EXAMINATION

INTRODUCTION

In the assessment of a patient with eye disease, it is

important to take a good history, examine the eyes with

adequate illumination and test the visual function.

Recently, retinal and macular diseases have become

more common as causes of severe visual loss. In these

cases, a fundal examination with dilatation of the pupils in

a darkened room is necessary.

HISTORY

A careful history of the patient’s ocular symptoms is essential. His

past history and general illnesses, such as diabetes and hypertension,

frequently provide useful clues.

Myopia, squint, open-angle glaucoma and dystrophic conditions

have a hereditary tendency which is revealed by an inquiry into the

patient’s family history. It is also useful to take note of allergies and of

the medical therapy the patient is undergoing.

OCULAR SYMPTOMS

The more important symptoms include decreased visual acuity,

floaters, ocular pain, headaches, itching, flashes, watering and double

vision (diplopia).

Decreased visual acuity

Decreased visual acuity must always be investigated and the cause

found. The cause for a sudden loss of vision could be vascular in

nature such as retinal vein occlusion, retinal artery occlusion or vitreous

haemorrhage. It could also be due to acute glaucoma, retinal

detachment or inflammatory conditions such as acute uveitis and

optic neuritis.

Gradual loss of vision is usually due to a refractive error such as

myopia or presbyopia, or to degenerative conditions of which cataract

is the most common. It could also be due to macular degeneration or

chronic glaucoma.

Floaters

Another common ocular symptom which calls for further

investigation is the appearance of floaters usually described by the

patient as small, semi-translucent particles of varying shapes moving

across the visual field with the movement of the eye. Single or double

floaters of many months or years are common and usually harmless.

But a sudden increase in floaters, especially when associated with

lightning flashes and visual loss in patients with high myopia or in the

elderly, suggests retinal disease, particularly retinal detachment.

Flashes

Flashes are momentary flashes of light due to stimulation of the

retina and are seen in retinal tears and detachments and also in

vitreous detachment. Other sensations of light may arise from migraine

or lesions of the visual pathway.

Eye pain and headaches

Eye pain and headaches may be due to either ophthalmic or non-

ophthalmic causes. Of the ophthalmic causes, acute glaucoma is the

most important. Less frequent but just as important is iritis. Uncorrected

refractive error, migraine and anxiety are common causes of

headaches.

Itchy eyes

Itching around the eyes is frequently due to allergy. It may also be

due to blepharitis.

Watering

In infants, watering is usually due to a blocked nasolacrimal duct.

A rare but important cause of watering and irritable eyes is congenital

glaucoma. Another cause is entropion of the lower lid.

In adults, watering has many causes, a common one being a blocked

nasolacrimal duct. It can also occur in association with surface

irritation, as in conjunctivitis, keratitis or when a foreign particle is in

the eye.

Double vision (diplopia)

It is important to note whether double vision (binocular diplopia)

occurs only when both eyes are opened or when one eye is occluded

(monocular diplopia).

Binocular diplopia is usually due to extraocular muscle paralysis.

Monocular diplopia is caused by diseases in the eyeball, such as

early cataract, lens dislocation or corneal opacity.

EXAMINATION

VISUAL ACUITY

The assessment of distant and near visual acuity is important as it

reflects the state of the macular function (central vision). The visual

acuity can be tested by asking the patient to cover one of the eyes

with a cardboard or with the palm of his hand. By testing the ability

of the patient to see objects such as the clock or the newspaper in his

own environment, it is possible to get a gross assessment of the visual

acuity as blind, grossly defective, subnormal or normal.

Distant visual acuity

It is usually necessary to record a patient’s distant visual acuity

more accurately with Snellen’s chart. It is read at six metres, with the

letters diminishing in size from above.

The patient has normal vision if he is able to read the line of letters

designated as 6/6 at or near the bottom of the chart. The scale for

decreasing distant visual acuity is 6/9, 6/12 (industrial vision), 6/18,

6/24, 6/36 and 6/60 (legal blindness in some countries).

If the patient is unable to read the letters, he is asked to count the

examiner’s fingers which are held a metre away. If his answers are

correct, he has distant visual acuity of “counting fingers” at a metre.

If he is unable to count the fingers, the examiner should move his

hand in front of the patient’s eyes. The visual acuity is then said to

be “hand movement”. If he can see only light, visual acuity is

recorded as “perception of light”. If he cannot see any light, visual

acuity is recorded as

“no perception of light” which is total

blindness.

VISUAL ACUITY TRANSCRIPTION TABLES

(Adopted by the International Council of Ophthalmology, 1954)

Decimal V

6 metre

20 feet

Visual Angle

Notation

Equivalent

(minutes)

1.0

6/6

20/20

1.0

0.9

1.1

0.8

5/6

20/25

1.3

0.7

6/9

20/30

1.4

0.6

5/9

15/25

1.6

0.5

6/12

20/40

2.0

0.4

5/12

20/50

2.5

0.3

6/18

20/70

3.3

0.2

5.0

0.1

6/60

20/200

10.0

In some countries, patients with less than 6/60 vision are classified

as legally blind. Patients who can see 6/12 have sufficient vision to

work in most industries and are said to have ”industrial vision”

which is also the visual requirement for driving.

Pinhole

In testing distant visual acuity, looking through a pinhole is useful

for patients with blurred vision. Vision can be improved if the defective

vision is due to refractive error. It cannot be improved if it is due to

organic eye disease.

Near visual acuity

The common near visual acuity tests are the Jaegar test and the ‘N’

chart, usually read at a distance of 30 cm. The Jaegar test is recorded

as J1, J2, J4, J6, etc., and the ‘N’ chart as N5, N6, N8, N10, etc.

Standard small newsprint is approximately J4 or N6. Each eye is

tested in turn with the other covered. Middle-aged patients

(presbyopic age) must be tested with their reading glasses.

Difficulties in examination

It is often difficult to test visual acuity in young children as well

as patients who are illiterate, uncooperative or malingering.

Frequently only an estimate can be made. The E-chart, picture cards

or small coloured objects may be used. It can be extremely difficult

to determine whether a patient is malingering without the use of

special tests.

VISUAL FIELDS

Confrontation

The visual fields can be recorded approximately by using the

confrontation test. The patient covers the eye which is not being

tested with his palm and fixes the other at the examiner’s nose, ear

or eye. A target is then brought into his field of vision from the side

and the point at which the patient sees the object is noted. The eye is

tested in the different meridians, usually 8.

Alternatively, the examiner’s fingers are held at a distance of one

metre and the patient is asked to count them in the different quadrants,

that is, the superior temporal, the inferior temporal, the superior nasal

and the inferior nasal quadrants.

EXTERNAL EYE EXAMINATION

This is done with good illumination from either a window or a

bright torch. A magnifying glass facilitates examination and should be

used whenever available.

The position and appearance of the eyelids should be noted,

especially with regard to their position in relation to the limbus.

Also note whether there is eyelash crusting, watering, oedema,

discharge or inflammation. Common problems include drooping of

the upper eyelid (ptosis), lid retraction, inability to close the lids

(lagophthalmos), eversion of the lid margins (ectropion) and inversion

of lid margins (entropion).

The conjunctiva and sclera should be almost white with only a

few small vessels. The transparent disc-like cornea is best seen with

either a good oblique light from a torch or window. Staining with

fluorescein dye will help to show ulcers or abrasions of the cornea.

The fluorescein is highlighted by blue light. The colour and pattern

of the iris should be observed. A dense cataract can be seen through

the pupil as a white reflex.

Eversion of upper eyelid

It is sometimes necessary to evert the upper lid to examine the

tarsal conjunctiva if the patient is suspected of having a foreign body

under the lid. This is also done for diagnosis of the conjunctival

follicles of the upper lid as in trachoma. The lid is everted by asking

the patient of look downwards and by applying slight pressure on the

lid with a finger or rod. The lid margin is then gently pulled upwards

to evert it.

PUPIL RESPONSES

The response of light directed at one pupil in a darkened room is

known as the direct pupillary response. The reaction of light by the

fellow pupil is called the consensual pupillary response.

Where a darkened room is not available, the pupillary response

can be tested by having the patient cover both his eyes with his

palms. The contraction of the pupil is observed when the palm is

removed from one eye. This indicates the response of the pupil to

direct light.

If there is no pupillary reaction to light, the reaction to

accommodation is tested by asking the patient to fix his eyes on an

object at a distance and then to focus on another object at about

10 cm away from him.

EXTRAOCULAR MUSCLES

The extraocular muscles are examined by observing the position of

the eyeballs with the patient looking straight ahead. Any gross

malposition of the eyes can be easily seen. One eye may be observed

to be turned inwards (convergent squint) or outwards (divergent squint).

Occasionally, one of the eyes may be seen to be higher than the

other (vertical squint).

Corneal light reflex

The corneal light reflex is a useful method of determining whether

one of the eyes is turned inwards or outwards, or vertically

displaced. Normally, when the patient is asked to look at a torch, a

light reflex is seen at the centre of the pupil. If one of the eyes is

misaligned, the reflex will not be at the centre of the pupil. In a

convergent squint, the light reflex will be at the outer side of the

cornea, and in a divergent squint, at the inner side of the cornea. A

general guide is that if the reflex is at the limbus, the degree of

convergence or divergence is approximately 40°. If it is halfway

between the centre of the cornea and the limbus, it is approximately

20°. The corneal light reflex is also a useful means to exclude

pseudosquints where there is an appearance of a convergent squint

because of medial epicanthal lid folds. In pseudosquints the corneal

light reflex is central in both eyes.

Ocular movements

When the extraocular muscles are severely paralysed, the

restriction in movement is tested by asking the patient to look in

different directions (positions of gaze). If the extraocular muscles are

less severely affected, special techniques have to be used.

Movement

Right Eye

Left Eye

Right

Right lateral rectus

Left medial rectus

Up and right

Right superior rectus

Left inferior oblique

Down and right

Right inferior rectus

Left superior oblique

Left

Right medial rectus

Left lateral rectus

Up and left

Right inferior oblique

Left superior rectus

Down and left

Right superior oblique

Left inferior rectus

The six cardinal positions of gaze and their corresponding primary

extraocular muscle actions.

OPHTHALMOSCOPY

The ophthalmoscope is used to observe abnormality in the ocular

media, optic disc, retinal vessels, fundal background and the macula.

Red reflex

With the lens power of the ophthalmoscope turned to 0 and the

ophthalmoscope held one metre away from the patient’s eye a red

reflex is seen through the pupil. Alternatively the lens power can be

turned to about +5 dioptres and the eye examined approximately

10 cm away. This is caused by the reflection of the light of the

ophthalmoscope from the choroidal vessels. It appears as a bright red

round area which is evenly lighted. Any opacity in the cornea, lens

(cataract) or vitreous will be seen as a dark area. In retinal detachment,

the reflex appears grey instead of red.

Fundus

Examination of the fundus is usually done with the direct

ophthalmoscope. The refractive error in both the patient and examiner

has to be compensated for by adjusting the lens power of the

ophthalmoscope. Alternatively, the examiner and patient may use

their glasses or contact lenses in which case no adjustment will be

required. The patient is then instructed to look at a distant object.

When the right fundus is examined, the ophthalmoscope is held in

the right hand. The examiner uses his right eye to examine the

patient’s right eye approaching from the right side. The patient’s left

fundus is examined with the examiner’s left eye and the patient is

approached from the left. It is important to get near enough so that

the examiner’s forehead touches his own thumb which is used to lift

the upper lid of the eye being examined.

It is best to approach the eye from the temporal side so that a good

view of the disc can be seen before the pupil contracts when light is

shone on the macula. The nasal retinal vessels and the temporal

retinal vessels are examined before the macula. Because of the extreme

sensitivity of the macula to light which results in rapid constriction of

the pupil, examination of the macula is difficult and usually requires

a mydriatic eyedrop to dilate the pupil.

Difficulties in examination of the fundus

Examination of the fundus can be difficult because of:

• Uncooperative patient

• High myopia

• Opacity in the cornea, lens or vitreous

• Poor ophthalmoscope or old batteries

• Bright room

• Small pupils

In high myopia, examination is simplified by looking through the

patient’s glasses or his contact lenses. As the lenses of an

ophthalmoscope can sometimes be fogged with dust or mould,

especially in the tropics, they may have to be cleaned to enable

adequate examination of the fundus.

The small pupil

In order to see the fundus clearly, the pupils should be dilated.

Examination in a darkened room may be adequate for patients who

have naturally large pupils. For patients with small pupils, examination

can be difficult and a short-acting mydriatic such as Tropicamide,

which acts in less than 30 minutes and has an effect of about four

hours, should be used. Long-acting mydriatics are no longer used

because of their length of action: Homatropine (one day) and Atropine

(one week).

SPECIAL TECHNIQUES

Modern technology has enabled ophthalmologists to examine

ocular conditions with greater precision. The techniques and

equipment commonly used by ophthalmologists are described here

to help other practitioners understand ophthalmic reports.

• Tests for extraocular muscles

The cover-uncover test is done by covering one of the patient’s

eyes while the other eye looks at an object. When the cover is

removed, the uncovered eye may move to look at the object. By

observing the movement of the eye, the presence of a squint may be

confirmed.

A number of tests can be carried out to analyse diplopia with the

use of red-green goggles to dissociate the eyes. The synoptophore is a

machine with specially designed pictures to measure accurately the

angle of a squint and to test the ability of the patient to see with both

eyes together (binocular single vision).

• Binocular slit-lamp microscopy

The binocular slit-lamp microscope enables accurate observation

of the eye up to a magnification of 40 times. It consists of two parts,

an oblique light which can be adjusted to a slit and a binocular

microscope. Other uses of the slit-lamp include examination of the

retina with magnification from a Hruby or contact lens and checking

the filtrating angle of glaucoma patients (gonioscopy).

• Tonometry

A tonometer is used to measure intraocular pressure. The most

widely used tonometer is the Goldmann Applanation Tonometer.

The Schiotz Indentation Tonometer is less accurate but it is

portable. The new non-contact tonometers do not require local

anaesthesia.

• Perimetry and scotometry

Perimetry gives a more exact record of the visual fields than the

confrontation test. The ability of the patient to see a small 5 mm

target on an arc moving into his view from the periphery at different

meridians is recorded on to a chart.

Scotometry is used to assess the central 30° part of the field of

vision. It involves using a small 1-5 mm target on a screen (Bjerrum

or Tangent screen) placed 1 or 2 metres away and noting when the

test target appears. The normal blind spot is found 15° lateral to the

fixation point.

• Goldmann and computerised perimetry

One problem in comparative field studies is the lack of

standardisation. The Goldmann bowl perimeter partially overcomes

this. More recently, the introduction of computerised perimetry has

sometimes been invaluable in serial visual field testing for glaucoma

and pituitary tumours.

• Tests for colour vision

The Ishihara test is most commonly used for colour vision. It is

very sensitive. Patients who are able to see colours for general purposes

may in fact be found to have a colour defect with it. Patients who fail

the Ishihara test but who respond accurately to the Lantern colour

matches or Farnsworth Munsell 100 hue test should not be prevented

from pursuing their occupation of choice. This includes pilots who

generally need to have perfect or near perfect vision.

• Indirect ophthalmoscopy

The indirect ophthalmoscope is now commonly used by

ophthalmologists. Its advantages are a binocular view, a wide field

and easy examination of the retinal periphery. It is particularly valuable

in assessing patients with opacity in the ocular media, high myopia

and retinal detachment.

Fundal photography and fundal fluorescein angiography

Fundal photography and fundal fluorescein angiography are

methods which supplement the examination of the fundus. In fundal

fluorescein angiography, fluorescein dye is injected intravenously and

serial fundal photographs are taken to show up the retinal and

choroidal circulation.

Refraction

It can be objective with retinoscopy. Subjective tests are done with

a trial frame and a set of lenses. Alternatively, the lenses may be

mounted on a series of rotating discs (phoropter). More recently,

computerised scanning machines print out the refraction with

remarkable accuracy.

Ultrasonography

Ultrasonography is now commonly used to evaluate the state of

the posterior segment of the eyeball when the ocular media is opaque

from corneal opacities, dense cataract or vitreous haemorrhage. It is

particularly useful in severe ocular injuries and vitreous haemorrhage

prior to posterior vitrectomy. Ultrasonography is also used for

measuring the thickness of the cornea (pachymeter) and the axial

length of the eye. In addition, it can provide essential data for

calculating the required lens power prior to intraocular lens

implanation in cataract extraction.

CT scan and Magnetic Resonance Imaging (MRI)

The CT scan is used for many ophthalmic conditions, but

especially for orbital tumours and localisation of intraocular foreign

bodies. It is also widely used for investigations of neuro-ophthalmic

disorders.

Magnetic resonance imaging is a noninvasive imaging procedure

that does not involve the use of ionising radiation. Its mode of action

is based on the interactions of three physical properties, viz. a

powerful magnetic field, radiowaves and atomic nuclei with an

electric charge.

Compared to the CT scan, MRI possesses greater sensitivity to soft

tissue contrast. It is also useful in detecting demyelinating lesions. A

disadvantage of MRI is that, unlike the CT scan, it does not detect

calcification well and is therefore less valuable in the diagnosis of

retinoblastoma and bony lesions.

Macular potential acuity

It is frequently important to predict the visual outcome prior to

surgery, especially cataract surgery. This can be done by testing

visual acuity with the pinhole or careful examination of the macula.

Special tests have recently been introduced. Evaluation with the

potential visual metre (PAM) seems to be more valuable than the

laser interferometer or Blue Field entoptoscope.

Electrophysiology

Clinical electrophysiology which includes electroretinography

(ERG), electrooculography (EOG) and visual evoked response study

(VER) is now available in small practical units for ophthalmic clinics.

ERG is useful in the diagnosis of retinal dystrophy, such as retinitis

pigmentosa. It is also valuable in vitreous haemorrhage when the

surgeon is unsure of visual function. EOG measures retinal pigment

epithelial function, and VER is diminished in optic nerve disease.

Extraocular Muscles

Corneal reflexes at centre of pupils signify normal ocular (alignments)

muscle balance.

