Optic neuritis/

retrobulbar

neuritis

• Visual reduction over hours

• Usually aged 20–50

• Pain exacerbated by eye movement

• RAPD

• Reduced colour sensitivity

• Swollen optic disc in optic neuritis (Fig. 8.7F) or

normal appearances in retrobulbar neuritis

Corneal

disease

• Usual association with pain

• Foreign body sensation

• Corneal opacity may be visible (e.g. Fig. 8.7D)

Amaurosis

fugax

• Painless loss of vision for minutes

• History of cardiovascular disease

• May have associated atrial fibrillation or carotid bruit

• Normal ocular examination

Bilateral

Giant cell

arteritis

• Painless loss of vision

• Age >50 years

• Weight loss

• Loss of appetite, Fatigue

• Jaw or tongue, claudication

• Temporal headache

• Pale or swollen optic disc

Cerebral infarct • May have associated headache and/or neurological

signs

• Usually specific field defects dependent on how the

visual pathway is affected (Fig. 8.5)

• Normal fundus examination

• If post chiasmal visual pathway affected, bilateral

visual field abnormalities

Raised

intracranial

pressure

• Headache

• Often asymmetric

• Pulsatile tinnitus

• Swollen optic discs

Migraine • Gradually evolving usually bilateral visual loss

• Vision loss is usually preceded by visual aura

• Normal ocular examination

• Ocular examination: normal

• Vision usually returns to normal after hours

RAPD, relative afferent pupillary defect (p. 162).

8.2 Common causes of a gradual loss of vision

Cause Clinical features

Refractive error • No associated symptoms

• Normal ocular examination

• Vision can be improved by pinhole (Fig. 8.4D)

Glaucoma • Usually bilateral but asymmetric loss of visual field

• Cupped optic discs on examination

Cataract • Gradual clouding of vision

• May be associated with glare

• Usually seen in the elderly

• Examination: clouding of the pupil and altered red

reflex (see Fig. 8.8A and B)

Cause Clinical features

Diabetic

maculopathy

• History of diabetes

• Central vision reduced or distorted

• Haemorrhages and exudates at the macula on

examination (Fig. 8.17A)

Compressive

optic neuropathy

• Gradual unilateral loss of vision

• Pale optic disc on examination (Fig. 8.8D)

Retinitis

pigmentosa

• Gradual bilateral symmetric loss of peripheral

visual field

• Nyctalopia (poor vision in dim light)

• Family history

• Examination: bone spicule fundus, attenuated

blood vessels and waxy optic disc (Fig. 8.8E)

The history • 157

8

D E F

C A B

Fig. 8.7 Common causes of an acute change in vision. A Central retinal vein occlusion. B Retinal detachment. Elevation of the retina around

the ‘attached’ optic disc; the retina may even be visible on viewing the red reflex. C Central retinal arterial occlusion. D Herpes simplex virus keratitis.

E Wet age-related macular degeneration. F Swollen optic nerve head in acute optic neuritis.

D E

C

A B

Fig. 8.8 Common causes of a gradual loss of vision. A Cataract. B Altered red reflex in the presence of cataract. C Dry age-related macular

degeneration. D Compressive optic neuropathy. Optic nerve sheath meningioma causing optic disc pallor and increased disc cupping with sparing of the

outer optic nerve rim. E Retinitis pigmentosa, with a triad of optic atrophy, attenuated retinal vessels and pigmentary changes. The latter typically start

peripherally in association with a ring scotoma and symptoms of night blindness.

8.2 Common causes of a gradual loss of vision – cont’d

Cause Clinical features

Dry age-related

macular

degeneration

• Gradual loss of central vision

• Usually bilateral

• Examination: drusen, atrophy and pigmentation at

the macula (Fig. 8.8C)

158 • The visual system

8.3 Causes of a painful eye

Cause Clinical features

Blocked gland

on lid

Pain on lid

Tenderness to touch

Ocular examination: redness and swelling of lid

Corneal foreign

body

Foreign body sensation

Watery eye

Photophobia

Ocular examination: foreign body visible or found

under the eyelid

Corneal

infection

Foreign body sensation

Photophobia

Red eye

Ulcer on cornea, which can be highlighted with

fluorescein staining (see Fig. 8.7D)

Ocular examination: white infiltrate may be visible

Scleritis Severe pain that keeps the patient awake at night

Soreness of the eye to touch

Association with recent infection, surgery or

rheumatic disease

Ocular examination: scleral injection

Angle-closure

glaucoma

Constant pain around the eye

Acute reduction in vision

Possibly, haloes seen around lights

Association with nausea and vomiting

Ocular examination: fixed mid-dilated pupil, hazy

cornea and usually a cataract

RAPD, relative afferent pupillary defect (p. 162).