Fig. 1.11

Looking straight ahead.

Fig. 1.12

Fig. 1.13

Up and right. Right superior rectus

Up and left. Right inferior oblique

and left inferior oblique.

and left superior rectus.

Fig. 1.14

Fig. 1.15

Right. Right lateral rectus and left

Left. Right medial rectus and left

medial rectus.

lateral rectus.

Fig. 1.16

Fig. 1.17

Down and right. Right inferior

Down and left. Right superior

rectus and left superior oblique.

oblique and left inferior rectus.

Six cardinal positions of gaze and their corresponding primary

extraocular muscle actions.

DESCRIPTION OF THE FUNDUS

Optic disc

Colour

— Pink, temporal side usually paler.

Margin

— Sharp and flat. Nasal margin may be relatively blurred

and raised (in hypermetropia). Many normal variations

including pigmentation and myopic crescent.

Cup

— Varies in size and depth. Situated at centre of disc and

slopes temporally.

Cup/disc ratio — is ratio of diameter of cup to that of

optic disc.

Retinal vessels

Colour

— Arteries lighter than veins.

Diameter — Arteries narrower than veins. Ratio approximately 2:3.

Crossing

— Arteries cross anterior to veins at arteriovenous

crossings.

Fundus background

Colour

— Red fundal background because of the choroidal

vessels and retinal pigment layer. Darker in pigmented

races. In lightly pigmented persons, large choroidal

vessels seen against the white sclera. Tesselated (tigroid

appearance) in myopia.

Macular area

Colour

— Normally darker than rest of fundus. At centre, normal

foveal light reflex.

Special Examination

Fig. 1.29

Fig. 1.30

Slit-lamp microscopy permits not only

Indirect ophthalmoscopy permits

magnified examination of anterior

good binocular examination of retinal

segment but also filtration angles,

periphery, especially useful in retinal

intraocular pressure with applanation

detachment or cloudy media.

tonometer, vitreous and retina with

special contact lens.

Fig. 1.31

Fig. 1.32

Schiotz tonometry, one of the

Applanation tonometry using

methods of measuring intraocular

fluorescein and blue cobalt light is

pressure.

most accurate method of measuring

intraocular pressure.

Special Examination

Fig. 1.33

Fig. 1.34

Fundal photography with intravenous

Ultrasonography now extensively

fluorescein dye injection

(fundal

used in ophthalmology especially

fluorescein angiography).

when ocular medium is opaque (note

total retinal detachment).

Fig. 1.35

Fig. 1.36

CT scan useful in numerous conditions.

Electrophysiological studies now used

Helps to confirm diagnosis of intraocular

clinically in many retinal conditions.

foreign body (note intraocular foreign

body near optic disc).

LID, LACRIMAL APPARATUS

AND ORBIT

INTRODUCTION

Most lid conditions are related to inflammation,

malposition or tumours. A common lacrimal disease is

blockage of the lacrimal drainage system which results in

tearing.

The most common condition of the orbit is

exophthalmos, indicating the possibility of thyroid disease

or a space-occupying lesion. It may require the care of

several specialists.

EYELID INFLAMMATION

Blepharitis (inflammation of the lid margin)

Squamous blepharitis is the more common of the two main types

of blepharitis. It is frequently associated with dandruff or seborrheic

dermatitis and presents with small white scales at the roots of the

eyelashes. The patient often has chronically irritable eyes.

Ulcerative blepharitis is due to staphylococcal infection of the

follicles at the lid margin. It is accompanied by falling of the lashes

and, later, by deformity of the lashes, some of which may turn inwards

(trichiasis).

Treatment is frequently difficult and tedious as the condition is

chronic. The crusts may be removed by cleaning the lid margins with

boiled cotton wool, followed by application of an antibiotic ointment

at night. It is best to avoid local steroids although they may relieve

the symptoms. In squamous blepharitis, scalp lotion to control the

dandruff may help.

Stye (hordeolum)

This is a small abscess of the eyelash follicle seen clinically as a

small inflamed nodule. The symptoms are acute irritation and local

pain. Treatment is with local heat applied with a folded face towel.

If the abscess points, the affected eyelash may be pulled out and

local antibiotics applied.

Chalazion (Meibomian cyst)

Blockage of the duct of a tarsal gland may cause a cyst

(Meibomian cyst) due to the retained secretion. A small chalazion

which presents as a painless nodule at the tarsal plate may

sometimes become inflamed. It usually resolves spontaneously. It can

be treated with local heat and topical antibiotics. Systemic antibiotics

are rarely necessary. Surgery may be necessary if the cyst is large,

becomes inflamed or ruptures, resulting in a granulomatous lesion on

the conjunctiva or skin.

Allergic or contact dermatitis

The skin around the eyelids becomes oedematous, inflamed and

scaly. There is intense itching. This is due to allergy to cosmetics or a

variety of ophthalmic medication, especially sulphonamides.

Treatment consists of identifying and stopping the offending

cosmetics or medication. The application of local steroid cream to

the skin of the eyelids helps.

Herpes zoster ophthalmicus

Herpes zoster ophthalmicus affects the skin supplied by the

ophthalmic division of the fifth cranial nerve. It presents with pain

and skin vesicles which may become secondarily infected. If the

nasociliary nerve is affected, the skin lesions appear on one side of

the nose. In this case the eye is at risk from complications which

include corneal inflammation, iridocyclitis and occasionally,

secondary glaucoma.

Treatment consists of providing general hygiene and the application

of local antibiotics to prevent secondary infection of the skin lesion.

Application of local steroids to the eye is needed if keratitis or

iridocyclitis develops. Ocular complications may require regular

ophthalmic care. Systemic antiviral drugs may be indicated in severe

cases during the acute stage. Prolonged pain over the scalp and eye

(post-herpetic neuralgia) may be troublesome.

EYELID MALPOSITION

Ptosis (drooping upper lid)

Ptosis can be unilateral or bilateral, complete or partial, and

congenital or acquired. In bilateral ptosis, the patient’s head is

characteristically tilted backwards in order to see through the narrowed

palpebral fissure.

Congenital ptosis is usually due to dystrophy in the levator palebrae

superioris muscle, and may lead to amblyopia if severe and untreated.

The causes of acquired ptosis are senile ptosis (degeneration of levator

aponeurosis), nerve-related causes

(third nerve lesion, Horner's

syndrome), muscular causes (myasthenia gravis and other myopathies)

and, mechanical causes (trauma to the lids, inflammation and tumours).

Treatment for congenital ptosis consists of an operation to shorten

the levator palpebrae superioris, usually with good cosmetic results.

Treatment for other types of ptosis depends on the cause.

Lid retraction

Instead of covering the upper edge of the cornea, the upper lid is

retracted several millimetres. The usual cause is overactivity of the

levator muscle from hyperthyroidism. In severe cases, a recession of

the levator muscle may be done.

Control of hyperthyroidism may be helpful. In severe cases, a plastic

bridging of the lids (tarsorrhaphy) or alternatively, a recession of the

levator muscle may be done.

Entropion (inversion of lid margin)

This condition is associated with inturned eyelashes (trichiasis) which

may lead to complications including chronic conjunctivitis, corneal

abrasion and even ulceration.

The cause may be scar tissue on the conjunctival surface, a common

complication of the end stage of trachoma, or spasm of the orbicularis

oculi (spastic entropion). It may also be due to weakness of the eyelid

tissues as in senile entropion.

Lubricants may help but surgical eversion of the lid is usually

required.

Trichiasis (inturned eyelashes)

Trichiasis can cause a unilateral red eye from chronic irritation of

the cornea or conjunctiva. It is frequently associated with entropion.

For a permanent cure, the hair follicles of the inturned lashes have to

be destroyed by diathermy or cryotherapy. Alternatively, the eyelid

may be everted surgically.

Ectropion (eversion of lid margin)

The patient usually complains of tearing (epiphora) due to failure

of the tears to gain access to the lacrimal drainage apparatus. This is

sometimes accompanied by exposure conjunctivitis or keratitis.

The cause of ectropion is weakness of the orbicularis oculi muscles

associated with seventh nerve lesion or senile weakness from loss of

muscle tone. Occasionally, it is caused by scar tissue on the skin of

the eyelid (cicatricial ectropion).

When the watering is disturbing or when it is complicated by

exposure conjunctivitis or keratitis, a plastic operation may be

necessary to restore the lid to its normal position.

EYELID DEPOSITS AND TUMOUR

Xanthelasma

Xanthelasma is a fatty deposit in the skin, usually bilateral and

occurring at the medial part of the upper lid. Less commonly, it

develops on the lower lid. It is a local condition which has no

symptoms. Surgical removal is for cosmetic reason.

Basal cell carcinoma (rodent ulcer)

Basal cell carcinoma usually appears on the lower lid margin as a

raised nodule with a characteristic pearly rolled edge. This is common

in Caucasians living in hot climates. If left untreated, the lesion may

ulcerate and infiltrate into the adjacent tissues. It may, although rarely,

lead to loss of the eye or the invasion of the bone and may even

reach the surface of the brain. The lesion is locally invasive and does

not metastasize.

The choice of treatment is between surgery and radiotherapy.

Careful follow-up is essential in order to prevent recurrence.

LACRIMAL SYSTEM

Blockage of the lacrimal drainage system may occur either in the

punctum, the canaliculus or the nasolacrimal duct, resulting in tearing.

Very often, the blockage occurs in the nasolacrimal duct and this

secretion may cause the lacrimal sac to become chronically infected

(chronic dacryocystitis). The patient complains of persistent watering

in the eye with reflux of mucopurulent material when pressure is

applied on the lacrimal sac.

If the condition persists, an operation (dacryocystorhinostomy) to

create a new drainage channel may have to be performed. In acute

dacryocystitis, systemic antibiotics and surgical drainage of the pus

are required.

ORBIT

Orbital cellulitis

This condition is unilateral. It presents with intense lid oedema,

chemosis and restriction of eye movements. It often occurs as a result

of the spread of infection to the orbit from one of the surrounding

paranasal sinuses. Sometimes there is disc oedema.

The infection may spread backwards and cause cavernous sinus

thrombosis, a condition which can be fatal. The patient usually has

systemic manifestations of fever and malaise.

Treatment is urgent. Intensive medication with systemic antibiotics

usually clears the infection. X-ray of the sinuses should be taken and

an ear, nose and throat specialist consulted.

Preseptal cellulitis

Preseptal cellulitis can simulate orbital cellulitis. It presents with

swollen and inflamed eyelids, but there is no proptosis, ocular

movements are not affected, and the patient is generally well. The

condition is mild and treatment with antibiotics is effective.

Exophthalmos (proptosis or forward protrusion of the eyeball)

This is recognised clinically by the position of the lower lid margin

which normally just covers the limbus but which is separated away

in exophthalmos. The protrusion is sometimes more obvious when

the patient is examined from above and the positions of both eyes are

compared.

Thyroid disease is the commonest cause. Other causes include

space-occupying lesion behind the eyeball which may arise from

orbital structures

(e.g. optic nerve tumours, haemangioma or

lymphangioma) which may have spread from the middle cranial fossa

(meningioma) or the posterior nasal space (e.g. nasopharyngeal cancer).

It may also be caused by metastatic tumours.

It is important to distinguish exophthalmos from pseudo-

exophthalmos which occurs in lid retraction (hyperthyroidism) and in

myopia when the eyes may appear to protrude forward.

Owing to the variety of causes, investigations often involve the

neurologists, the endocrinologist, the radiologist and the ear, nose

and throat surgeon.

Treatment depends on the cause. A local intraocular space-

occupying lesion may require surgical removal. If the cornea is at

risk, it needs protection, usually a tarsorrhaphy.

CONJUNCTIVA, SCLERA AND

CORNEA

INTRODUCTION

Bilateral red eyes from infection or allergy are common

and relatively harmless. However, a unilateral red eye

requires careful ocular examination as the common causes

are acute glaucoma, acute iritis, keratitis, or a foreign

body. These conditions can lead to blindness if untreated.

Corneal diseases may lead to visual loss because of

scarring. Of particular importance are trachoma and herpes

simplex infection. Corneal graft surgery may restore vision

to patients with central corneal opacities.

BILATERAL RED EYES

Bacterial conjunctivitis

Acute bacterial conjunctivitis is a common cause of bilateral red

eyes. It presents with yellowish mucopurulent discharge and sticky

eyelids, especially in the morning. The sensation of grittiness or of

having a foreign body in the eyes is due to the rubbing of the

inflamed palpebral conjunctiva against the cornea. The diagnosis is

usually straightforward, especially when it occurs during an epidemic.

Intensive application of local antibiotic eyedrops every three hours

should cure the condition. It is, however, important to continue with

the eyedrops for two days after the infection has cleared clinically.

At night, an antibiotic ointment may be used for prolonged effect

and to prevent stickiness of the lids in the morning.

Padding of the eyes should be avoided as it tends to aggravate the

infection. If the condition does not improve in 48 hours, treatment

should be reviewed. Bacteriological swabs and cultures may then be

helpful.

Viral conjunctivitis

Viral conjunctivitis presents with bilateral watering red eyes. The

discharge is less than that in bacterial conjunctivitis. Sometimes, the

eyes are irritable and photophobic, owing to an associated keratitis

which may lead to blurred vision. The virus may also cause

preauricular and submandibular lymphadenopathy. A fever or an

upper respiratory infection may be associated. There is no specific

treatment. When there is corneal involvement, steroids can be used

under slit-lamp control. To prevent bacterial infection, antibiotics

may help.

Preventive measures, especially washing the hands after

examining each patient, must be taken during epidemics. Patients

should wash their hands, and handkerchiefs and hand towels should

not be shared. The family should be kept apart during the acute

stage.

Allergic conjunctivitis

Allergic conjunctivitis presents with intense itchiness, in addition

to watering, red eyes. Sometimes it is associated with vasomotor-

rhinitis or a history of allergies such as rashes, reaction to drugs or

cosmetics and hay fever.

Treatment with a decongestive or antihistamine eyedrop combined

with oral antihistamine is usually effective. Steroids should not be

used except in the occasional severe cases.

Spring catarrh (vernal conjunctivitis)

A specific allergic conjunctivitis which is less common is

spring catarrh. It is usually seasonal, mostly affecting boys. Large flat

papillary conjunctival thickenings form on the upper tarsal

conjunctiva. Corticosteroid eyedrops give relief. Corneal

complications occasionally develop.

Chronic non-specific conjunctivitis

Chronic non-specific conjunctivitis is a condition presenting with

a multitude of symptoms which include a sensation of dryness,

discomfort, irritation, burning, redness, and sometimes, watering and

pain as well. The eyes are constantly irritable particularly when

exposed to irritants which include bright sunlight, dust, smoke,

airconditioning and wind.

Examination usually shows no abnormality. Investigations should

be carried out to exclude specific causes such as inturned lashes

(trichiasis), defective tear flow

(dry-eye), chronic allergy or eyelid

infection (blepharitis).

Treatment depends on identification of contributory factors and

use of artificial tears, antihistamine drops and sometimes weak

vasoconstrictors. Antibiotics and steroids should not be used. The

condition tends to persist despite treatment and the patient requires

frequent reassurance.

Dry eyes

Dry eyes or keratoconjunctivitis sicca is due to defective tear

formation. Patients frequently present with symptoms similar to those

of chronic non-specific conjunctivitis.

The more common form is idiopathic. A more severe form is often

associated with secondary systemic conditions such as Sjogren's

syndrome (dry eyes, dry mouth and arthritis), connective tissue

diseases (rheumatoid arthritis, systemic lupus erthematosus), sarcodosis

and Steven Johnson's syndrome. Occasional serious corneal

complications, including corneal perforation, may develop.

Treatment

If mild, tear substitutes will help. Avoiding low humidity such as

air-conditioning and use of goggles are also useful. If more severe,

methods to preserve tears include occluding the punctum or

tarsorrhaphy.

UNILATERAL RED EYE

A unilateral red eye is a potentially dangerous condition. It may

be due to serious ocular conditions such as acute closed-angle

glaucoma, iritis, keratitis, corneal ulcer or a foreign body. Less

commonly it is due to scleritis. Of particular importance is acute

closed-angle glaucoma which presents with a unilateral red eye

associated with headache, pain in the eye or blurred vision. Prompt

consultation with an ophthalmologist is required.

Unilateral conjunctivitis is usually due to an underlying cause

such as a blocked nasolacrimal duct or trichiasis (inturned eyelashes).

It is important to carry out a thorough investigation of a unilateral

red eye to establish the cause.

Subconjunctival haemorrhage

This condition also presents as a unilateral red eye. Rubbing of

the eyes and severe coughing may cause capillary rupture resulting

in haemorrhage into the subconjunctival space. It is sometimes

spontaneous.

No treatment is normally required except to reassure the patient

that the haemorrhage will take one to two weeks to absorb.

Occasionally, the condition recurs. If it does, investigations to exclude

blood dyscrasia may be carried out.

TRACHOMA

This is a major worldwide blinding condition caused by infection

brought about by an organism known as “chlamydia trachomatis”. It

has a varying pattern in different countries. In the less developed

countries, it is endemic with up to 90% of some populations showing

signs of trachoma. In some areas 10% of those infected become

blind. It is not entirely clear why the organism behaves differently in

different environments.

The chlamydia presents a different clinical picture in developed

societies where it is benign and affects the genitals as well as the

eye and is called TRIC (trachoma inclusion conjunctivitis).

The clinical features vary considerably. At the initial stage, it may

be asymptomatic, or may present with acute conjunctivitis. The

signs of active infection are white, round follicles on the conjunctival

surface of the upper lids associated with a velvety papillary

hypertrophy. Follicles at the limbus leave small depressions known

as Herbert’s pits, which are permanent diagnostic signs of previous

trachoma. A layer of new blood vessels and connective tissue (pannus)

usually invades the upper cornea. Healing leads to scars. If

compounded by cyclical reinfection and superimposed bacterial

infection, entropion (inturned eyelid), trichiasis (inturned eyelashes)

and blindness due to opaque cornea or even endophthalmitis may

result.

In active trachoma, local broad spectrum antibiotics such as

tetracycline may be repeated twice a day for six weeks. This may be

combined with oral broad spectrum antibiotics or oral sulphonamides.

If mass surveys reveal that over 20% of the population are actively

infected, treatment is given to the whole population to eliminate the

infectious pool of chlamydia.

Surgical correction of entropion and trichiasis relieves discomfort

and decreases the risk of visual loss from corneal scarring and

infection. If there is corneal scarring, it is sometimes possible to

improve vision with corneal graft surgery.

In spite of advances in modern medicine, trachoma remains one of

the most difficult eye diseases to eradicate in developing countries

mainly because of poor and unhygienic living conditions which

include lack of water supply, dust and flies. These encourage cyclical

reinfection and superimposed bacterial infection.

RAISED CONJUNCTIVAL LESIONS

Pinguecula

This is a tiny, cream-coloured, slightly raised opaque lesion on

the conjunctiva, usually on the nasal side of the cornea but sometimes

on the temporal side. The pinguecula usually causes no symptoms. It

is common in the tropics, and may be related to exposure to the sun.

No treatment is required except for reassurance that it is not a

growth. Surgical removal for cosmetic reason is seldom required.

Pterygium

Pterygium is a triangular fleshy wing of conjunctiva which

encroaches on the cornea usually on the nasal side. Some pterygia

are vascular, thick and fleshy while others are avascular and flat. It

is usually bilateral and harmless but may cause mild astigmatism. In

rare cases, visual disturbance may result from the spread of the

pterygium across the pupillary area. This condition is common in

the tropics and is associated with exposure to the sun.

Simple excision by a variety of methods may be considered if the

pterygium encroaches on the cornea by 3 mm or more. Recurrence

is high in some countries (50%). To prevent recurrence, betatherapy

or thiotepa eyedrops may be applied with great care as they may

cause scleral necrosis. A newer technique, using conjunctival graft

from the same eye to cover the bare sclera after pterygium excision,

has a much lower recurrence rate and is preferred.

Conjunctival melanoma (naevus)

Benign conjunctival melanoma is a common harmless condition.

The lesion occasionally grows in size during puberty. It may be

removed for cosmetic reasons. Malignant conjunctival melanoma is

uncommon.

CORNEAL ULCER

Corneal ulcers are usually due to herpes simplex virus infection,

bacterial infection or trauma.

Herpes simplex dendritic ulcer

Herpes simplex dendritic ulcer is a serious infection of the cornea

caused by the herpes simplex virus. The eye is usually irritable, red,

watering and photophobic.

A typical branched dendritic ulcer usually develops. Sometimes,

there are complications such as disciform keratitis, a deep stromal,

disc-like inflammation of the cornea and iritis. The condition tends

to recur especially during periods of stress or fever. A number of

antiviral agents, such as ldoxuridine, are specific against the virus. In

some cases, the infected loose epithelium may be removed with

either a cotton bud after application of Amethocaine eyedrops, or by

the use of some other mechanical of chemical method. Steroid

eyedrops are absolutely contraindicated, as they lead to serious

corneal complications or even perforation of the eye. They should

be avoided even when the condition is quiet as they can precipitate

an attack of the infection.

Small marginal corneal ulcers

These are frequently associated with ulcerative blepharitis and are

believed to be due to hypersensitivity to staphylococcal antigens.

Treatment with antibiotic eyedrops is effective and may be combined

with steroids.

Bacterial corneal ulcer

The signs and symptoms are those of a unilateral red eye which is

painful, watering and photophobic. The vision is blurred. It is caused

by bacterial infection from a variety of organisms. The commonest

organisms are pseudomonas aeroginosa, staphylococcus, and

streptococcus. Of these, pseudomonas is the most dangerous as it

can lead to large destructive corneal ulcers rapidly. The risk factors

for bacterial ulcer are contact lens wear (especially prolonged wear

and unhygienic maintenance of lens), corneal trauma and

immunosuppression. Bacteriological studies are essential for precise

diagnosis and treatment. The ulcer should be scraped for examination

with gram stain.

Severe corneal ulcer

Severe corneal ulcers can often be prevented by adequate initial

treatment of minor injuries. Application of drops of broad-spectrum

antibiotics are particularly important in rural areas where ophthalmic

care is not immediately available. Severe and neglected corneal

ulcers lead to blindness from corneal scarring, corneal perforation,

secondary glaucoma and panophthalmitis.

Treatment is urgent. It includes intensive application of broad-

spectrum antibiotics drops usually consisting of an aminoglycoside

(gentamycin or tobramycin) and a cephalosporin

(cephazolin)

topically. In severe cases, subconjunctival injections and systemic

antibiotics are sometimes also required. Dilatation of the pupil with

Atropine eyedrops prevents synechiae (iris adhesions) and subsequent

glaucoma. In severe cases, therapeutic corneal grafting may be

required.

Fungal corneal ulcer

Corneal ulcers caused by a wide variety of fungi have a more

insidious and protracted cause. They are particularly likely to occur

in susceptible eyes with depressed immunity after prolonged treatment

with steroid or antibiotic drops and in eyes after injury with organic

material. Scrapings may reveal the fungus. Treatment is with local

and sometimes systemic antifungal agents. Eradication is often difficult

and corneal grafting may be required. Prognosis is poor.

CORNEAL OPACITY

If the corneal scarring is in the periphery, the vision remains

good, but when it is central it can interfere severely with vision.

Common causes are healed herpes keratitis, or ulcer trachoma, trauma

and keratomalacia from Vitamin A deficiency. In many cases a

corneal graft can restore vision.

Arcus senilis

This is a white ring at the periphery of the cornea, caused by lipid

deposits at the limbal region. The central cornea is never affected. It

is sometimes found in young adults (arcus juvenilis). The condition

is harmless.

Corneal dystrophies

Corneal dystrophies affect both eyes symmetrically. Keratoconus

is a dystrophic condition in young adults where the cornea becomes

conical in shape. The patient becomes highly short-sighted with

severe irregular astigmatism. Vision is initially improved with glasses.

Later, contact lenses may help to improve vision considerably. But if

the condition is advanced, contact lenses will not help. Corneal

graft surgery is highly effective.

Hereditary corneal dystrophies of various types cause minute

opacities in the central cornea. Some will lead to severe visual loss

early life and may require corneal grafting.

Fuch’s endothelial dystrophy presents with corneal oedema and

opacity. It can lead to severe visual loss. It usually occurs in the

middle-aged or the elderly and is more common in Caucasians than

Asians. It is caused by dystrophic changes in the corneal endothelium.

Sometimes, it follows a cataract extraction. Corneal graft surgery

may help.

Non-ulcerative (interstitial) keratitis

In the active stage, interstitial keratitis is bilateral and presents

itself as a patch of vessels with corneal opacity. In the later stages,

the eye is quiet with residual opacity of varying intensity in the deep

corneal layer and ghost vessels which are best seen under the slit-

lamp microscope. Congenital syphilis is the usual cause.

The acute stage responds rapidly to local steroids. Antibiotics may

be used if desired but the effect is usually insignificant. Defective

vision due to corneal opacity can be improved with corneal graft

surgery.

Corneal grafts

Corneal grafting is a surgical procedure in which donor cornea is

used to replace a diseased recipient cornea. Progress in transplantation

research and microsurgical techniques has improved graft survival

and visual prognosis in recent years.

The indication for corneal graft is usually for visual improvement

(optical). Common causes include post cataract surgery bullous

keratopathy

(corneal decompensation), keratoconus, corneal

dystrophies and corneal opacities. Corneal grafts can also be used for

therapeutic purposes for severe corneal ulcers.

LENS AND GLAUCOMA

INTRODUCTION

Cataract is a common cause of gradual painless visual

loss in the elderly. The usual indication for surgery is

when the patient’s vision has deteriorated to such an

extent that it interferes with his normal activities. Mature

cataracts can lead to complications. Cataract extraction

with an intraocular lens implant is the usual surgical

operation.

Glaucoma is a major cause of blindness. Open-angle

(chronic) glaucoma is asymptomatic. Acute closed-angle

glaucoma presents as a red eye associated with sudden

visual loss, ocular pain and headache. It blinds an eye

rapidly unless urgently and adequately treated.

CATARACT

A cataract is an opacity in the clear lens. Normally, the human

lens converges light rays. An opacity in the lens will scatter or block

the light rays. If the opacity is small and at the lens periphery, there

will be little or no interference with vision. On the other hand,

when the opacity is central and dense, the light rays can be severely

interfered with. This will lead to blurred vision.

The most common cause of cataract is old age and this is known

as senile cataract. Other causes are less common but should be

excluded in younger patients, including: trauma, drug toxicity (steroid),

metabolic diseases (diabetes and hypoparathyrodism) and ocular

diseases (uveitis and retinal detachment).

Management

The indications for surgery depend on the patient’s visual

requirements. Cataract extraction should be considered when the

patient’s normal activities are seriously interfered with. This is highly

subjective. For example, a young person may want earlier cataract

removal if it interferes with his occupation. On the other hand, an

elderly sedentary person may defer cataract surgery because of lower

visual requirements. Cataract extraction is also required if the cataract

is mature as it can lead to complications. Today, age and poor general

health are usually not contraindications for surgery because of early

mobilisation and the use of local anaesthesia.

Surgical removal of cataract is by the intracapsular or extracapsular

method. In intracapsular cataract extraction, the whole lens together

with its capsule is removed.

In extracapsular extraction, the nucleus and the cortex are removed

through an opening in the anterior capsule (anterior capsulectomy)

leaving the posterior capsule intact. It is the operation of choice in

countries where modern technology, in particular a good operating

microscope, is available. Ultrasonic disintegration of the nucleus

(phacoemulsification) to remove the cataract through a small incision

(3 mm) has been introduced and is becoming popular.

Phacoemulsification is a new variation of the extracapsular cataract

technique. In this operation, ultrasonic disintegration of the nucleus

enables the surgeon to remove the nucleus through a small incision

(less than

3 mm). While the final visual outcome between the

conventional extracapsular technique and phacoemulsification is the

same, there are certain advantages of phacoemulsification. These

include faster rehabilitation and less postoperative astigmatism.

However, this operation is machine dependent and is more expensive.

Optical correction

After cataract extraction, the eye will be without its lens. Therefore

an intraocular lens has to be inserted or cataract glasses have to be

used in order that objects can be focused sharply on the retina.

Unfortunately, the thick cataract glasses lead to difficulty in adjustment

owing to the enlarged image size, the peripheral distortion, and the

image jump. The use of contact lenses minimises the problem but

are difficult to manage. An intraocular lens placed within the eyeball

at the time of surgery gives excellent post-operative vision. It is now

the procedure of choice. After the cataractous lens is removed, the

intraocular lens implant is inserted behind the iris (posterior chamber

implant).

With the aid of the operating microscope, the cataract incision is

made and sutured with precision. Patients are not required to be

confined to bed and most can walk with help, as soon as they

recover from the effects of anaesthesia and sedation. Cataract surgery

is now usually performed as an outpatient procedure.

Cataract extraction is one of the most satisfying operations for

both the surgeon and the patient. Most patients regain their eyesight

or experience a considerable improvement in vision following a

successful extraction. Failure to restore normal vision is usually due

to an abnormality of the retina or the optic nerve.

Postoperative complications

Although cataract surgery is generally simple and effective, a

number of postoperative complications can occur. The most serious

is postoperative endophthalmitis (infection of the entire eye), which

can lead to blindness. Other complications include: wound leaks,

glaucoma, severe astigmatism, opacification of the intact posterior

capsule, retinal edema and retinal detachment.

Secondary cataract

Secondary cataract can develop in association with other diseases

of the eye such as following iridocyclitis or retinal detachment. It is

sometimes associated with trauma from injury or surgery.

Mass cataract blindness

Mass cataract blindness is on the increase, and in some nations

accounts for 80% of blindness. There is a need for eye surgeons to

put together an international plan to remove cataracts. Unnecessary

blindness can be prevented with low cost implant surgery,

extracapsular cataract extraction and posterior chamber lens

implantation. There are several organisations including The World

Cataract Surgeons Association recently formed for this purpose.

Quality cataract surgery is achievable in the hands of experienced

surgeons who have been well taught in extracapsular cataract

extraction and posterior chamber implantation under a good operating

microscope — successful results are obtained in 95% of cases and

some surgeons have attained almost 100% success.

GLAUCOMA

In the normal eye, there is a delicate balance between the inflow

and outflow of aqueous. When the outflow is blocked, the intraocular

pressure rises, leading to optic nerve damage. This condition is known

as glaucoma.

There are two main types of glaucoma:

• Open-angle glaucoma, which develops insidiously and leads to

slow and progressive damage to the optic nerve and visual loss

with few or no symptoms. Open-angle glaucoma has been referred

to as the "thief of sight."

• In contrast, acute closed-angle glaucoma, which develops suddenly,

is associated with pain, sudden visual loss and congestion of the

eye. Acute closed-angle glaucoma frequently presents as a painful

unilateral red eye.

Open-angle glaucoma is more common than closed-angle

glaucoma among Caucasians, while closed-angle glaucoma is more

common among the Chinese. Glaucoma causes 10% of blindness in

most countries.

PRIMARY OPEN-ANGLE GLAUCOMA (POAG)

Primary open-angle glaucoma is a condition of visual loss usually

associated with raised intraocular pressure. Although the filtration

angle is open, the trabecular meshwork at the filtration angle is

defective, leading to increased resistance to the outflow of aqueous.

The diagnosis is confirmed by visual field loss and glaucomatous

cupping of the optic disc. This is usually combined with raised

intraocular pressure. When the pressure is normal, the condition has

been referred to "normal pressure glaucoma". It is an insidious

condition usually presenting with no symptoms. The symptoms, if

present, are not dramatic and consist of frequent changes of glasses,

vague tiredness, ocular discomfort and increased difficulty with

reading.

Ocular hypertension

An intraocular pressure of more than 20 mm Hg suggests the

possibility of glaucoma. It is useful to note that a number of patients

with raised intraocular pressure of 30 mm Hg do not suffer any visual

field loss. This condition is called “ocular hypertension” and usually

requires no treatment, except for careful and regular reviews.

Visual field loss

Typical visual field changes develop in chronic open-angle

glaucoma. Early changes include an arcuate scotoma and later, the

loss of the nasal field. Late changes leave the patient with restricted

central vision although sometimes some temporal vision remains.

Optic cup

There is usually an increase in size of the optic disc cup in

association with the visual field loss. In advanced chronic open-

angle glaucoma, the cup reaches the edge of the disc. The retinal

vessels dip sharply over the edge of the cup and there is optic

atrophy.

Cup/disc ratio

As the size of the normal physiological cup varies with different

individuals it can be difficult to distinguish a glaucomatous cup from

a physiological cup. A method used to record the size of the optic

disc cups is the cup/disc ratio. The vertical diameter of the cup is

compared with the diameter of the disc and these are recorded as a

ratio. If the cup reaches the margins of the disc, it is designated 1.0.

If the cup extends across 40% of the disc diameter, it is recorded as

0.4. If the cup/disc ratio is greater than 0.5 or if there is asymmetry,

the possibility of glaucoma should be excluded.

Prevention and early diagnosis

Diagnosis is frequently made too late because of the lack of

symptoms in chronic open-angle glaucoma. To prevent this, periodic

measurement of intraocular pressure in all patients over the age of

40 is advisable, as open-angle glaucoma has been found in 1% -2 %

of older patients in many countries.

There is also a familial tendency in this condition. All relatives of

patients with chronic open-angle glaucoma should be regularly

reviewed.

The treatment for glaucoma can be either medical, via laser or

surgical. Medical treatment involves the use of different eyedrops to

control the intraocular pressure. The drugs act via either inhibition of

aqueous production or promote greater aqueous outflow.

The traditional medical therapy of choice is 2-4% Pilocarpine

(Cholinergic agonist) or 0.25-0.5% Timolol (Beta adrenergic blocker).

Additional drugs used include

1-2% Adrenaline, 1% Propine

(Adrenaline prodrug) and oral Acetazolamide (Carbonic anhydrase

inhibitor). New eye drops recently developed include: latanoprost (a

prostaglandin agonist), apraclonidine

(Adrenaline agonist),

dorzolamide (Carbonic anhidrase inhibitor) and brimonidine (alpha

adrenergic agonist). These drugs promise greater pressure lowering

effects as well as better patient tolerability. Current research includes

developing drugs which can protect the optic nerve against the

effects of high intraocular pressure (Neuroprotective agents).

If medical therapy proves unsatisfactory, laser trabeculoplasty,

which involves laser treatment of the trabecular meshwork, may be

used.

When both medical treatment and laser are not effective,

trabeculectomy is performed. This creates an artificial communication

between the inside of the eyeball (anterior chamber) and the outside

of the eyeball (the subconjunctival space). Failure due to scarring

has led to the use of inhibitors of scarring

(the antimetabolites

Mitomycin C or 5 fluorouracil).

ACUTE CLOSED-ANGLE GLAUCOMA

Acute closed-angle glaucoma is common in middle-aged patients.

Any middle-aged patient with a unilateral red eye associated with

blurred vision, pain or headache, should be suspected of having

acute closed-angle glaucoma. It occurs when the iris periphery

suddenly apposes itself to the corneal periphery and blocks the

filtration angle. This prevents aqueous from flowing into the outflow

channel, leading to a sudden rise in intraocular pressure.

The patient is frequently in pain, the eye is congested, and the

cornea is hazy due to epithelial oedema which is the initial cause of

the blurred vision. The pupil is semi-dilated and not reactive to light.

The anterior chamber is shallow but this is not easily observed. If

this is unrelieved, the increased pressure will cause permanent damage

to the eye, resulting in severe visual loss or blindness.

Treatment is urgent. The patient should be referred to an

ophthalmologist as soon as possible. Surgery is required after the

intraocular pressure has been medically reduced.

Medical therapy

Immediate intensive medical therapy to lower the intraocular

pressure is important. 1%- 4% Pilocarpine should be instilled every

ten minutes for the first hour, then less frequently. Acetazolamide

(500 mg) should be administered intravenously. Oral Acetazolamide

(1000 mg) should be given and repeated every four hours. Osmotic

agents such as Glycerol or intravenous Mannitol may be used. An

analgesic or tranquilliser should be given where appropriate.