Cause Clinical features

Conjunctivitis Increased clear or purulent discharge

Ocular examination: red eye

Vision is usually unaffected

Uveitis Floaters

Blurry vision

Photophobia

Ocular examination: ciliary flush

Optic neuritis Reduction in vision

Reduction in colour sensitivity

Constant pain worsened by eye movement

Ocular examination: swollen disc in optic neuritis

(see Fig. 8.7F), normal disc in retrobulbar neuritis

Orbital cellulitis Constant ache around the eyes

Reduced vision

Double vision

Association with a recent viral infection

Ocular examination: conjunctival chemosis and

injection, restricted eye movements; in severe cases,

visual reduction with RAPD

Thyroid eye

disease

Symptoms of hyperthyroidism (p. 197)

Sore, gritty eyes

Double vision

Ocular examination: lid retraction, proptosis,

restricted eye movements and conjunctival injection,

conjunctival chemosis (see Fig. 10.4)

8.4 Common causes of a red eye

Causes Clinical features

Allergic

conjunctivitis

Itchy eyes

Clear discharge

Possibly, more frequent occurrence at certain times

of year

Viral conjunctivitis Watery discharge

Possible itch

Swollen conjunctiva

Usually bilateral

Ocular examination: gland swelling and follicles

under the lid

Bacterial

conjunctivitis

Purulent discharge

Pain

Trauma History of trauma

Ocular examination: may reveal subconjunctival

haemorrhage or injection

Acute angleclosure glaucoma

Acute-onset reduction in vision

Pain

Blurring of vision

Haloes seen around lights

Nausea

Ocular examination: fixed, mid-dilated pupil with a

hazy cornea

Acute anterior

uveitis

Gradual onset of pain

Photophobia

Floaters

Ocular examination: ciliary flush

Causes Clinical features

Episcleritis Focal or diffuse injection

Possible association with a nodule

No pain

Vision not affected

Scleritis Focal or diffuse injection

Vision may be affected

Association with recent infection, surgery or

rheumatic disease

Severe pain that keeps the patient awake at night

Pain to touch

Dry eyes Gritty or burning sensation

Watery eyes

Ocular examination: corneal fluorescein staining

Subconjunctival

haemorrhage

No pain

Vision unaffected

Ocular examination: mildly raised conjunctiva with a

bleed

Corneal ulcer/

abrasion

Vision usually reduced

Foreign body sensation

Photophobia

Watering

Ocular examination: ulcer seen on fluorescein

staining (see Fig. 8.7D)

May be associated with a white corneal infiltrate

The history • 159

8

RAPD, relative afferent pupillary defect (p. 162).

8.4 Common causes of a red eye – cont’d

Causes Clinical features

Orbital cellulitis Usual occurrence in young children

Recent history of intercurrent viral illness

Vision may be affected

Possible double vision

Ocular examination: reduced vision and colour

vision, proptosis, eye movement restriction; in

severe cases, RAPD

Causes Clinical features

Thyroid eye

disease

Chronic red eyes

Sore, gritty sensation

Foreign body sensation

Double vision

Ocular examination: lid retraction, proptosis,

conjunctival injection and chemosis (see Fig. 10.4)

8.5 Causes of double vision

Monocular

• High astigmatism

• Corneal opacity

• Abnormal lens

• Iris defect

Binocular

• Myasthenia gravis (p. 125)

• VI nerve palsy (Fig. 8.9)

• IV nerve palsy

• III nerve palsy (Fig. 8.10)

• Internuclear ophthalmoplegia

• Thyroid eye disease (see

Fig. 10.4)

• Complex or combined palsy

• Severe orbital cellulitis or

orbital inflammation

A

B

Fig. 8.10 Third nerve palsy. A Complete ptosis in right III nerve

palsy. B The same patient looking down and to the left. The right eye

is unable to adduct or depress due to a complete right III nerve palsy. It

remains in slight abduction due to the unopposed action of the right

lateral rectus muscle and an intact VI nerve. From Forbes CD, Jackson

WF. Color Atlas of Clinical Medicine. 3rd edn. Edinburgh: Mosby; 2003.