Treatment must continue until the pressure is reduced.

Laser or Surgery

Laser iridotomy done with either the argon or neodymium YAG

laser is the treatment of choice. It is simple and safe. A new procedure

is to use contracting laser burns, known as iridoplasty, for angle

closure glaucoma. Alternatively surgical peripheral iridectomy is done

when the laser is not available. A filtrating operation (trabeculectomy)

may be necessary especially for patients who have failed to respond

to medical therapy. The decision on the type of surgery to be

performed and the timing for it can be determined only after careful

evaluation of the patient’s condition by an ophthalmologist.

The fellow eye

Acute closed-angle glaucoma is bilateral. The fellow eye is at risk

of developing an acute attack in 50% of cases in five years. A

prophylactic peripheral iridectomy should be performed on the fellow

eye. More recently, laser iridotomy has been used successfully.

Subacute and chronic closed-angle glaucoma

When the filration angle is less rapidly closed, the rise of pressure

will be subacute (subacute glaucoma). Accordingly, the symptoms

will be milder. The patient may complain of having transient blurred

vision, mild headache and of seeing ”halos“ (rainbow colours around

lights). Closed-angle glaucoma may even simulate chronic open-

angle glaucoma and has no symptoms until there is severe visual

field loss at an advanced stage of the condition (chronic closed-

angle glaucoma). Diagnosis for chronic closed-angle glaucoma is

made by gonioscopy.

SECONDARY GLAUCOMA

The intraocular pressure may be increased by a disease

process which blocks the outflow channel of the aqueous. In severe

iridocyclitis, the inflammatory proteins and cells or iris adhesions

may block up the outflow channel. In hyphaema (blood in the

anterior chamber), the outflow channel may be blocked by the

blood. New iris vessels (rubeosis iridis) which may develop following

central retinal vein occlusion and proliferative diabetic retinopathy

may lead to secondary haemorrhagic glaucoma

(neovascular

glaucoma) which is difficult to treat. Sometimes, glaucoma is a

complication of a mature cataract or intraocular tumours.

UVEAL TRACT, RETINA AND

VITREOUS

INTRODUCTION

Inflammation of the uvea (uveitis) is sometimes related

to systemic disease. Similarly, various retinal vascular

conditions, including retinal artery and vein occlusions

are associated with cardiovascular diseases.

Retinal detachment is a cause of sudden painless visual

loss. It should be referred for urgent surgery. With modern

surgical techniques, the prognosis is good.

Pathologic macular conditions are important. More than

half of recent blindness in developed countries is due to

diseases affecting the macula. Of particular importance

are age-related macular degeneration, high myopia and

diabetic retinopathy.

UVEITIS

Iridocyclitis (iritis)

Iridocyclitis, the inflammation of the iris and ciliary body, usually

presents as a painful unilateral red eye. It must be differentiated from

other common causes of a unilateral red eye, including acute closed-

angle glaucoma, foreign body injury, keratitis and corneal ulcer.

The symptoms include photophobia, mild pain, blurred vision and

watering. The pupil is small and slit-lamp examination shows flare

(proteins) and cells in the anterior chamber as well as deposits of

white cells (keratic precipitates) on the posterior surface of the cornea.

The inflamed iris may adhere to the anterior capsule of the lens

(posterior synechia). When the iridocyclitis is severe, secondary

glaucoma and secondary cataract may result. This condition tends to

recur.

The cause is usually difficult to determine. It may be associated

with joint diseases such as ankylosing spondylitis or Still’s disease

(juvenile rheumatoid arthritis) but rarely with sarcoidosis, syphilis,

leprosy, tuberculosis or viral infection.

Cycloplegics such as Atropine or Homatropine are used to dilate

the pupil and prevent posterior synechia. They also relieve the pain.

Steroid eyedrops reduce the inflammation. Investigations should be

carried out to exclude the known causes in severe and recurrent

iridocyclitis.

Chorioretinitis

Inflammation of the choroid and the retina, chorioretinitis, usually

presents with visual loss.

In the acute stage, if the inflammation is at the macula, the

patient will present with visual loss. Lesions which are not at the

macula may be silent and are found only when routine examination

shows a chorioretinal scar. In pars planitis

(chorioretinitis at the

extreme fundal periphery), the condition may remain silent for many

months or years and it only manifests itself when the vision is affected

by vitreous opacities or macular oedema.

In the majority of cases, the cause is unknown. In some cases, it

may be due to toxoplasmosis. Less commonly, it is associated with

syphilis, tuberculosis, sarcoidosis, toxocariosis

(worm infestation),

histoplasmosis and AIDS.

Investigations to find the cause should be carried out. Treatment

can be difficult. The use of systemic steroid may help in addition to

therapy for specific infections. Recurrences are common.

CHOROIDAL TUMOUR

Naevus (benign choroidal melanoma)

A naevus is a flat, round, pigmented, choroidal lesion rarely causing

any visual disturbance. It is usually easy to distinguish between a flat

benign naevus and a raised malignant choroidal melanoma.

Malignant choroidal melanoma

A pigmented, raised lesion of the choroid is usually a malignant

choroidal melanoma. It sometimes presents with retinal detachment,

and occasionally with vitreous haemorrhage or secondary glaucoma.

Because of this, malignant melanoma should be excluded in unilateral

blind eyes of uncertain etiology. It is more common in Caucasians

than in other races.

Enucleation of the eye is usually required. In selected patients

with only one good eye left, or those with small tumours, irradiation,

photocoagulation or surgical excision may be used. Recent statistics

indicate that small, malignant choroidal melanoma may be kept

under observation but without treatment, provided they are regularly

evaluated.

Choroidal matastasis

Choroidal metastasis may result from a wide variety of cancers

including breast and lung cancer. It is rare. It usually presents in the

eye as flat multiple deposits at the posterior pole. Usually it is

associated with an exudative retinal detachment. Treatment with

radiotherapy may help to retain vision for the limited lifespan of the

patient.

VASCULAR OCCLUSION

Central retinal artery occlusion

In occlusion of the central retinal artery the patient notices sudden

visual loss in one eye and, within a few minutes, the eye may become

totally blind.

Complete obstruction of the central retinal artery presents a

characteristic ophthalmoscopic picture a few hours after the attack.

The larger retinal arteries are constricted and look like thin threads

while the smaller vessels are scarcely visible. The fundus appears

milky white because of retinal oedema. In contrast to this, there is a

cherry-red spot at the macula where the retina is thin and where the

red choroidal circulation shows through. Haemorrhages are not seen

in central retinal artery occlusion unless the vein is also occluded.

After a few weeks, the retinal swelling subsides and the retina

regains its transparency but the disc becomes pale because of atrophy

of the optic nerve. The retinal arterioles remain narrow.

The use of vasodilators and emergency attempts to lower the

intraocular pressure are normally ineffective. However, if treatment

is given within a few hours of the onset, there is a slight chance of

visual recovery. For this reason, treatment should be attempted.

Elderly patients with central retinal artery occlusion must exclude

temporal arteritis by blood ESR and occasionally, by biopsy of the

temporal artery. Failure to recognise this cause, which is controlled

with high doses of steroids, may lead to blindness in the fellow eye.

The more common causes of central retinal artery occlusion include

arteriosclerosis with or without hypertension and emboli from diseased

heart valves or carotid atheroma.

Central retinal vein occlusion

Occlusion of the central retinal vein is less abrupt in presentation

than occlusion of the central retinal artery. Visual impairment occurs

gradually and the loss of sight is less complete. The patient is left with

visual acuity of counting fingers.

The predisposing causes are hypertension, diabetes mellitus,

arteriosclerosis in the elderly, open-angle glaucoma and factors or

conditions which increase coagulability of the blood including the

use of oral contraceptives.

Examination with the ophthalmoscope shows grossly tortuous and

engorged retinal veins, especially near the optic disc. Very often,

unilateral disc oedema is present. Scattered all over the retina, from

the disc to the periphery, are haemorrhages of all shapes and sizes.

These are accompanied by soft exudates.

After a period of many weeks, the haemorrhages clear gradually

and there is little evidence of the occlusion, except for shunt vessels

on the optic disc. Vision fails to be restored in the majority of the

elderly but the prognosis for younger patients is better.

The development of new vessels on the iris (rubeosis iridis) is due

to ischaemia of the retina. These vessels may obstruct drainage in

the filtration angle and cause painful secondary thrombotic glaucoma.

This happens in about one-third of the patients if untreated with

laser.

Medical investigations may reveal predisposing systemic diseases.

Photocoagulation is used to prevent secondary thrombotic glaucoma.

If this condition develops, medical therapy to lower the pressure

may control the pain.

Branch retinal vein occlusion

The visual symptoms depend on the site of occlusion. If the macula

is involved, the patient will complain of blurred vision. The fundal

changes show a characteristic fan-shaped distribution of retinal

haemorrhages which radiate from the arteriovenous crossings. The

haemorrhages are usually flame-shaped.

Macular oedema may sometimes persist, and swelling disrupt the

fovea leading to visual loss. Moreover, vitreous haemorrhage from

abnormal retinal vessels, either shunt or new vessels, may cause

sudden visual loss.

After some months, there is re-establishment of local circulation

around the site of the occlusion and the haemorrhages and exudates

are absorbed.

Branch retinal vein occlusion usually occurs at an arterovenous

junction, that is, where a vein is crossed by a sclerotic artery. The

superior temporal vein is the branch most commonly affected. If

either this vein or the inferior temporal vein is occluded, the macula

may be involved. The main predisposing causes of branch retinal

vein occlusion are longstanding hypertension (85%), arteriosclerosis

and diabetes.

Laser photocoagulation may be used to ablate the damaged

capillary bed if macular oedema decreases vision or when there is

danger of vitreous haemorrhage from abnormal new vessels.

RHEGMATOGENOUS RETINAL DETACHMENT

Retinal detachment is the separation of the retinal neurosensory

layer from the retinal pigment epithelium. It is caused by tears (holes)

which are usually located at the peripheral areas of the retina. These

tears develop in degenerate or thin retina. An important factor is

degenerate vitreous which collapses with age and may cause traction.

Retinal detachment is most common in patients with degenerative

(high) myopia, in the elderly and as a result of ocular injuries.

The symptoms of a retinal tear include seeing multiple floaters of

recent onset and flashes of light. Vitreous floaters have been described

by patients as dots, flies or cobwebs in their field of vision. If the

patient has seen single floaters for many months, it is usually harmless.

On the other hand, a large number of floaters appearing suddenly

together with flashes of light in patients with myopia or in the

elderly requires retinal assessment by an ophthalmologist. Retinal

tears may cause vitreous haemorrhage or lead to separation of the

retina from the pigment epithelium and choroid, resulting in sudden

visual loss.

With the development of retinal detachment there is in addition

loss of peripheral visual field. The typical symptom described is “a

curtain obstructing part of the vision”. If the macula is affected, there

is a sudden loss of central vision.

Ophthalmoscopy shows a loss of the red reflex with areas of

detached retina appearing grey and undulating.

A superior temporal detachment is an ocular emergency. The

spread of the subretinal fluid due to gravity may detach the macula

leading to permanent defective central vision. Bed rest is urgently

required until surgery can be carried out.

Diagnosis is confirmed by an ophthalmologist by examining the

retina with full dilatation of the pupils with an indirect

ophthalmoscope. The indirect ophthalmoscope gives a better view

of the peripheral retina than the direct ophthalmoscope.

It is important to find all the retinal tears (holes) as all tears have

to be sealed with firm scars. These scars are produced by

cryoapplication, diathermy or photocoagulation. For technical reasons,

laser photocoagulation and cryoapplication are the most popular.

Silicone material is frequently used to push the wall of the sclera

inwards to close the tear. Drainage of subretinal fluid helps to flatten

the retina against the sclera. Occasionally, intravitreal surgery

(vitrectomy and gas injection) may be required.

As retinal detachment is a bilateral disease, similar changes are

frequently found in the other eye which should also be thoroughly

examined with the indirect ophthalmoscope.

Exudative and traction retinal detachment

Less commonly, retinal detachment is not due to a retinal tear but

to exudation as in malignant choroidal melanoma, severe uveitis or

toxaemia of pregnancy. Another cause of detachment is fibrous

traction in proliferative diabetic retinopathy, penetrating injury and

retinopathy of prematurity.

MACULAR DISEASES

Macular diseases are major causes of blindness. In developed

countries, blindness today is rarely caused by infection or

malnutrition but mainly by degenerative, metabolic and vascular

conditions affecting the macula.

Common chronic macular lesions which cause gradual loss of

central vision include degenerative high myopia, juvenile macular

dystrophy and age-related macular degeneration. The common acute

macular conditions are central serous retinopathy, macular

haemorrhages, and disciform macular degeneration. Diffuse retinal

conditions which affect the macula include retinal vein occlusion

and diabetic retinopathy.

Many macular diseases are as yet untreatable. More effective

treatment can be developed only with a better understanding of

retinal metabolism and pathophysiology.

Juvenile macular dystrophy

This occurs in the young who often has a history of a similar

disease in the family. It is bilateral and symmetrical and causes

gradual painless loss of vision. A variety of clinical entities exist with

presumably different underlying genetic defects.

There is no effective treatment. Precise diagnosis, visual aids and

genetic and occupational counselling are useful.

Age-related maculopathy

Age-related maculopathy (senile macular degeneration) is a bilateral

degeneration of the macula. It causes loss of central vision. It accounts

for over 20% of blindness in Caucasians (less than 6/60 visual acuity)

but is less prevalent in other races.

The patient usually complains of gradual increasing disturbance

of central vision. One letter or word may appear at a different level

from its neighbour or there may be missing letters or words.

The ophthalmoscopic picture varies. The macula usually has fine

pigmentary clumps and patches of atrophy. White round spots called

drusen (colloid bodies) are frequently seen. They are waste deposits

located just beneath the retinal pigment epithelium. Drusen by

themselves are usually harmless, especially if they are few in number

and are sharply-demarcated. Large or confluent drusen are frequently

associated with macular degeneration.

Sometimes, vision may be suddenly lost because of an acute

complication of age-related maculopathy. A localised, raised

exudative lesion due to subretinal bleeding from new vessel

proliferation from the choroid (subretinal neovascularisation) may

develop at the macula. If untreated, this may lead to scarring and

loss of vision.

Urgent fundal fluorescein angiographic tests should be carried out,

as subretinal neovascularisation at an early stage may be effectively

treated with laser photocoagulation.

It is important to emphasize to patients with macular degeneration

that they will not go totally blind from the condition as peripheral

vision will not be affected. Some patients benefit from the use of

strong glasses and a variety of visual aids for distant and near vision.

These include magnifying lenses and special telescopic spectacles.

Central serous retinopathy

This condition is common in males from 20 to 50 years of age. It

occurs spontaneously and is characterised by fluid leaking from the

choroidal capillaries through the pigment epithelium and subsequently

accumulating under the macula. The aetiology is unknown.

The patient complains of sudden disturbance of central vision

which is generally described as a dulling, darkening or blurring of

vision. In most cases, there is micropsia (objects appearing smaller)

and the ability to discriminate colour is sometimes reduced.

Ophthalmoscopically, the macula shows a characteristic round

swelling with a ring reflex at its border. Diagnosis is confirmed by

fundal fluorescein angiography which shows a leaking defect in the

retinal pigment epithelium.

The condition is usually self-limiting and benign. If severe or if it

persists for many months, photocoagulation may be used. Recurrences

are common.

Degenerative (high) myopia

Degenerative myopia is often familial and is characterised by a

progressive increase in the axial length of the eye and by chorioretinal

atrophy. The atrophy is more pronounced at the posterior pole of the

eye and may cause loss of central vision, sometimes from macular

haemorrhage. The loss of central vision is proportional to the amount

of macular involvement. Another complication which may develop

is detachment of the retina.

Direct ophthalmoscopy is difficult owing to the high refractive

error. The view is improved by examining the fundus through the

patient’s glasses or contact lenses. The disc shows a typical crescent

or ring of chorioretinal atrophy surrounding its margin.

No treatment can change the progress of this condition. Vocational

guidance may be useful prior to the loss of central vision. The rate of

deterioration is unpredictable.

Retinitis pigmentosa

Retinitis pigmentosa is characterised by detective vision in dim

light and progressive loss of peripheral field. The hereditary pattern

may be recessive, dominant or sex-linked. Onset of symptoms is in

the first or second decade of life. The vision usually deteriorates to

blindness by the fifth or sixth decade. The ophthalmoscopic signs

include proliferation of retinal pigment with a characteristic dark

brown spider-like appearance, a waxy-yellow disc and attenuated

retinal vessels.

It is important to study the family history in this condition to

establish genetic risks. Electroretinography is abnormal before

ophthalmoscopic signs develop.

Retinitis pigmentosa is sometimes associated with a variety of rare

systemic abnormalities such as deafness, cataract and glaucoma.

Therefore, regular ophthalmic examination is recommended.

VITREOUS CONDITIONS

Degeneration of the vitreous occurs as a result of age and in high

myopia. The vitreous becomes more fluid and may spontaneously

detached itself from the retina. As it causes flashes and floaters, the

presence of a retinal tear has to be excluded. Floaters are a particularly

common ocular complaint and are usually harmless.

Other forms of vitreal degeneration which are sometimes present

but harmless are white deposits, asteroid bodies and synchisis

scintillans.

Vitreous haemorrhage is a cause of sudden visual loss. It is caused

by trauma, retinal tear or abnormal blood vessels, especially in

diabetic retinopathy. The blood may be absorbed over many months.

However, if the blood does not absorb, vitrectomy — a surgical

method of removing blood from the vitreous — may help to restore

vision in blind eyes.

OCULAR MANIFESTATIONS OF

SYSTEMIC DISEASES

INTRODUCTION

Many systemic diseases have ocular manifestations.

The most important is diabetic retinopathy. Laser

photocoagulation prevents blindness in the majority of

patients if treatment is started early.

Other systemic conditions affecting the eye are

hypertension, thyroid and rheumatoid diseases. In some

developing countries, keratomalacia (vitamin A deficiency)

and onchocerciasis (filarial worm infection) are major

causes of blindness.

DIABETES MELLITUS

Refractive changes

Blurring of vision in a diabetic patient is sometimes the result of

refractive changes in the eye. These are due to fluctuation in the

blood-sugar level and occur frequently when diabetics commence

treatment. The patient should be assured that the refractive changes

will stop once the blood-sugar level is stabilised and that the condition

will not cause any permanent loss of vision.

Extraocular muscle paralysis

Diabetes sometimes affects the third or sixth cranial nerve. A third

cranial nerve lesion due to diabetes may be associated with a

unilateral headache. The pupil is usually not affected. The condition

resolves itself within three months.

Pupil and iris abnormalities

The pupils may respond sluggishly to light or fail to dilate with

mydriatic eyedrops. Neovascularisation of the iris may develop

(rubeosis iridis) in some patients with severe proliferative diabetic

retinopathy.

Cataract

Senile cataract develops more often in a diabetic and at a younger

age. It may develop rapidly as a dense fluffy white cataract in a

young diabetic with severe uncontrolled diabetes.

DIABETIC RETINOPATHY

The most important ocular manifestation of diabetes is diabetic

retinopathy. It is now a major cause of blindness in developed

countries and is rapidly becoming an important cause of blindness

in some developing countries.

The development of diabetic retinopathy is related to the length

of time that the patient has had diabetes. The main reason for the

increase in diabetic retinopathy in recent years is that with better

medical treatment diabetics now live longer. In some countries

diabetic retinopathy has been found in one-third of the diabetic

population.

Classification of diabetic retinopathy

(1) Background diabetic retinopathy

(2) Proliferative diabetic retinopathy

(1) BACKGROUND DIABETIC RETINOPATHY

The changes are usually found at the posterior pole, in the area

between the superior temporal and the inferior temporal retinal

vessels. They consist of retinal microaneurysms, round dot

haemorrhages and hard exudates. The characteristic minute red round

spots are either microaneurysms or dot haemorrhages. The hard

exudates appear as minute yellow, well-defined deposits. These are

usually multiple and scattered. They may become more extensive

later and form large confluent patches.

Preproliferative diabetic retinopathy

In preproliferative diabetic retinopathy, vascular obstructive changes

are seen. These obstructive features include soft exudates (cotton

wool spots), large blot haemorrhages, dilated or segmented veins

and venous loops. These changes indicate more severe (ischaemic)

retinal damage and fundal fluorescein angiography shows loss of

capillary circulation.

With maculopathy

Background diabetic retinopathy progresses slowly over the years.

The majority of the patients do not lose their central vision. Some

develop changes in the macula resulting in the deterioration of central

vision. This complication of diabetic retinopathy is known as

maculopathy. Depending on the amount of haemorrhage and exudate,

the degree of oedema and capillary loss at the macula, the vision

can fall to less than 6/60 in severe maculopathy.

(2) PROLIFERATIVE DIABETIC RETINOPATHY

A more severe type of diabetic retinopathy known as proliferative

diabetic retinopathy sometimes develops. This must be recognised

early as severe visual loss, otherwise blindness can ensue rapidly.

Fortunately, a pre-proliferative stage can be recognised and may

remain for many years before the dangerous proliferative changes

develop.

The proliferative stage is established when new vessels develop.

This occurs in about 10% of patients with diabetic retinopathy. The

new vessels grow on the retinal surface and at the optic disc. They

tend to bleed into the vitreous. Fibrous tissue formation leads to

traction retinal detachment.

Prognosis

The visual prognosis depends on the type and severity of the

retinopathy. Most patients with background diabetic retinopathy do

not develop visual loss. In proliferative diabetic retinopathy, the

visual outlook is worse. The presence of diabetic retinopathy,

especially proliferative diabetic retinopathy, usually reflects the

general state of health of the patient. Renal and microvascular

complications may result in a shorter life span.

Management

If laser photocoagulation is done at an early stage, the majority of

blindness from diabetic retinopathy is preventable.

As the early fundal changes can be easily missed, the fundus of all

diabetics should be regularly examined with the pupils dilated.

All diabetics without fundal changes require strict metabolic control

and dietary advice to delay or prevent the development of diabetic

retinopathy and other complications. The patients should have annual

fundal examination to detect early retinal changes.

Diabetics with retinopathy require an analysis of their diet,

metabolic control and life-style. The presence of retinopathy should

be regarded as a warning that the control may have been sub-

optimal over an extended period of time. Ophthalmic assessment

should include colour fundal photography and fundal fluorescein

angiography. If vision is threatened, photocoagulation should be

carried out.

Photocoagulation

A photocoagulator produces intense light (argon laser or xenon)

which is focused on the retinal pigment epithelium where the light

beam is converted to heat. The resulting small chorioretinal burns

form scars and destroy abnormal vessels.

Photocoagulation is effective in preventing blindness due to diabetic

retinopathy. It should be carried out in the presence of diabetic

maculopathy or pre-proliferative diabetic retinopathy. In proliferative

diabetic retinopathy, extensive photocoagulation (known as pan retinal

photocoagulation) is necessary to prevent vitreous haemorrhage and

traction retinal detachment.

HYPERTENSION AND ARTERIOSCLEROSIS

Hypertension primarily affects the retinal arterioles. In young

patients the arterioles react to moderately raised blood pressure by

constriction. The ophthalmic signs are either diffuse or focal

constriction of the arterioles.

In middle-aged patients however, the walls of the arterioles become

thickened (arteriosclerosis) and are unable to constrict. The thickened

walls show a widening of the normal light reflex. As the thickening

of the wall progresses, it gives a copper appearance to the blood

column (copper wiring) and then a white appearance (silver wiring).

At the arteriovenous crossings, the thickened arteriolar walls displace

and constrict the veins (arteriovenous nipping). These changes are

common in middle-aged patients with chronic hypertension. They

may lead to a branch retinal vein occlusion.

In more severe hypertensives, the arteriolar wall is damaged by

necrosis leading to flame-shaped haemorrhages and soft exudates

(cotton wool spots) caused by microinfarcts of the retina. Sometimes

retinal oedema is present. Chronic retinal oedema at the macula

results in hard exudates radiating from the macula (macular star).

Finally papilloedema results. When this happens, the patient has

malignant hypertension. Vision is usually normal except when there

is associated macular involvement.

Hypertensive retinopathy

Many attempts have been made to classify hypertensive retinopathy,

of which the Keith-Wagner classification is the most useful. In the

first two grades changes are limited to the retinal vessels, but in

Grade III, retinal haemorrhages and soft exudates are present. In

Grade IV there is papilloedema.

Grade I

In young patients with mild hypertension, minimum constriction

and irregularity of the arterioles are found. In older hypertensives

however, there is often no arteriolar constriction but a widening of

the light reflex of the arterioles because of the thickened sclerotic

arteriolar wall.

Grade II

The arteriolar changes in Grade II are similar to those in Grade I

except that they are more obvious. The retinal veins at the

arteriovenous crossings appear constricted and are seen

ophthalmoscopically as arteriovenous nippings.

Grade III

Superficial flame-shaped haemorrhages appear near the disc with

soft exudates. The retina is oedematous. Occasionally, small hard

exudates may also appear.

Grade IV

Papilloedema is an ominous sign of malignant hypertension. When

retinal oedema is substantial and prolonged, small hard exudates

collect and radiate from the macula in a characteristic star-shaped

formation.

Significance

The significance of grading is that the fundal changes reflect the

severity of the hypertension and the state of the arterioles elsewhere

in the body. Furthermore, when the fundal changes are reversed, it

serves as a good indication of the control of the hypertension.

Pre-eclamptic hypertension

In pre-eclamptic toxaemia or hypertension of pregnancy, there is

a marked spasm of the arterioles as they are not sclerotic in young

patients. All the more severe signs of hypertension may be

superimposed. The condition is frequently associated with bilateral

exudative inferior retinal detachment.

Other vascular retinopathies

Severe anaemia is frequently associated with flame-shaped

haemorrhages and soft exudates. The retinopathy has no unique

features and is common in conditions where there is an associated

platelet deficiency such as in pernicious anaemia and leukaemia.

Hyperviscosity retinopathy occurs in any condition which increases

the blood viscosity such as hyperglobulinaemia and polycythaemia

vera. The retinal veins are engorged, associated with retinal

haemorrhages, occasional soft exudates and oedema. The fundus is

very similar to that found in central retinal vein occlusion.

Sickle-cell anaemia is a hereditary condition (ss or sc haemoglobin)

common in Negroid populations. Owing to occlusion of small vessels

at the retinal periphery and ischaemia, fibrovascular proliferation

occurs. Localised chorioretinal scars are also characteristic of the

condition. Vision may be lost from vitreous haemorrhage or traction

retinal detachment but this can be prevented with photocoagulation.

Peripheral retinal vasculitis with vitreous haemorrhage

(Eales’

disease) is characterised by recurrent vitreous haemorrhages associated

with abnormalities of the peripheral retinal veins. This condition

occurs particularly in young adult males who are otherwise well.

The cause is unknown but was once thought to be due to sensitisation

to tuberculosis. Photocoagulation or cryotherapy of abnormal retinal

vessels can prevent recurrent vitreous haemorrhage. Blindness from

vitreous haemorrhage can be reversed in many cases by vitrectomy.

THYROID DISEASE

Hyperthyroidism (Graves disease)

Hyperthyroidism is associated with lid retraction and lid lag, and

sometimes, with exophthalmos. The eyelid signs may be unilateral

or bilateral. Bilateral lid retraction gives a typical staring appearance.

Other signs include poor convergence and infrequent blinking.

Thyroid exophthalmos

Thyroid exophthalmos is caused by orbital oedema and lymphocyte

infiltration. It may develop with or without hyperthyroidism, or

following treatment for hyperthyroidism. The ocular signs are

exophthalmos with oedema of the lids and conjunctiva. Sometimes

there is restriction of ocular movement, particularly for elevation. As

a result, the patient is unable to look upwards. Although the

exophthalmos is usually bilateral it can be unilateral. A CT scan is

useful for diagnosis. It helps to differentiate a unilateral exophthalmos

from that of a retrobulbar space-occupying lesion and it usually

shows typical thickened extraocular muscles.

Complications

Severe thyroid exophthalmos may lead to difficulty in closing the

eyelids, a condition known as lagophthalmos. This may cause

exposure keratitis with corneal dryness, ulceration and infection.

The increased intraorbital pressure may also damage the optic nerve.

Treatment

Hyperthyroidism should be treated. High doses of oral steroids

may control the progressive exophthalmos. Surgery may be necessary

to protect the cornea or to decompress the orbit. Surgical correction

of diplopia after the disease has burnt itself out may also be

necessary.

AIDS

Cotton-wool spots in the fundi are the most common ocular lesions

in AIDS. They are ischaemic lesions possibly caused by vasculitis

and may be associated with flame-shaped haemorrhages. More severe

vasculitis can lead to necrosis and haemorrhagic retinitis.

Other ocular features include neoplasms in the eyelid, conjunctiva

or orbit., e.g. Kaposi sarcoma, neuro-ophthalmic lesions and

opportunistic infections.

The most common ocular opportunistic infection is

cytomegalovirus (CMV) retinitis. This produces a characteristic picture

of white retinal lesions associated with haemorrhage resembling

“crumbled cheese and ketchup”. Treatment includes the use of

gancyclovir, an anti-viral agent. Other opportunistic pathogens include

toxoplasma gondii, herpes simplex and zoster, candida albicans and

pneumocystis carinii.

INFECTION AND MALNUTRITION

In developing countries, infection and nutritional diseases like

onchocerciasis and keratomalacia are major causes of blindness.

Their eradication depends on dealing with the problems of poverty

— poor living conditions, diet and health education at grass root

level with the help of thousands of paramedics. In the People’s

Republic of China, the “barefoot” doctors are reported to be effective

in controlling blindness which has resulted from malnutrition and

infection.

Keratomalacia (Vitamin A deficiency)

Keratomalacia is an acute condition of the cornea due to Vitamin

A deficiency in the child. It is frequently precipitated by a

gastrointestinal upset. It starts with xerosis (dryness of the conjunctiva)

and may lead to melting and perforation of the cornea (keratomalacia).

The International Agency for the Prevention of Blindness has estimated

that a quarter of a million children in the world are blinded annually

by this condition.

Onchocerciasis (river blindness)

This major blinding condition is due to the invasion by

microfilariae resulting from the bite of the jinja-fly which is common

in parts of West Africa. The eye complications include iritis,

secondary glaucoma, cataract and vitreoretinal damage. Blindness is

common in the affected communities. The condition is prevented by

the elimination of the vector fly. This is unfortunately not always

possible. Treatment of the established condition with antihelminthic

drugs or surgery does not restore vision.

Leprosy

This affects the eye in 30% of the cases but most of the ocular

complications are not serious. The facial nerve may be involved

resulting in paralysis of the orbicularis oculi muscle ectropion

(everted lid) and lagophthalmos (inability to close the lids) leading to

exposure keratitis. There may also be madarosis (loss of eyebrows

and eyelashes). Keratitis and anterior uveitis are uncommon.

Syphilis

This may affect the eye at all stages of the disease. The primary

sore rarely occurs on the eyelid or conjunctiva. At the secondary

stage, it may cause uveitis. Optic atrophy occurs as a complication

of tertiary syphilis. In congenital syphilis, bilateral interstitial keratitis

and chorioretinal scars may develop.

Tuberculosis

Many inflammatory ocular conditions, including scleritis and

uveitis, are said to be associated with a focal tuberculous infection.

However, it is unlikely that tuberculosis is a significant causative

agent in these and other ocular diseases of unknown etiology.

OTHER CONDITIONS

Rheumatoid arthritis

Rheumatoid arthritis can affect the eyes in several ways. It may

cause persistent irritation and congestion on account of dry eyes.

Episcleritis is a common cause of localised redness of the eyes in

rheumatoid patients. Scleritis may be localised, nodular or diffuse.

When severe, there is necrosis of the sclera known as scleromalacia.

Rheumatoid arthritis can also be complicated by long-term therapy

with Chloroquine or steroids. Chloroquine can cause maculopathy

and corneal deposits. Cataract may develop with long-term systemic

steroid therapy.

Muco-cutaneous diseases

Acne rosacea may cause chronic conjunctivitis or blepharitis and

more importantly, severe superficial keratitis with corneal

vascularisation. It is usually bilateral with a tongue-like opacity of

the cornea and, if it affects the pupillary region, severe visual loss

will result. Acne rosacea is common among Caucasians in Europe.

Treatment is with steroid eyedrops.

Stevens-Johnson’s syndrome is an acute inflammation of the skin

and mucous membrane. The eruptions are sometimes caused by a

drug. The most common ocular manifestation is severe conjunctivitis

which may result in corneal scarring with dry eyes and corneal

opacity. Treatment with artificial tears, contact lenses and plastic

surgical procedures may help.

NEURO-OPHTHALMOLOGY

INTRODUCTION

The visual pathway or the third, fourth, fifth and sixth

cranial nerves are frequently affected by diseases of the

central nervous system. Because the clinical features are

often sensitive indicators of neurological diseases, a

special field of ophthalmology has developed — neuro-

ophthalmology.

An important problem is to determine whether the optic

disc swelling is due to papilloedema, papillitis or

ischaemic optic neuropathy. Optic atrophy is a common

clinical manifestation which requires diagnosis and a full

neurological evaluation. A chiasmal lesion causes a

bitemporal hemianopic field defect whereas a post-

chiasmal lesion causes a homonymous field loss.

OPTIC DISC SWELLING

The ophthalmoscopic picture of optic disc swelling shows blurring

of the disc margin and swelling of the optic nerve head, with filling

in of the central physiological cup. The veins are dilated and venous

pulsations are absent. There are often small superficial haemorrhages

confined to the immediate disc area, and oedema of the surrounding

retina. In early disc swelling, fundal fluorescein angiography may

help to determine its presence.

Papilloedema or papillitis

The ophthalmoscopic appearance of disc oedema in papilloedema

and papillitis is the same. Papilloedema is differentiated from papillitis

by the presence of other clinical features.

Papilloedema is a passive swelling of the optic disc commonly

caused by raised intracranial pressure. The condition is usually

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bilateral. Vision is normal unless the macula is affected by oedema

or exudates. Rarely is the vision diminished because of optic atrophy

in severe unrelieved papilloedema. The visual fields and colour vision

are also normal although the blind spot is sometimes enlarged. The

pupillary reflex to light is normal.

Papillitis is an inflammation of the optic nerve, frequently of

uncertain aetiology. Disseminated sclerosis is an important cause.

The condition is usually unilateral. Because the optic nerve is

inflamed, there is usually marked visual loss. A central scotoma is

present and the eye may have defective colour vision, especially to

red. The pupil is dilated, with sluggish or no reaction to direct light.

PAPILLOEDEMA

PAPILLITIS

Visual Acuity

Normal (usually)

Reduced

Pupil

Normal

Poor response to

direct light

Visual Field

Normal (increased

Central scotoma

blind spot)

or field defect

Colour Vision

Normal

Defective

Usually

bilateral

unilateral

Differential diagnosis of papilloedema and papillitis.

Ischaemic optic neuropathy

Ischaemia to the optic nerve head from arteriolar sclerosis and

temporal arteritis also causes sudden visual loss with a swollen optic

disc in the elderly population. It is important to exclude temporal

arteritis by blood erythrocyte sedimentation rate

(ESR). Systemic

steroids will protect the unaffected eye. The prognosis for the affected

eye is usually poor and optic atrophy usually follows.

Pseudo-papilloedema

Pseudo-papilloedema is a variation in the appearance of the optic

disc which is sometimes mistaken for true disc oedema. It should be

clearly differentiated from the latter in order to avoid unnecessary

investigations and anxiety to the patient.

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One common cause of pseudo-papilloedema is hypermetropia

where the disc margin is blurred. Other common causes include

drusen (yellowish-white deposits at the optic disc) and opaque

myelinated nerve fibres. Fundal fluorescein angiography can help to

distinguish pseudo-papilloedema from true disc oedema.