Fig. 8.9 Sixth nerve palsy causing weakness of the lateral rectus

muscle. The patient is attempting to look to the left.

Past ocular history

Ask the patient whether they have any known ophthalmic

conditions. Enquire specifically about amblyopia, which is a

reduction in vision in one eye from childhood, as this may limit

best-corrected visual acuity. Check whether the patient normally

wears glasses or contact lenses, and the last time they had their

eyes checked for refractive correction. Ask about any previous

eye operations that may also affect vision.

Past medical history

Focus on systemic diseases that can affect the eyes directly or

as a side effect of treatment, in particular:

a history of diabetes or hypertension, especially in the

context of visual loss or double vision

thyroid disease in the context of red, swollen eyes and

double vision

asthma, chronic obstructive pulmonary disease (COPD) or

peripheral vascular disease if starting glaucoma medication.

Drug and allergy history

The eyes may be affected by medication given for other conditions

(such as glaucoma exacerbated by conjunctival absorption of

nebulised anticholinergic drugs in COPD). Medication given for

the eyes (such as beta-blocker eye drops) can aggravate other

conditions like asthma.

Ask about a history of hay fever and allergies if the patient

has itchy eyes.

Family history

Several eye diseases have an inherited predisposition. Ask

specifically about a history of glaucoma in first-order relatives.

Genetic diseases affecting the eyes include retinitis pigmentosa

(see Fig. 8.8E). Patients with thyroid eye disease may have a

positive family history of autoimmune disease.

Social history

Visual impairment has a wide range of effects on daily life.

Ask about:

Daily activities requiring good vision: reading, television,

sport, hobbies and so on.

Driving.

Occupation: certain professions, including drivers of heavy

goods vehicles and pilots, require specific visual acuity criteria.

Smoking and alcohol use: this may affect vascular and

optic nerve function within the eye.

160 • The visual system

8.6 Common causes of increased discharge from the eyes

Causes Clinical features

Bacterial

conjunctivitis

Red eye

Yellow or green sticky discharge

Vision usually unaffected

Viral

conjunctivitis

Red eye

Clear, watery discharge

Possible itchy eye

Vision usually unaffected

Ocular examination: conjunctival chemosis and injection

Blocked

tear duct

White eye

Clear, colourless tearing

Possible occluded punctum

Possible malposition of the lid

Trichiasis/

foreign body

Foreign body sensation

Clear discharge

Possible positive fluorescein staining

Allergic

conjunctivitis

Possible red eyes

Possible itchy eyes

Clear discharge

Possible history of hay fever or atopy, or recent start of

eye medication

Blepharitis Mild injection of lids

Deposits on lashes

Poor tear

film/dry

eyes

Constant tearing

Watering increased in the wind

Improvement with tear supplements

Ocular examination: early break-up time (<3 seconds)

with fluorescein staining of tear film

8.7 Common causes of periorbital swelling

Causes

Category Unilateral Bilateral

Infective Orbital cellulitis

Inflammatory Granulomatous polyangiitis

Idiopathic orbital

inflammatory disease

Vasculitis

Neoplastic Orbital tumours

Lymphoma

Metastases

Systemic Thyroid eye disease

(asymmetric)

Thyroid eye disease

Vascular Caroticocavernous fistula

Orbital varices

Pseudoproptosis Ptosis Severe viral

conjunctivitis

Myopia

Lid retraction

The physical examination

General examination

Carefully and systematically examine:

posture and gait

head position

facial asymmetry and dysmorphic features

eyelid position and periocular skin

position and symmetry of gaze (any squint/strabismus?).

Visual acuity

Assessment of visual acuity is mandatory in all ophthalmic patients.