RETROBULBAR NEURITIS

Retrobulbar neuritis is an inflammation of the optic nerve with

similar symptoms and signs as papillitis except that the optic disc

oedema is absent. The clinical features include pain on movement

of the eyes, sudden blurred vision, defective colour vision and a

central scotoma. The cause is usually unknown but some patients

have underlying disseminated sclerosis. There is no specific treatment.

Steroids may be used to speed up recovery of the central vision.

OPTIC ATROPHY

Because the colour of the optic disc varies in normal individuals,

a pale optic disc does not necessarily signify the presence of optic

atrophy. Optic atrophy is confirmed where a pale optic disc is

associated with defective visual acuity and visual field.

There are numerous causes of optic atrophy and they include

optic neuritis, meningitis, encephalitis, central retinal artery

occlusion, chronic ischaemia of the optic nerve, compression of the

optic nerve or chiasma, trauma, chronic glaucoma, retinitis

pigmentosa, congenital and familial disorders, and exogenous factors

such as toxic processes, malnutrition, vitamin B deficiency and

syphilis. The cause is frequently undetermined.

Neurological investigations must be carried out to exclude

compression of the optic nerve by intracranial tumours and other

treatable causes.

CHIASMAL LESION

A chiasmal lesion causes a characteristic bitemporal hemianopic

field defect. A chromophobe adenoma is the most common cause.

The presence of optic atrophy and poor visual acuity usually indicates

that the condition is already at a very advanced stage. Diagnosis is

made by finding the characteristic field defect and confirmed by

radiology of the skull. It should be differentiated from other causes

of a chiasmal lesion such as a suprasellar cyst (craniopharyngioma)

or meningioma.

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Post-chiasmal lesion

A post-chiasmal lesion causes a homonymous hemianopic field

defect. It is usually due to either a cerebrovascular occlusion or a

tumour. The optic tract, the optic radiation or the visual cortex may

be affected. If the lesion is further back at the occipital lobe, the

homonymous hemianopia tends to be congruous (similar). If

the lesion occurs further forward and affects the optic tract, the

homonymous hemianopia will tend to be incongruous (dissimilar). At

the optic radiation, a homonymous quadrantic field defect may

occur because the visual pathway is spread out over a relatively

large area.

Computerized tomography and nuclear magnetic

resonance scans

CT scan and now NMR are commonly used in neuro-ophthalmic

investigations. They permit accurate localisation of pathology

affecting the visual pathway. These investigations are also particularly

valuable in evaluating the extent of intracranial lesions.

PUPILS

The pupils may be abnormal in size or shape or in their reaction

to light and accommodation.

Large pupil

A large pupil may be caused by mydriatic eyedrops, optic neuritis,

optic atrophy and oculomotor nerve paralysis. It may also be caused

by blunt injury to the eye which has damaged the pupillary sphincter

(traumatic mydriasis), or by advanced disease of the retina. Less

commonly, it is due to Adie’s tonic pupil.

Small pupil

A small pupil can be caused by miotic eyedrops such as

Pilocarpine. Other causes include iritis, Argyll Robertson pupil due

to syphilis, morphine and Horner’s syndrome (sympathetic paralysis).

In Horner’s syndrome, pathology in the sympathetic pathway manifests

as an ipsilateral miosis, partial ptosis, apparent enophthalmos and

anhidrosis.

Irregular pupil

A pupil which is irregular may be due to a congenital iris defect,

posterior synechiae from iritis, Argyll Robertson pupil, or surgery.

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Reaction to light

A pupil which is not reactive to direct light but which is reactive

to consensual light suggests that the eye is severely damaged or

blind from disease of the retina or the optic nerve (Marcus Gunn

pupil). A pupil which is not reactive to either direct or consensual

light indicates local disease or injury to the sphincter of the iris, or

damage to the third cranial nerve, the nerve supply of the pupillary

sphincter. Sometimes it is due to the use of a mydriatic.

In the Argyll Robertson pupil there is no reaction to light but the

pupils react to accommodation.

EXTRAOCULAR MUSCLES

Paralytic squints

In severe paralysis of the extraocular muscles, the diagnosis is

usually obvious. Lesions of the third nerve lead to ptosis and a

relatively immobile eyeball which deviates downwards and outwards.

This deviation is due to the paralysis of all the extraocular muscles

except for the lateral rectus and the superior oblique. The pupil is

dilated.

In lesions of the sixth nerve, there will be a convergent squint. In

lesions of the fourth nerve, the superior oblique muscle is paralysed.

The eye is elevated when it is in an adducted position because of

the overaction of the inferior oblique muscle. The patient often has a

compensatory head posture to avoid double vision.

Numerous conditions may result in paralysis of the extraocular

muscles. The cause is often difficult to determine and special

investigation may be required. Trauma, diabetes, arteriosclerosis,

intracranial aneurysms and tumours are the most common causes.

In slight paralysis the ocular movements are apparently normal.

The patient complains of double vision and the diagnosis can be

difficult. The following simple questions may help to confirm the

presence of muscle paralysis.

• Is double vision present when both eyes are open? Is double

vision present when one eye is closed? Extraocular muscle paralysis

causes binocular double vision. If double vision is present when

one eye is occluded, it is not due to paralysis of the extraocular

muscles.

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• Does the separation of images occur side by side or one above

the other? In sixth nerve paralysis the separation is side by side

while in third or fourth nerve paralysis the separation is one

above the other.

• In which direction of gaze does the maximum separation occur?

Maximum separation of images occurs in the direction of action

of the affected muscle. For example, there will be maximum

separation of images when the patient looks to the left if the left

lateral rectus muscle is affected.

• In which eye is the image fainter? The fainter image is seen by the

eye with the paralysed muscle. If there is left lateral rectus muscle

paralysis, there will be a horizontal separation of images and the

fainter image is seen with the left eye.

The cover test for diagnosis of strabismus and special optical tests

are required to investigate patients with diplopia and to chart their

progress.

Myasthenia gravis

Myasthenia gravis causes weakness of the skeletal muscles,

especially in young adults. The extraocular muscles are frequently

affected. Thus, the patient may present with intermittent and varying

double vision and ptosis which is usually bilateral. The symptoms

are classically more pronounced in the evening. They can be

precipitated clinically by asking the patient to keep a sustained

upward gaze for a minute or two.

Diagnosis can be confirmed by demonstrating a reversal of

symptoms with intravenous tensilon.

NYSTAGMUS

Nystagmus is an involuntary, oscillatory movement of the eyes.

Jerk nystagmus has a slow and fast component and is usually

maximum in a particular position of gaze. It is caused by neurological

conditions which affect either the cerebellum, the vestibular system

or their connection. Patients with jerk nystagmus require a full

neurological evaluation.

Ocular (pendular) nystagmus has no slow or fast component. It is

caused by poor vision and the patient’s inability to fix his gaze. As a

result the eye develops a pendular movement.

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Both jerk and pendular nystagmus are often congenital.

MIGRAINE

Migraine is a common cause of headaches. Often there is visual

disturbance prior to the onset of the unilateral headache. This

presents as sparkling or flashing lights followed by a positive field

defect. The symptoms are unilateral. The headache is frequently

associated with nausea and vomiting. The symptoms are usually

relieved by resting quietly in a darkened room. There is frequently a

family history of migraine.

Occasionally, migraine-like attacks are due to pathological lesions

such as intracranial aneurysms and tumours. Severe, atypical

persistent migraine or migraine of late onset requires neurological

investigation.

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Complete Third Nerve Paralysis

Fig. 7.19

Complete left ptosis (looking straight ahead).

Fig. 7.20

Fig. 7.21

Left inferior oblique paralysis

Left superior rectus paralysis

(looking up and right).

(looking up and left).

Fig. 7.22

Fig. 7.23

Left medial rectus paralysis

Normal left lateral rectus

(looking right).

(looking left).

Fig. 7.24

Fig. 7.25

Left superior oblique action

Left inferior rectus paralysis

is limited (because of inability

(looking down and left).

to adduct: looking down and

right).

Note: Third cranial nerve supplies levator palpebrae superioris besides

medial, superior and inferior rectus and inferior oblique muscles.

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EYE DISEASES IN CHILDREN

INTRODUCTION

A rare but important ocular condition in children is

retinoblastoma, a malignant tumour which usually presents

as a “white pupil”. Early diagnosis may save the life of the

child.

Squint is common in children, especially in Caucasians,

and should be evaluated and treated early to prevent loss

of vision from amblyopia (lazy eye).

Other common conditions include conjunctivitis,

blocked nasolacrimal duct and congenital cataract.

WHITE PUPIL (DIFFERENTIAL DIAGNOSIS)

White pupil or leukocoria is diagnosed in a child when the red

reflex is abnormally white. The most important condition to exclude

is retinoblastoma. Other causes include:

• Retinopathy of prematurity

(retrolental fibroplasia). In this

condition, there is a history of prematurity and the use of oxygen.

• Dense congenital cataract. This is easily recognised.

• Persistent primary hyperplastic vitreous. The eye is abnormally

small.

• Coats’ disease. There is massive exudates from abnormal retinal

vessels.

• Endophthalmitis (inflammation of the whole eye due to infections).

• Organised vitreous haemorrhage.

Retinoblastoma

Retinoblastoma is the commonest intraocular malignancy in

children. It is a developmental tumour of retinal origin. There is a

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strong genetic component and the patient's family should undergo

genetic counselling and screening for possible retinoblastoma.

Retinoblastoma is an important cause of the white pupil (cat’s eye

reflex) in children. Usually, the condition is detected when an

abnormal whiteness appears in the child’s pupil. This is most obvious

in dim light when the pupil is partially dilated. In most cases, the

presence of the white reflex indicates that the condition is at an

advanced stage.

As retinoblastoma is highly malignant and can spread rapidly, it

must be differentiated from other causes of a white pupil.

The differential diagnosis can be difficult even for an experienced

ophthalmologist. A child with a white pupil should be urgently referred

to an ophthalmologist to establish the cause. Examination under general

anaesthesia with full dilatation of the pupils is required to determine

the diagnosis and exclude retinoblastoma.

Management

An eye with an advanced retinoblastoma usually requires removal

as soon as possible. As retinoblastoma frequently affects the fellow

eye, this should also be examined under anaesthesia with full dilatation

of the pupil. These examinations have to be repeated at regular

intervals. If early retinoblastoma is found, it can be treated with a

combination of chemotherapy, radiotherapy, photocoagulation and

cryoapplication.

Retinopathy of prematurity

All premature babies, especially those who require oxygen, should

have their fundus examined by an ophthalmologist for early signs of

retinopathy. Oxygen causes constriction and obliteration of premature

blood vessels in the peripheral retina. This leads to new vessel

proliferation exudation, scarring and retinal detachment. Treatment

by photocoagulation, cryotherapy or even vitreous surgery may be

indicated.

SQUINTS IN CHILDREN

A squint (or strabismus) is a deviation of an eye, so that its visual

axis is no longer parallel with that of its fellow eye.

Squints can be congenital (occurring at birth) or acquired (occurring

later on in life). They may be latent (suppressed when both eyes are

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open) or manifest (present all the time). Squints may also be divided

into those associated with paralysis of a muscle (paralytic squint) or

where no obvious evidence of paralysis exists (non-paralytic or

concomitant squint). In a paralytic squint the degree of deviation of

the eyes is not the same in all fields of gaze. In a non-paralytic or

concomitant squint the degree of deviation is the same in all directions

of gaze.

Paralytic squints

The ocular manifestations of paralytic squints in children are

generally similar to those in adults, except that the child does not

complain of double vision. To avoid double vision, the child suppresses

the use of one eye, leading to amblyopia. Sometimes, the child adopts

a compensatory head tilt to avoid double vision.

Non-paralytic squints

This is the commonest form and can be either horizontal or vertical.

Horizontal squint can be either convergent (esotropia), where one of

the eyes is turned inwards, or divergent (exotropia), where one of the

eyes is turned outwards. In vertical squints, one eye is higher than the

other.

A convergent squint is often associated with hypermetropia (long

sight). Correction of the hypermetropia with glasses can reduce the

squint. This type of squint is known as accommodative convergent

squint. It is common in Caucasian children but not in other races. A

divergent squint in a child usually develops after the age of three

years and is often associated with myopia.

Frequently, a non-paralytic squint is precipitated by illnesses such

as measles or chicken pox. An important consideration in young

children is that the squint may occasionally be due to poor vision or

secondary to ocular disease, of which retinoblastoma is the most

important.

Effects of squint on children

There are three effects of squint on children

• Amblyopia (lazy eye)

• Failure to develop binocular single vision.

• Cosmetic blemish. This can lead to emotional and socioeconomic

problems.

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Management

The child should be referred to an ophthalmologist as soon as a

squint is suspected for exclusion of ocular pathology, especially

retinoblastoma, and to commence treatment for amblyopia.

Refraction with Atropine or other cycloplegics should be carried

out and, where necessary, appropriate glasses prescribed. Glasses for

children with accommodative convergent squint may be adequate to

correct the squint and these glasses should be used constantly.

Early diagnosis and treatment may prevent the development of

amblyopia or increase the chances of reversing it. Treatment includes

patching of the good eye until maximum improvement of the

amblyopic eye is obtained. This is usually supervised by an

orthoptist. Patching can be tedious, and needs the co-operation of

the child and its parents.

Surgery may be necessary. In a convergent squint, surgery is directed

at weakening the medial rectus muscle and strengthening the lateral

rectus muscle. The opposite procedure is done in a divergent squint.

In squints which have a vertical element, surgery becomes more

complicated as it involves surgery on one of the vertically acting

muscles, that is, the superior or inferior rectus, or one of the oblique

muscles. Although it is usual for the eyes to be straightened at one

operation, it may occasionally require more than one operation.

It is important to explain to the parents that even after surgery to

straighten the eyes, patching of the good eye and continued supervision

are required.

Amblyopia

Amblyopia is an important condition in children and is present in

up to 5% of some populations. In a squint, whether paralytic or non-

paralytic, the child suppresses the use of one eye in order to avoid

double vision. Persistent suppression of the eye causes amblyopia,

(sometimes referred to as a lazy eye).

It is important to treat a child with squint as early as possible since

amblyopia can frequently be prevented or reversed by patching the

good eye to stimulate the squinting eye to function.

Refractive amblyopia is due to anisometropia

(difference of

refraction in each eye), bilateral high astigmatism or hypermetropia

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(long-sight). Amblyopia can also be caused by ptosis, corneal scar,

cataract or congenital nystagmus.

Pseudo-squint

Pseudo-squint is usually due to marked medial epicanthal eyelid

folds which give the appearance of a convergent squint. Diagnosis is

confirmed by observing the corneal reflex and the cover test. As the

child grows older, the skin folds tend to become less marked. No

treatment, only reassurance, is required.

INFECTIOUS CONJUNCTIVITIS

Conjunctivitis occurring in the first 28 days after birth is referred to

as ophthalmia neonatorum. In the past, the infection was usually due

to gonorrhoea. In recent years, better antenatal care in most countries

has made gonorrhoea less common. Other causative organisms include

staphylococcus, streptococcus, haemophilus, pneumococcus, coliform

organisms, herpes simplex virus and chlamydia (TRIC organism found

in the genital tract of females).

In gonococcal infection, there is acute purulent conjunctivitis which

can perforate the cornea and lead to blindness.

If the conjunctivitis is severe, urgent treatment with systemic and

local therapy is required. The child may have to be hospitalised with

barrier nursing to prevent the spread of the infection. However, many

milder cases of conjunctivitis can be treated as outpatient cases, with

hourly applications of antibiotic eyedrops until the infection clears. It

is important to clean the discharge regularly with sterile (boiled) cotton

wool soaked in saline or water.

LACRIMAL SYSTEM (TEARING)

Blockage of the lacrimal drainage system in a child usually occurs

at the nasolacrimal duct. Within the first few weeks of life one eye is

noticed to water and to be stickier than the other. Pressure with the

finger on the lacrimal sac often produces a reflux of mucopurulent

material. This is due to late canalisation of the lacrimal drainage

system which first develops as a solid cord of epithelial cells and

normally canalises at about the time of birth. Occasionally, it is not a

developmental abnormality but is due to blockage of the nasolacrimal

duct by debris.

Treatment is conservative, with application of astringent eyedrops

(Zinc sulphate 1/4%) and daily massage of the lacrimal sac with the

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pulp of the finger (with short nail) for the first six months. Antibiotics

are used only where there is an infection. Most cases will clear. If the

condition persists, or if the infection is recurrent or severe, the child

should be referred to an ophthalmologist for syringing under general

anaesthesia. If there is a blockage, it may be necessary to probe the

nasolacrimal duct. Surgery to anastomosise the sac to the nasal mucosa

(dacryocystorhinostomy) is rarely required in children.

CONGENITAL CATARACT

Congenital cataract with minimal lens change which does not

interfere with vision usually requires no surgery. When it is bilateral

and dense, surgery should be performed in the first six months. Dense

congenital cataracts should therefore be referred for an ophthalmic

opinion as soon as possible. Where the cataract is not dense and

where there is a fair view of the fundus, the decision for surgery can

be difficult. It is advisable to wait until the child is older, when visual

acuity can be more accurately determined.

In addition to surgery, an important part of management is to

ensure good visual function. The main objective is to prevent

amblyopia. Orthoptic support and cooperation from parents are

important.

To see clearly the child requires either cataract glasses or contact

lenses. Recently some surgeons have tried lens implantation in selected

situations.

If the cataract is unilateral, the conventional approach is not to

remove it surgically unless there is an unsightly white reflex at the

pupil. This is because despite surgery, the eye usually remains

amblyopic. However, recent reports suggest that the vision can be

good if appropriate steps to prevent amblyopia are taken early in life.

This requires intensive treatment by a dedicated team and is only

pursued in some centres.

Surgery involves aspiration of the lens after opening the anterior

capsule under the operating microscope. This is possible because the

nucleus of the child’s lens is soft.

CONGENITAL GLAUCOMA

Congenital glaucoma is rare. In infants, raised intraocular pressure

causes the cornea to increase in diameter from 11 mm to over 13

mm. Because of the increase in size, this condition is also known as

buphthalmos (ox eye). It causes tears in the Descemet’s membrane,

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leading to corneal oedema, irritation and watering of the eye combined

with photophobia. If left unrelieved, the raised intraocular pressure

will damage the optic nerve, resulting in glaucomatous cupping and

optic atrophy.

Referral to an ophthalmologist of an infant with photophobia and

tearing or a large and opaque cornea enables early diagnosis and

treatment, and may prevent blindness. Surgery and life-long follow-

up is necessary.

PHAKOMATOSES

This is a group of congenital or hereditary abnormalities which

affect the skin, the nervous system and also the eye in varying

degrees.

Neurofibromatosis (von Recklinghausen’s disease) is characterised

by pigmented patches of the skin (cafe-au-lait spots) and subcutaneous

tumours of varying sizes. The brain stem or cerebellum may be affected

by the tumours. The ocular manifestations include neurofibromas in

the eyelids, orbit, retina and optic nerve gliomas.

Tuberous sclerosis (Bourneville’s disease) is a disease in which

gliomas of the brain are associated with sebaceous adenoma of the

face. These are distributed across the nose and face in a typical

butterfly pattern. Occasionally, the retina or optic disc has a yellowish

raised nodule which looks like a mulberry.

Sturge-Weber syndrome is a capillary haemangioma or “portwine

stain” affecting the distribution of the fifth nerve on the face. Capillary

haemangioma may also affect the cerebral cortex. Sometimes, the

eye on the side of the lesion, develops congenital glaucoma which

can be difficult to treat. Choroidal angioma may also be present.

Von Hippel-Lindau disease is a condition with an elevated

haemangioma at the retinal periphery associated with large feeding

retinal vessels. Many have associated cerebellar or brain stem

haemangioma. The haemangioma often causes exudates and

haemorrhages in the retina and vitreous and can lead to retinal

detachment. The retinal lesions should be treated with

photocoagulation, diathermy or cryoapplication.

DEVELOPMENTAL ABNORMALITIES

There are a large number of developmental abnormalities which

occur in mild or severe forms. The mechanism is not fully known.

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Some are associated with antenatal infections, teratogenic drugs and

chromosomal abnormalities or hereditary defective genes.

The abnormalities may affect the whole skull and face, giving rise

to a number of syndromes such as craniofacial dysostosis, mandibulo-

facial dysostosis and meningo-encephalocele.

The whole eye may be affected in anophthalmos (absence of one

eye, congenital cyst and microphthalmos — small eye). Coloboma of

the iris or choroid is due to the absence of a part of the eye as a result

of incomplete closure of the choroidal fissure.

Common abnormalities which affect the lids include congenital

ptosis, coloboma of the lid and obstruction of the lacrimal apparatus.

The lens may be abnormal in shape or dislocated as in Marfan’s

syndrome and homocystinuria. Persistent hyaloid (embryonic vitreous)

artery and hyperplastic primary vitreous which presents itself as a

white pupil may also occur.

A number of abnormalities may occur at the optic disc. These

include optic pits and hypoplasia of the optic nerve, which is an

occasional cause of poor vision in childhood.

ANTENATAL INFECTIONS

Antenatal infection can lead to congenital syphilis, rubella or

toxoplasmosis. The common manifestations of rubella are congenital

cataract and nystagmus. Both syphilis and rubella can cause

pigmentary changes of the retina. Congenital toxoplasmosis causes a

typical localised pigmented chorioretinal scar at the macula.

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OCULAR INJURIES

INTRODUCTION

Ocular injuries are common. Some may be so trivial

that only reassurance is required. On the other hand, some

injuries are so severe that the eye is inevitably lost.

Ocular injuries may be due to any of the following:

• Chemical injury

• Injury from “flying” particles

• Injury from sharp instruments

• Blunt injury

• Ocular injury associated with head injury

• Welding burns

Visual acuity is extremely important in the assessment

of ocular injuries for evaluation and for medico-legal

reasons. The eye should be systematically examined.

However, when a large penetrating wound of the cornea

or sclera is suspected, it would be prudent not to examine

the eye in detail, as a forceful examination may cause

further ocular damage. Antibiotic eyedrops should be

applied and the eye covered with a sterile eyepad. The

patient should be referred immediately to an

ophthalmologist.

PREVENTION

Many ocular injuries are preventable, and the physician may be in

the best position to give advice.

Chemical Injury

Chemical injuries due to strong alkalis or acids are potentially

blinding and require urgent treatment.

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It is important to dilute the chemical as soon as possible: it is really

quite futile to try to determine whether the chemical is an acid or an

alkali — as is frequently recommended in textbooks. The time to act

is immediately after the injury has occurred, and it is important to

advise that treatment should be started immediately by whoever is

available and not wait for the arrival of the doctor.

The eye should be irrigated with sterile fluid (if available) or with

tap water immediately, and this should be continued for at least ten

minutes.

The severity of the damage to the eye depends on the nature of the

chemical. Strong alkalis and acids can cause severe irreversible

damage with total blindness.

Alkaline burn injuries are more serious because the alkali penetrates

the eye and destroys its internal structure leading to complications

such as cataract, severe iridocyclitis and glaucoma. Acid coagulates

collagen and this forms a barrier which may prevent penetration of

the chemical into the eye. Therefore it does not normally cause damage

to the internal structures.

Chemical injuries occur in laboratories and in chemical industries.

Supervisors, teachers, students and workers should be warned that if

any chemical gets into the eye, it should be immediately washed off

with any available bland fluid or tap water. Protective eyeshields for

those at risk should be used. Welding burns and injuries from “flying”

particles in industries can be prevented by the use of goggles or

special guards.

Injury From “Flying” Particles: Superficial Corneal

Foreign Particle

Flying particles usually come from two sources: a working hammer

or chisel or a revolving machine. When the velocity of the foreign

particle is great, it will penetrate the eye. Otherwise, it is commonly

embedded in the cornea presenting as a corneal foreign body, leading

to severe photophobia, congestion and irritation of the eye. Infection

is prevented by the use of antibiotic eyedrops. The foreign body is

removed after administering a drop of local anaesthetic with the aid

of a magnifying loupe.

Foreign bodies within the pupillary area should be referred to an

ophthalmologist as a corneal scar at this site can lead to severe visual

loss.

130

For removal of foreign bodies, the use of a blunt instrument is

recommended to avoid perforation of the globe — a sharp instrument

such as a hypodermic needle should be used with caution because

the danger of perforation is great.

Injury From Sharp Instruments

Penetrating wound

A penetrating wound is usually due to a sharp or pointed

instrument which has penetrated the eyeball. Loss of vision may be

the result of direct damage to the cornea or to the lens, causing

cataract. There may also be intraocular haemorrhage or retinal

damage. The patient usually gives a history of a sharp or pointed

instrument hitting the eye. It is important to obtain a precise history of

the nature of the injury. The patient may complain of pain, watering

eye and photophobia. The pupil is sometimes deformed due to a

prolapsed iris.

Treatment is urgent. Antibiotic eyedrops are applied locally after

the affected area has been cleaned. The eye should be covered with

a sterile eyepad to immobilise the eyelids. It is unwise to try to

examine the eye in detail, especially if there is a large penetrating

wound, as the eye can be further damaged during examination. The

patient should be referred immediately to an ophthalmologist as surgery

is generally urgently required.

Blunt injury

Blunt injuries may damage the eye in many ways. Hyphaema is

an important common injury. It is due to bleeding in the anterior

chamber from a torn blood vessel in the iris. As the blood settles to

the lowest part of the anterior chamber, a horizontal level of blood

is seen. Often associated with this is a semi-dilated, immobile pupil

known as “traumatic mydriasis” resulting from damage to the iris

sphincter.

If neglected, further bleeding may occur leading to secondary

glaucoma, and a blood stained cornea. Because of this, hyphaema is

an ocular emergency. The patient should be urgently referred for

hospitalisation and bed-rest to prevent further bleeding.

If there is evidence of secondary glaucoma, surgery may be

necessary to evacuate the blood clot from the anterior chamber.

131

Other complications which may develop from a blunt injury are

cataract, dislocation of the lens, damage to the macula, vitreous

haemorrhage and retinal detachment. Because so many structures

may be damaged, patients with severe blunt injuries of the eye should

be referred for ocular assessment as soon as possible.

Blowout fracture

A blunt injury sometimes does not injure the eyeball itself, but

may instead fracture one of the thin walls of the orbit, usually the

floor. This will cause the contents of the orbit to protrude into the

maxillary antrum. The inferior rectus and inferior oblique muscles

may be involved and result in double vision and limited elevation

of the eye. Further evaluation is necessary and surgery is usually

required.

Ocular Injury Associated With Head Injury

An ocular injury associated with a head injury is sometimes

overlooked because the lid swelling makes it difficult to examine the

eye and also attention is often diverted to problems.

In patients with severe head injuries, especially if there is bruising

around the orbit, it is important to carry out a careful examination of

the eyes and orbits.

Ocular injuries include damage to:

• Orbital wall — blowout fracture

• Optic nerve

• Extraocular muscles or their nerve supply

• Ocular structures

Welding Burns (Arc Burns)

Within eight hours following exposure to intense ultraviolet light,

the worker and even those observing the job may complain of severe

photophobia, blepharospasm, pain and watering of the eyes.

A drop of local anaesthetic can be used to facilitate examination

to ensure that the symptoms are not due to some other injury.

Treatment consists of relieving the symptoms of pain and photophobia

with analgesics and patching the eyes. Use of local anaesthetic drugs

for pain relief should be avoided. This conditions usually subsides in

24 hours.

132

REFRACTIVE ERRORS

INTRODUCTION

A common cause of blurred vision is refractive error.

This is a physiological condition where the refracting system

of the eye fails to focus objects sharply on the retina. It is

usually corrected with glasses. A useful rapid test to

distinguish between refractive error and disease of the eye

is the use of a pin-hole.

In modern societies, contact lenses are sometimes

preferred to glasses mainly for cosmetic reasons. When

contact lenses are used, it is important for the wearer to

take the necessary precautions to prevent complications

as serious ocular damage may occasionally develop.

REFRACTIVE ERROR

Myopia

Myopia (short sightedness) is an optical condition where distant

objects are focused in front of the retina so that vision for distance is

blurred, but near vision is normal. Myopia is measured by the power

in diopters of the concave lens needed to focus the light onto the

retina.

Myopia is common in Asians, especially the Chinese. Studies have

shown that up to 80% of the Chinese student population may be

myopic compared to 25% in Caucasians. In addition, there are

indications that myopia is becoming more common and more severe

with time. Myopia exerts a socioeconomic burden on society. The

cost of myopic correction in the United States alone is estimated to

be 2 billion dollars per year.

A strong genetic component probably exists with myopia but there

have been also suggestions that myopia is related to changing

140

environmental factors, especially in Asia. These include increasingly

prolonged close work activities among the young in Asia.

There are 2 types of myopia. The commonest form of myopia is

known as simple or physiological myopia. It is usually slow or non-

progressive and not associated with any degeneratives changes of the

retina.

It is important to distinguish simple myopia from the other form,

pathological myopia. The latter is more serious but found in only a

small percentage. Pathological myopia is usually seen in people with

more than 6 diopters of myopia associated with progressive

degenerative changes of the retina, affecting, in particular, the macula.

This degeneration, known as myopic maculopathy, sometimes leads

to blindness. In addition, patients with pathological myopia have a

higher risk of developing glaucoma, cataract, retinal tears and retinal

detachment.

Glasses are the usual way of correcting myopia, and they are

usually prescribed by an ophthalmologist or an optometrist. Contact

lenses are also a popular and efficient means of correcting myopia.

Laser refractive surgery is increasing in popularity as an alternative

means for correction.

Current research is focused on preventing or slowing the progression

of myopia. Studies include the use of bifocal glasses, contact lens and

eye drops (atropine).

Common myopia is known as simple myopia, and it is not associated

with any degenerative changes of the retina. It is important to

distinguish simple myopia from progressive myopia. The latter is a

serious form of myopia found in a small percentage of people,

frequently associated with progressive degenerative changes of the

retina, affecting, in particular, the macula. This sometimes leads to

blindness, unlike simple myopia.

Fig. 10.1

Simple myopia corrected with a concave lens.

141

Hypermetropia

Hypermetropia (long sightedness) is a condition where a distant

object is focused behind the retina. In the young, because of the

strong accommodative power of the lens, hypermetropia is

compensated for. With age, however, the power of accommodation

decreases and the patient soon finds that he is unable to compensate.

This begins with difficulty in focusing for near vision and later, for

distance. Because of this, the patient requires the use of reading

glasses earlier in life. With time, glasses are required for distant vision

as well.

Fig. 10.2

Hypermetropia corrected with a convex lens.

Astigmatism

Astigmatism is a condition where the image cannot be focused

sharply on a point because either the cornea or the lens is not spherical

and has greater power in one meridian. Marked astigmatism causes

poor vision, both distant and near. It is corrected with a cylindrical

lens. A cylinder is shaped like a food can with no power in one axis

and maximum power at right angles to that axes. Sometimes the

astigmatism is irregular. This is caused by corneal scarring or by

keratoconus (conical cornea). Irregular astigmatism is usually difficult

to correct with glasses. Contact lenses frequently help.

Fig. 10.3

Astigmatism corrected with a cylindrical lens.

142

Presbyopia

(old-age sightedness) is a condition of weak

accommodation brought about by age. A young child has considerable

ability to accommodate. This diminishes with age owing to progressive

weakness in accommodation and near vision becomes progressively

worse. Glasses for near vision are required even though the distant

vision is perfect. For people who require correction for both distant

and near vision in a single pair of glasses, bifocals are sometimes

recommended.

EYE STRAIN

Uncorrected refractive errors or wrongly prescribed glasses may

lead to symptoms which include red eyes, blurring, watering, tired

eyes and headaches which may be ocular, frontal or diffuse. There is

often a close relationship between eye strain and the use of the eyes

for reading, driving, or an occupation which requires close visual

concentration. Patients show great individual variation in the tolerance

of refractive error. Some are sensitive to minor changes in their glasses

while others are not bothered by gross refractive errors.

The symptoms of eye strain may also be due to muscle imbalance,

poor convergence, a patient’s neurotic state, or a variety of drugs,

and occasionally, systemic diseases.

In presbyopic patients, the symptoms are relieved by the use of

reading glasses and stronger focal light when reading.

CONTACT LENS

Contact lenses are now widely used. There are basically two types

of contact lenses — hard and soft. Hard contact lenses have been

available for about 30 years. However, they are not as comfortable to

wear and require careful fitting. For this reason, soft lenses have

become more popular, being easy to fit and well-tolerated.

Optically, contact lenses function in the same way as glasses. They

help to focus the image sharply on the retina.

There are several reasons why contact lenses are used. The most

common one is cosmetic. The lenses are very popular with young

female myopic patients who are willing to tolerate any discomfort or

inconvenience in order to improve their appearance.

Contact lenses are also used by sportsmen who find that glasses

fog with perspiration and by stage or television personalities who find

143

it less attractive to wear glasses. They may be contraindicated in

dusty or industrial conditions.

Soft contact lenses are sometimes used therapeutically to bandage

a corneal ulcer which fails to heal or to prevent discomfort from

chronic corneal epithelial disturbance.

Complications

A common complication, especially with hard lenses, is overwear.

This leads to corneal oedema. The patient gives a history of having

used the lenses longer than usual. He complains of pain, watering,

photophobia and eyelid spasm

(blepharospasms). Because of

complications, any contact lens wearer who complains of persistent

pain or discomfort should have the cornea assessed by an

ophthalmologist.

The main problem with soft contact lenses, however, is the risk of

corneal infection which may lead to corneal ulcers and blindness.

Another problem with soft lenses is the development of giant

papillary conjunctivitis due to a hypersensitivity reaction. The patient

complains of redness, itching, irritation and mucoid discharge. Eversion

of the upperlid will reveal characteristic giant papillae. If severe, the

patient should stop wearing the contact lenses.

Refractive surgery and the Excimer laser

There has been rapid progress in the correction of refractive errors

by either laser or surgical means.

Initially, radial keratotomy, which involved partial incisions into

the cornea to change the curvature, was the common surgical

procedure to reduce simple myopia.

More recently, photorefractive keratectomy using excimer laser

has been found to have less complications and to be more predictable.

Photorefractive keratectomy involves the use of ultraviolet light to

remove a few microns of superficial corneal tissue. This reduces the

refractive power by reshaping the anterior surface of the cornea and

so reduces myopia.

With greater severity of myopia, photorefractive keratectomy has

been shown to be less predictable and a new technology called

LASIK (Laser assisted intrastromal keratomileusis) has been introduced.

In this technique, a flap of cornea is created and excimer laser is

144

applied to the corneal stroma to remove tissue, as in photorefractive

keratectomy. The flap is then replaced at the end of the procedure.

LASIK has been found to achieve excellent results even with myopia

of beyond −10 diopter.

Clear lens extraction and more recently, the insertion of an

intraocular lens in front of the normal crystalline lens have been used

effectively in severe myopia but both have all the dangers of intraocular

surgery.

Aphakia

Aphakia is the optical condition of the eye without its lens (following

cataract extraction). A strong convex (plus) lens has to be used to

replace the power of the removed lens so that images can be focused

on the retina. The thick cataract glasses can cause adjustment difficulty

because of the optical distortion and the increased image size. The

use of contact lens decreases the adjustment problems and is an

advantage for those who can tolerate their use. In many countries

intraocular implants are routinely inserted during surgery to overcome

this problem.

145

OPHTHALMIC DRUGS

COMMON OCULAR DRUGS

Local eyedrops are useful for disease affecting the anterior part of

the eye. Ointments may be used instead of eyedrops. In general

eyedrops are preferred as they will not blur vision and can deliver the

drugs in higher concentration. Conditions affecting the back of the

eye will require either subconjunctival or retrobulbar injections, or

systemic therapy.

THERAPEUTIC DRUGS

These drugs are usually dispensed as eyedrops, but may be used as

eye ointments.