Each eye must be tested separately. The most commonly used

method of testing distance visual acuity is using a Snellen chart,

which displays a random selection of letters at diminishing font

size in successive lines. Ask patients to wear their distance

spectacles if they usually require them. Near/reading spectacles

should be worn only when testing reading vision.

Examination sequence

• Use a backlit Snellen chart positioned at 6 metres and dim

the room lighting.

• Cover one eye and ask the patient to read the chart from

the top down until they cannot read any further. Repeat

for the other eye.

If the patient cannot see the largest font, reduce

the test distance to 3 metres, then to 1 metre if

necessary.

If they still cannot see the largest font, document

instead whether they can count fingers, see hand

movement or just perceive the difference between light

and dark.

On the Snellen chart, lines of decreasing font size are

numbered according to the distance in metres that a

person with normal vision could read them. Express

visual acuity as the distance at which text is read

(usually 6 metres) over the number of the smallest font

line read correctly on the chart. For example, 6/60

means that the patient sees at 6 metres the font size

that is seen at 60 metres by a person with normal

vision.

If the patient cannot read down to line 6 (6/6), place a

pinhole directly in front of the eye (with the patient keeping

their usual spectacles on, if they wear them) to correct any

residual refractive error (see Fig. 8.4D).

If the visual acuity is not improved with a pinhole, this

indicates the presence of eye disease not related to the

refractive apparatus alone, such as retinal or optic nerve

pathology.

Note that 6/6 is regarded as normal vision; in the UK,

6/12 or better with both eyes is the requirement for

driving.

• Assess near vision with a similar test using text of

reducing font size held at a comfortable reading

distance. It is important to consider the need for

reading spectacles in patients over the age of 40 years

because of presbyopia (age-related deterioration in

near vision).

The physical examination • 161

8

If the degree of anisocoria is greater in brighter lighting, then

it is the larger pupil that is abnormal; if it is more pronounced

in dim lighting, the smaller pupil is the abnormal one. An equal

degree of anisocoria in all levels of lighting indicates physiological

anisocoria.

Direct and consensual light reflex

Examination sequence

With the patient fixating on a point in the distance and in

ambient lighting, shine a bright light from the temporal side

into one eye and look for constriction of the ipsilateral

pupil.

To test the consensual reflex, assess the pupil response in

the contralateral pupil when light is directed towards the

ipsilateral pupil. Repeat for the other pupil.

Orbit and periorbital examination

Examination sequence

Observe the face and orbit for asymmetry and any obvious

abnormality, including swelling, erythema or any other skin

changes.

• Look for any abnormality in the position of the lids and

ptosis (Box 8.8).

• Look for any asymmetry in the position of the eyeballs.

Eyeball protrusion (proptosis) is best detected by looking

down on the head from above.

Palpate around the orbital rim and orbit, looking for any

masses.

• Check eye movements (Fig. 8.11).

• Use an ophthalmoscope (Fig. 8.12) to look for optic disc

swelling from compression.

Pupils

First inspect generally for squint and ptosis. Examine pupil shape

and symmetry. Physiological anisocoria (unequal pupil size) is

seen in 20% of the population.

Anisocoria

The eyes should be assessed to determine which is the abnormal

pupil.

Examination sequence

With the patient fixating at a point in the distance, increase

and decrease the illumination and look for any change in

the degree of anisocoria.

8.8 Causes of eyelid ptosis

Cause Diagnosis

Associated distinguishing

features

Neurogenic Horner’s syndrome Ptosis, miosis, eye

movement spared

Cranial nerve III

palsy

Dilated pupil, eye

movements affected (see

Fig. 8.10)

Myogenic Myotonic dystrophy Frontal balding, sustained

handgrip

Chronic progressive

external

ophthalmoplegia

Bilateral ptosis and

impairment of eye

movements, often without

diplopia, sparing of pupil

reflexes

Oculopharyngeal

dystrophy

History of swallowing

abnormalities

Neuromuscular

junction

Myasthenia gravis History of variable

muscular fatigue

Mechanical Eyelid tumour Evident on inspection

Eyelid inflammation/

infection

Evident on inspection

Trauma Scarring/history of trauma

Degenerative Levator aponeurosis

degeneration

Often unilateral, eye

movement normal

Long-term contact

lens wear

History of contact lens use

Fig. 8.12 Ophthalmoscopy. Ask the patient to focus on a distant target.

To examine the left eye, use your left eye to look through the

ophthalmoscope and left hand to hold it, index finger on the wheel. Hold

the patient’s head with your free hand. Gradually move in to visualise the

optic disc. Rotate the wheel to obtain a clear, focused image.

Fig. 8.11 Testing the six positions of gaze. Sit facing the patient, 1

metre away. Perform the test with both eyes open. Hold a pen torch or

target in front of the patient and ask them if they see the target as double.

Move the target to the six positions of gaze (blue arrows).

162 • The visual system

Adie’s pupil

This is a mid-dilated pupil that responds poorly to both light

and accommodation. With time, however, the affected pupil

can become constricted. Adie’s pupil is thought to result from

parasympathetic pathway dysfunction in the orbit. It typically

affects young women and is benign. When associated with

diminished Achilles tendon reflexes, it is referred to as Holmes–

Adie syndrome.

Argyll Robertson pupil

The pupil is small and irregular, and reacts to accommodation

but not light. This is classically the result of neurosyphilis. There

are other causes of light-near dissociation, however, including

diabetes mellitus, severe optic nerve disease and midbrain

lesions.

Visual fields

The normal visual field extends 160 degrees horizontally and

130 degrees vertically. Fixation is the very centre of the patient’s

visual field. The physiological blind spot is located 15 degrees

temporal to the point of visual fixation and represents the entry

of the optic nerve head into the eye.

The aim of the visual field examination is to test the patient’s

visual fields against your own (making the assumption that you

have normal visual fields). The visual field can be tested using

the fingers for gross examination. Finer examination can be

performed using a small hatpin.

Examination sequence

• Check visual acuity and ensure that the patient has at

least enough vision to count fingers.

• Sit directly facing the patient, about 1 metre away.

With your eyes and the patient’s eyes open, ask the

patient to look at your face and comment on whether they

have any difficulty seeing parts of your face.

• Ask the patient to keep looking straight at your face. Test

each eye separately. Ask the patient to close or cover one

eye and look directly across to your opposite eye; you

should also close your other eye.

Hold your hands out and bring an extended finger in

from the periphery towards the centre of the visual field.

For an accurate assessment of the patient’s fields, it is

vital that the testing finger is always kept in the plane

exactly halfway between yourself and the patient. Wiggle

your fingertip and ask the patient to point to it when they

first see it (Fig. 8.13). If the patient fails to notice your finger

when it is clearly visible to you, their field is reduced in

that area.

• Test all four quadrants separately.

More subtle visual field defects can be elicited using a

small white hatpin or a white Neurotip. With the patient

looking directly at your eye, bring the white target in from

the periphery to the centre (again always in the plane

halfway between you and the patient). Ask the patient to

say when they first see the target.

• Undertake this for all four quadrants, testing each eye

separately.

To assess very early visual field loss, repeat the same test

using a red hatpin or a red Neurotip (Fig. 8.14).

Relative afferent pupillary defect

Relative afferent pupillary defect (RAPD) is an important clinical

sign that occurs when disease of the retina or optic nerve reduces

the response of the eye to a light stimulus. Testing for RAPD

is an extension of the direct and consensual light responses.

Examination sequence

• Use a bright light source.

Move the light briskly from one eye to the other, but place

it on each eye for a minimum of 3 seconds.

In normal patients, this results in symmetrical constriction of

both pupils. In RAPD, light in the affected eye causes weaker

constriction (apparent dilatation) compared to light shone in the

normal eye.

Accommodation

Examination sequence

Ask the patient to look at a close fixation target (do not

use a light source) after fixating on a distant target.

There should be constriction of the pupil on near gaze.

Failure to constrict to light but constriction on near gaze is

referred to as light-near dissociation.

There are many causes of a dilated or constricted pupil

(Box 8.9).

Pupillary examination will distinguish the various causes of

anisocoria, as described here.

Horner’s syndrome

Horner’s syndrome is the clinical picture resulting from dysfunction

of sympathetic nerve supply to the eye, which originates in the

hypothalamus and emerges in the root of the neck before

innervating the pupil (see Fig. 8.6B). Damage at any point in

this pathway will result in Horner’s syndrome. On examination,

there is a constricted pupil (loss of sympathetic dilator tone) and

a partial ptosis resulting from denervation of Müller’s muscle

in the upper eyelid. There may also be anhydrosis (loss of

sweating) on the affected side. Diagnosis may be confirmed by

administering cocaine eye drops, which will cause pupil dilatation

in the unaffected pupil but no dilatation on the affected side.

Causes of Horner’s syndrome include demyelination, neck trauma/

surgery, apical lung tumour (Pancoast tumour) and carotid artery

dissection.

8.9 Causes of anisocoria

Dilated pupil

• Cranial nerve III palsy

• Pharmacological treatment

with a dilating agent (e.g.

tropicamide or atropine)

• Physiological

• Post-surgical

• Adie’s tonic pupil

Constricted pupil

• Horner’s syndrome

• Mechanical, e.g. secondary to

posterior synechiae in iritis or

trauma

• Physiological

• Late-stage Adie’s tonic pupil

• Pharmacological treatment

with a constricting agent (e.g.

pilocarpine)

The physical examination • 163

8

on the cornea in relation to the pupil. The reflections

should be symmetrical between the two eyes. Ask the

patient if they see a single or double light. If they see

double, this may indicate the presence of a squint, but not

seeing double does not exclude a squint. If the reflection

is on the nasal aspect of the pupil in one eye, this

suggests that the eye is deviated outwards and is

described as an exotropia.

To confirm the presence of a squint, perform the cover/

uncover test:

• Ask the patient to look at the pen torch at all times and

then cover one eye.

Look at the uncovered eye for any movement. It may

be helpful to repeat this several times.

Inward movement of the uncovered eye suggests that

it was positioned abnormally outwards and is described

as an exotropia (divergent manifest squint).

It is important to show the patient the red target and ask

them to report what colour they see. A dull or pale red

suggests colour desaturation, which may indicate optic

nerve dysfunction.

• When testing each quadrant with a red target, be sure to

explain to the patient that they should say when they first

see that the target is red and not when they first see it.

The target may be visualised before they appreciate the

red colour.

• To test the blind spot, place a red-tipped target

equidistant between the patient and yourself at the visual

fixation point.

Move the target temporally until it disappears.

• Then move the target slowly up and down, as well as from

side to side, until it reappears. This allows you to compare

the patient’s blind spot with yours.

Ocular alignment and eye movements

The eyes are normally parallel in all positions of gaze except

for convergence. Any misalignment is referred to as a squint

(strabismus). Squints are described as manifest (tropia) if present

with both eyes open, or latent (phoria) if revealed only by covering

one eye. In addition, they can be concomitant (where the angle

of squint remains the same in all positions of gaze) or incomitant

(where the angle of squint deviation is greatest in a single position

of gaze). The latter is commonly the result of paralysis of particular

extraocular muscles.

Detection of squint

Examination sequence

• Sit directly facing the patient, approximately 1 metre away

and at a similar height.

• Check visual acuity as part of the examination.

• Look for any abnormal head posture such as head tilts

(seen in cranial nerve IV palsy) or head turns (cranial nerve

VI palsy). These signs may be subtle.

• Hold a pen torch directly in front of the patient and instruct

them to look at the light. Observe the reflection of the light

Fig. 8.13 Confrontation visual field testing. Sit facing

the patient, 1 metre away. To compare your visual field

(assumed normal) with the patient’s, present a white

target or wiggle your fingers at a point equidistant

between yourself and the patient in the periphery. Bring

the target inwards in the direction of the blue arrows,

asking the patient to alert you when they first see it. Test

each eye separately.

Fig. 8.14 Testing the central visual field. Sit facing the patient, 1 metre

away. Present a red target at a point equidistant between yourself and the

patient in the periphery, starting when you can first see the target as red.

Bring the target inwards in the direction of the blue arrows, asking the

patient to alert you when they first see the target as red. Test each eye

separately.

164 • The visual system

Ophthalmoscopy

The direct ophthalmoscope is a useful tool for assessing both the

anterior and the posterior segments of the eye. Pharmacological

pupil dilatation is essential for a thorough fundus examination,

though the optic disc can be examined sufficiently without

dilatation.

Examination sequence

• Ask the patient to sit upright and look at a distant target.

• When using the direct ophthalmoscope to examine

the patient’s right eye, hold it in your right hand and

use your right eye to examine. Hold it in your left

hand and use your left eye to examine the patient’s

left eye.

Place your free hand on the patient’s forehead and brow,

as this will steady the head and improve your

proprioception when moving closer to the patient with the

ophthalmoscope.

• Rotate the ophthalmoscope lens to +10. This will allow

a magnified view of the anterior segment. You will be

able to examine the eyelid margins, conjunctiva, cornea

and iris. If epithelial defects are suspected, fluorescein can

be administered and a cobalt blue filter used to reveal

these.

• To examine the fundus, dial the lens back to 0.

• With your hand on the forehead and the brow, use the

ophthalmoscope to see the red reflex (red light reflected

off the retina) at a distance of about 10 cm. When the red

reflex is in focus, look for opacities and determine whether

they are static or mobile. Static opacities are usually due

to cataract changes, while mobile opacities indicate

vitreous opacities.

• Slowly move the ophthalmoscope closer to the patient

almost to the point that your forehead touches your

thumb, which is resting on the patient’s forehead and

brow (see Fig. 8.12).

• Turn the lens dial until the optic disc comes into focus; if it

does not, focus on a blood vessel.

• The optic disc can usually be located easily; if not, follow a

blood vessel centrally (in the direction opposite to its

branches) to locate it.

• Examine the optic disc, paying particular attention to its

shape, colour, edges and cup size.

• Follow each blood-vessel arcade and examine each of the

retinal quadrants.

• To examine the macula, ask the patient to look directly at

the light.

The normal retina looks different in Asian and Caucasian

patients (Fig. 8.16).

Swelling of the optic disc is a very important clinical sign.

Causes of unilateral and bilateral optic disc swelling, and their

distinguishing features, are summarised in Box 8.10.

A variety of diseases that can damage the optic nerve cause

an abnormally pale optic disc (see Fig. 8.8D). The differential

diagnosis of optic disc pallor is summarised in Box 8.11.

• Conversely, if the eye moves outwards when the

contralateral eye is covered, this suggests that it was

abnormally positioned inwards and is described as an

esotropia (convergent manifest squint).

Repeat the cover/uncover test for the other eye.

• Failure of an eye to move despite an obvious corneal light

reflex may indicate that the eye has such poor vision that

it cannot take up fixation or else it is restricted from

moving.

• The alternating cover test involves covering the eyes

alternately and quickly while the patient is fixated on the

pen torch. Leave the cover on each eye for about 2

seconds but move between the eyes in less than 1

second. The movement is repeated multiple times. This

test will help to elicit latent squint.

Ocular movements

Examination sequence

In the same seating position, ask the patient to look at a

target or pen-torch light about 50 cm away.

• Ask them to say if and when they experience diplopia.

• Starting from the primary position, move the target in the

six positions of gaze (see Fig. 8.11) and up and down.

If diplopia is present, ask whether this is horizontal, vertical

or a combination of the two.

• Determine where the image separation is most

pronounced.

• Look for nystagmus and determine whether the eye

movement is smooth.

Interpretation of any limitation of excursion is made by

reference to the functions of the extraocular muscles (see

Fig. 8.2).

Oculocephalic (doll’s-eye) reflex

This reflex is the ability of the eyes to remain fixated while the

head is turned in the horizontal plane (Fig. 8.15). An impaired

reflex indicates a brainstem abnormality.

Examination sequence

• With the patient supine, ask them to look at your face.

Gently turn their head from side to side, noting the

movement of the eyes.

• This can also be performed on a comatose patient.

Nystagmus

Nystagmus is continuous, uncontrolled movement of the eyes.

Biphasic or jerk nystagmus is the most common type. It is

characterised by slow drift in one direction, followed by fast

correction/recovery in the opposite direction. The direction of the

fast phase designates the direction of the nystagmus. If there

are equal oscillations in both directions, it is called pendular

nystagmus.

Nystagmus commonly indicates vestibular disease, and the

examination sequence and differential diagnosis are covered

on page 174.

Investigations • 165

8

Retinopathies

Diabetes mellitus leads to a wide range of important abnormalities

in the retina, which are summarised on Fig. 8.17.

The eye also provides an opportunity to view the effects of

hypertension on the microvasculature. The retinal arteries are

effectively arterioles. Chronic arteriosclerosis with vessel-wall

thickening and hyalinisation appears as widening of the arterioles,

arteriovenous nicking where arterioles cross venules, and a ‘silver

and copper wiring’ light reflex.

More acute changes can also be seen in malignant hypertension.

Various grading systems have been created to try to link retinal

findings to end-organ damage. The retinal appearances in

hypertension are illustrated in Fig. 8.18 and classified using the

Modified Scheie classification:

Grade 0: no changes.

Grade 1: barely detectable arteriolar narrowing.

Grade 2: obvious retinal arteriolar narrowing with focal

irregularities.

Grade 3: grade 2 plus retinal haemorrhages, exudates,

cotton-wool spots or retinal oedema.

Grade 4: grade 3 plus optic disc swelling.

Inherited retinopathies result from a wide range of genetic

mutations. The most common inherited retinopathy is retinitis

pigmentosa, which causes symptoms of nyctalopia (difficulty

seeing in dim light) and tunnel vision. Examination reveals a

pale optic disc, attenuated arterioles and bone-spicule retinal

pigmentation (see Fig. 8.8E).

Investigations

Appropriate initial tests for a variety of common presenting eye

problems are summarised in Box 8.12.

Fig. 8.15 Oculocephalic reflex. Move the head in the horizontal plane. Note that the eyes move in the opposite direction to head movement.

A

B

Fig. 8.16 The normal fundus. A Caucasian. B Asian.

166 • The visual system

8.10 Causes of optic disc swelling

Unilateral

• Optic neuritis

• Anterior ischaemic optic

neuropathy

• Syphilis

• Lyme disease

• Bartonella infection

• Sarcoidosis

• Leukaemia

• Optic nerve glioma

• Secondary metastases

Bilateral

• Papilloedema

• Optic disc drusen

• Diabetic papillitis

• Pseudopapilloedema in

hypermetropes

• Hypertensive papillopathy

8.11 Differential diagnosis of optic disc pallor

Inherited

• Congenital optic atrophy, including Leber’s and Behr’s

End-stage glaucoma

Trauma

Compressive

• Orbital neoplasm

• Thyroid eye disease

• Orbital cellulitis

Neurological

• End-stage papilloedema • Devic’s disease

Metabolic

• Nutritional deficiency

• Toxic amblyopia

• Ethambutol

• Sulphonamide

• Diabetes mellitus

Vascular

• Central retinal artery occlusion • Giant cell arteritis

Inflammatory

• Meningitis • Postoptic neuritis

A B

C D

E F

Fig. 8.17 Retinal abnormalities in diabetes mellitus. A Diabetic maculopathy. B Background diabetic retinopathy. C Severe non-proliferative

diabetic retinopathy. D Proliferative diabetic retinopathy. E Proliferative diabetic retinopathy with a vitreous haemorrhage. F Previous panretinal laser

photocoagulation in treated proliferative diabetic retinopathy.

Investigations • 167

8

A B

C D

Fig. 8.18 Hypertensive retinopathy. A Increased reflectance, giving a silver wiring appearance to the arteriole (arrow). B Focal arteriolar narrowing

(double arrows) seen in grade 2 disease. C Exudates and flame haemorrhages in grade 3 retinopathy. D Signs of malignant hypertension in grade 4

disease with a swollen optic disc and macular exudate.

168 • The visual system

8.12 Investigations

Investigation Indication

Clinic tests

Refraction Refractive error, cataract and corneal disorders

Fluorescein staining Corneal epithelial disease

Schirmer’s test Dry eyes, Sjögren’s syndrome

Nasolacrimal duct washout Watery eyes

Blood pressure Hypertensive retinopathy, retinal vein occlusion

Bacterial culture and sensitivity Bacterial conjunctivitis

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