Anti-infection eyedrops

• Antibacterial eyedrops

The commonly used antibiotic eyedrops are those which are seldom

used systemically and have a broad spectrum of action. They are

Chloramphenicol, Neomycin, Soframycin, Gentamicin and Polymyxin.

Tetracycline or sulphur derivatives are particularly useful in the

treatment of trachoma. Fortified preparations are available for treatment

of severe corneal infections, including fortified Cephazolin,

Gentamycin and Vancomycin. Newer drugs with increased efficacy

and broader antibacterial spectrum include Tobramycin, Ciprofloxacin

and Norfloxaxin.

• Antiviral eyedrops

Idoxuridine, Adenine Arabinoside, Acycloguanosine and

Trifluorothymidine eyedrops or ointments are used for herpes simplex

infection of the eye. A new drug, acyclovir, has less toxicity.

148

Glaucoma therapy

There are a variety of eye drops for the treatment of glaucoma.

These include pilocarpine, beta adrenergic blockers, adrenaline,

prostaglandin agonists, topical carbonic anhydrase inhiitors, among

others (see Page 56).

Decongestants (and antihistamine) eyedrops

There are numerous combinations of decongestants and

antihistamine eyedrops used for non-specific conjunctivitis and mild

allergies, and also as a placebo for tired, irritable eyes.

Tear replacement and lubricating eyedrops

Normal saline eye drops can be used as an ocular lubricant in dry

eyes but are not retained in the conjunctival sac. Methylcellulose,

Hypromellose and Polyvinyl alcohol are examples of more viscid

compounds with longer duration of action. Popular brand names

include Tears naturale and Lacrilube. Refresh and Cellufresh have no

preservatives.

Other means of delivering medications

To increase the duration of action of eyedrops, patients can

compress the lacrimal sac with their fingers. In addition,

subconjunctival injections of drugs can be given. Recently, drugs in

the form of small pellets can be introduced into the conjunctival sac

or even the eyeball itself and have been shown to be relatively safe

and effective.

Mydriatics and cycloplegic eyedrops

Mydriatic and cycloplegic eyedrops are used in uveitis to dilate

the pupil and to paralyse the muscles of accommodation in order to

relieve pain and to prevent adhesion of the iris to the lens (posterior

synechiae). They are also used in the treatment of amblyopia and

sometimes after surgery. The common eyedrops used for longer action

in therapy are Atropine and Homatropine.

Steroid eyedrops

Steroids are used for treating inflammation from many conditions

such as iridocyclitis and surgical trauma. Because of their many

complications, some of which can lead to severe visual loss, there

should be specific indications for their use.

149

The combination of steroids with antibiotic eyedrops is particularly

dangerous, especially when used for prolonged periods. The

complications from steroid drops are glaucoma, cataract and

aggravation of corneal infection, especially from herpes simplex and

fungus.

DIAGNOSTIC DRUGS

• Short-acting mydriatic eyedrops are used for ophthalmoscopy and

retinoscopy. These include Tropicamide and Phenylephrine.

• Local anaesthetic eyedrops are used for ocular examinations to

overcome blepharospasm and for tonometry. Besides their

diagnostic uses, local anaesthetic eyedrops are used in the

removal of corneal or conjunctival foreign bodies.

• Fluorescein is used in strip-form in the assessment of corneal

injury and suspected ulceration. It is also used as an intravenous

preparation for fundal fluorescein angiography.

MISUSE OF EYEDROPS

Eyedrops, when misused, can lead to a number of complications.

Steroid eyedrops

The most important and common problem is the indiscriminate

use of steroid eyedrops, especially in combination with a broad

spectrum antibiotic. These eyedrops may cause dangerous

complications with prolonged use. The complications include:

• Glaucoma

• Cataract

• Herpes simplex and fungal infection

Contaminated eyedrops

Eyedrops which have been opened and left unused for many months

can be contaminated. It is important that unused eyedrops be

discarded. Many countries warn consumers to discard eyedrops one

month after they are opened.

Systemic effects

Local eyedrops, especially Atropine and related anti-cholinergics,

may lead to systemic effects especially in children and infants.

150

Pilocarpine eyedrops, if used intensively in acute glaucoma, can also

cause systemic effects. 10% Phenylephrine drops may cause serious

cardio-vascular effects including tachycardia and sudden increase in

blood pressure. Timolol may aggravate asthma.

Local anaesthetic eyedrops

Local anaesthetic eyedrops should never be prescribed for ocular

pain as they can de-epithelialize the cornea and mask serious eye

complications by relieving the pain. When local anaesthetic drops

are used for diagnostic purposes it is important that the patient be

told not to rub the eye immediately after application to avoid corneal

abrasion.

Antibiotic eyedrops

The prolonged use of antibiotic eyedrops locally sometimes cause

chronic conjunctivitis.

DIAGNOSTIC EYEDROPS

Main uses

(Chemical)

Remarks

Names

Ophthalmoscopy

Dilators

Short acting

(1) Tropicamide

(6 hours)

0.5% -1%

(2) Cyclopentolate

1%-2%

(3) Phenylephrine

2.5% -10%

Examination

Local anaesthetics

Not to be used for

(blepharospasm

(1) Proparacaine

pain relief

and tonometry)

(2) Tetracaine

Staining cornea

(1) Fluorescein

Use strips.

Drops may be

contaminated.

151

THERAPEUTIC EYEDROPS

Indication

Drug

Bacterial Infection

•

Chloramphenicol*

•

Neomycin

•

Gentamycin

•

Framycetin

•

Sulphacetamide

•

Tobramycin

•

Ciprofloxacin

•

Norfloxacin

Anti-viral

•

Idoxuridine

(Herpes simplex)

•

Adenine Arabino — side

•

Acycloguanosine

•

Trifluorothymidine

•

Vira A

•

Acyclovir

Glaucoma

•

Pilocarpine

•

Timolol

•

Epinephrine (adrenaline)

•

Dipiverin (adrenaline

prodrug)

•

Brimonidine (alpha

adrenergic agonist)

•

Apraclonidine (alpha

adrenergic agonist)

•

Latanoprost (prosta-

glandin agonist)

•

Dorzolamide (carbonic

anhydrase inhibitor)

Chronic non-specific

Decongestants (antihistamines)

conjunctivitis

Numerous:

• Phenylephrine (neosynephrine)

• Naphazoline

• Antazoline

• Zinc Sulphate

Dry eye

Artifical tears

• Methylcellulose

• Polyvinyl alcohol

• Hypromellose

Iridocyclitis and after

Mydriatics (dilators)

surgery

• Atropine

• Homatropine

• Tropicamide

Inflammation Iridocyclitis

Numerous steroids:

and after surgery

• Hydrocortisone

• Prednisolone

• Dexamethasone

*Chloramphenicol eye drops are not used in some countries because of possible

systemic complications.

152

Strength

Dosage

Remarks

Use frequently

3-4 hourly but

avoid prolonged

therapy

Toxic to cornea

1%-4%

Constricts pupil

0.25%-0.5%

No effects on pupil

1%-2%

Dilates pupil

0.1%

Long term use leads to

Follicular conjunctivitis

0.5%

0.005%

May exacerbate uveitis

Less effective than oral

Acetazolamide

Often used as

placebo

Apply at least

every 3 hours

Long-acting

0.5%-1%

1 week action

2%-5%

2 day action

0.5%-1%

4 hours

Serious complications

0.1%

include:

0.5%

• Glaucoma

0.1%

• Cataract

• Aggravate

Herpes Simplex

153

Index

secondary,

53, 65

Acetazolamide,

senile,

Acne rosacea,

treatment, extraction of,

52,

Acute closed-angle glaucoma,

Adie’s pupil,

103

Cavernous sinus thrombosis,

AIDS,

66, 87

Cellulitis, orbital,

33, 26, 32, 90

Amblyopia,

113, 115, 116, 118,

preseptal,

149

Chalazion (Meibomian cyst),

23,

Anhidrosis,

103

Ankylosing spondylitis,

Chlamydia,

Anophthalmos,

120

Chorioretinitis,

Anterior chamber, blood in,

131,

pars planitis,

137

scars,

Aphakia,

145

Choroidal metastasis,

Arcus senilis,

39, 49

Coats’ disease,

113

Argyll Robertson pupil,

104

Coloboma,

119, 127

Arteriosclerosis,

68, 69, 84, 104

Colour-blindness, tests for,

Astigmatism, 37, 39, 116, 142, 143

Conjunctivitis,

2, 24, 144

Atropine,

8, 39, 66, 116, 149,

acute,

allergic,

150, 152

bacterial,

33, 41

therapy in acute iritis,

chronic,

24, 34

follicular,

giant papillary,

144

Blepharitis,

2, 35, 89

infections,

116

squamous,

22, 28

unilateral,

ulcerative,

22, 28, 39

vernal (spring catarrh),

34, 45

Blindness, definition of,

viral,

34, 41

mass blindness,

Contact lenses,

143

Blowout fracture,

132, 139

hard,

143

Bourneville’s disease,

119, 126

soft,

144

Buphthalmos (‘ox eye’),

118, 124

wear,

Burn, arc (welding),

132

Cornea,

chemical,

130, 133

abrasion,

5, 24

complications,

conical (keratoconus),

39, 48

CT scan,

foreign body,

35, 130, 134

Candida albicans,

grafts,

33, 37, 40, 50

Capsulectomy,

indication for graft,

anterior,

infection,

144

Carcinoma of lid (basal-celled),

lacerated wounds,

136

25, 31

opacity,

3, 7, 8, 10, 33, 36,

Cataract,

3, 51, 58

39, 40, 49, 50

congenital,

113, 118, 124

perforation,

extracapsular extraction,

scars,

36, 39, 130

51, 53

ulcer,

39, 47

Figures in bold refer to illustrations

155

Corneal ulcer,

35, 39, 47, 65

Fuch’s endothelial,

39, 48

bacterial,

juvenile macular,

71, 78

dendritic,

38, 44

senile macular,

fungus,

hypopyon,

47, 134

marginal,

Eales’ disease,

Cryoapplication,

70, 114, 119

Ectropion,

5, 25, 30

Cryopencil,

Electrophysiology,

11, 21

Cupping of optic disc,

55, 61

Entoptoscope, Bluefield, II,

Cup/disc ratio,

17, 55, 61

electrooculography (EOG),

Cycloplegics,

electroretinography (ERG),

Cytomegalovirus (CMV) retinitis,

visual evoked response study

(VER),

Endophthalmitis,

36, 53

Enopthalmos, 102

Dacryocystitis,

Entropion,

5, 24, 30

Dacryocystorhinostomy,

26, 117

Epicanthal folds,

116

Dendritic ulcer,

Epiphora,

Detachment, retinal,

69,

70, 80,

Episcleritis,

Esotropia,

115

Developmental abnormalities, 118,

Exotropia,

115

127

Examination,

Diabetes,

difficulties in,

mellitus,

distant visual acuity,

3, 12

refractive changes,

external eye,

5, 13

retinal changes in,

82, 83

extraocular muscles,

6, 9, 14

retinopathy in,

82-85, 92-93

fundus,

7, 8, 16

Diathermy,

near visual acuity,

4, 12

Disc,

ophthalmoscopy,

7, 16

oedema,

100, 107

perimetry,

9, 18

pseudo,

101, 108

pupils,

rotating (phoropter),

red reflex,

7, 15

Discharge mucopurulent,

scotometer,

9, 18

Dry eyes,

special techniques,

Drugs,

147

Exophthalmos (proptosis),

22, 26,

diagnostic,

148, 150

32, 98

misuse of,

149

and keratitis,

therapeutic,

147, 151-152

in thyroid disease,

87, 98

anti-infection,

147

pseudo,

cycloplegic,

148

Exposure keratitis,

25, 30, 98

decongestants,

148

Extraocular muscles,

87, 104

glaucoma,

54, 147

paralysis,

81, 104, 111-112

lubrication,

148

Eye strain,

141

mydriatic,

148

Eyelids,

steroid,

148-149

basal-celled carcinoma of,

25,

tear replacement,

148

Drusen,

71, 102, 108

congenital malformations, 127

Dystrophy, corneal,

39, 48

deposits on,

25, 31

Figures in bold refer to illustrations

156

eversion of,

5, 13, 24, 25, 30

Histoplasmosis,

66, 76

inflammation of,

5, 22, 28, 29

History, importance of,

malposition of,

24, 30

Homatropine,

retraction of,

27, 32

Hordeolum (style),

23, 29

tumours of,

25, 31

Horner’s syndrome,

24, 103

wounds of,

131, 136

Hypermetropia,

108, 141

Hypertension,

malignant,

Floaters,

2, 73

ocular,

Fluorescein,

10, 20, 84, 94

pre-eclamptic,

Foreign body,

retinal changes,

85, 95

corneal,

134

Hyperthyroidism,

27, 87, 88

intraocular,

130, 133

Hyphaema,

57, 131, 137

Fundus, degenerative changes,

72,

Hypopyon,

47, 133

83, 85- 86, 94

examination,

Implant posterior chamber lens,

52, 53

Gancyclovir,

Infection,

Gas injection,

antenatal,

120

Glaucoma,

bacterial,

38, 41, 47

closed-angle,

35, 53, 55

opportunistic,

acute,

35, 43, 55, 62

staphylococcus,

chronic,

viral,

38, 66

sub-acute,

Injury, ocular,

129

congenital,

118, 124

associated with head injury,

intraocular pressure,

53-57

128, 139

neovascular,

chemical,

132, 129-130

open-angle,

54, 60

from blunt instruments,

field loss in,

55, 60

131-132, 138-139

optic disc cup,

54, 61

blowout fracture,

132,

secondary,

139

treatment,

55, 56, 64, 147

hyphaema,

131, 137

from ‘flying’ particles,

130-131, 134

Haematoma of eyelids,

139

intraocular,

135

Haemorrhage, in anterior chamber,

from sharp instruments,

131,

137

136

macular,

abrasion, cornea,

131,

retinal,

136

subconjunctival,

36, 139

laceration, lid,

136

vitreous,

73, 86, 132

penetrating,

131, 136

‘Halos’ in glaucoma,

from welding burn,

131

Herpes simplex,

Interstitial keratitis,

40, 49, 89

corneal opacity from,

Intracranial aneurysms,

106

dendritic ulcer,

38, 44

tumours,

106

Herpes zoster ophthalmicus,

23,

Intraocular foreign body,

121,

28, 88

134-135

Figures in bold refer to illustrations

157

Intraocular pressure, in glaucoma,

in aphakia,

144

53-57

intraocular implant,

Intraocular tumour,

Leprosy,

Intravitreal surgery,

Lesions,

Iridocyclitis,

57, 58, 65

bony,

Ipsilatreal miosis,

103

chiasmal,

100, 102, 110

Iridodialysis,

138

field defect,

102, 110

Iridectomy, peripheral,

ischaemic,

Iridotomy, laser,

57, 62

Leukocoria,

113

Iris,

neuro-ophthalmic,

coloboma,

119, 127

post-chiasmal,

100, 103, 110

prolapse,

131, 136

visual pathway,

103

Iritis,

42, 43, 65, 103

Lids (see eyelids)

Ischaemia,

86, 101

Lime burn,

133

Itch, in eyes,

Magnetic Resonance Imaging

Kaposi sarcoma,

(MRI),

Keratic precipitates,

Macula,

Keratitis,

central serous retinopathy,

disciform,

38, 49

72,

exposure,

25, 30, 89, 98

degeneration,

interstitial,

40, 49, 89

disciform,

71, 79

Keratoconus,

high myopia,

72, 78-79

Keratomalacia,

39, 49, 88

senile,

Keratectomy, photorefractive,

144

dystrophy, juvenile,

71, 78

Keratotomy, radial,

140, 144

haemorrhage,

potential acuity,

retinitis pigmentosa,

73, 104

Laser,

Marfan’s syndrome,

120

excimer,

144

Meibomian cyst (see chalazion)

interferometer,

Melanoma,

trabeculoplasty,

benign choroidal,

66, 77

Lacerations,

benign eyelid,

cornea,

136

malignant choroidal,

65, 77

lid,

136, 139

Metastasis, choroidal,

Lacrimal drainage system,

Microphthalmos,

119, 127

blockage,

25-26, 117-118

Microscope,

congenital,

117-118

slit-lamp,

9, 20, 40

Lagophthalmos,

5, 87, 98

Microaneurysms,

82, 93, 94

‘Lazy eye’,

116

Migraine,

106

Lens, dislocation of,

138

Morphine,

103

injury,

134

Myasthenia gravis,

105

opacity,

51, 58

ptosis in,

105, 111

Lenses,

Myopia,

140, 141

after cataract extraction,

high (degenerative),

contact,

39, 47, 143

ophthalmoscopy in,

complications,

143

pathological,

141

Figures in bold refer to illustrations

158

progressive,

141

Orbital cellulitis,

26, 32, 90

simple or physiological,

135,

Orbital tumour,

11, 32

141, 143

Panophthalmitis,

Naevus,

46, 66

Papilloedema,

100-101, 107

Nasolacrimal duct,

in hypertension,

85, 95, 107

congenital, blocked,

125

pseudo,

101

Neonatorum, ophthalmia,

115,

Papillitis,

100, 101, 107, 109

125

Paralytic squint,

104, 111-112,

Neovascularisation,

114

Neuritis, retrobulbar,

102

Pars planitis,

Neurofibromatosis,

119

Perimetry,

9, 18, 19

Night-blindness (see retinitis

Goldman,

pigmentosa)

Phakomatosis,

118, 126

Nystagmus,

105

Photocoagulation,

70, 84, 95,

114, 119

Pilocarpine,

55, 103, 147

Oblique muscles, paralysis,

Pinguecula,

37, 46

111-112

Pneumocystis carinii,

Occlusion,

Post-chiasmal lesion (see lesions)

branch retinal vein,

68, 75

Potential visual metre (PAM),

central retinal artery,

67, 75,

Pre-eclamptic hypertension,

109

Presbyopia,

142

central retinal vein,

68, 75

Preseptal cellulitis (see cellulitis)

in amblyopia,

116

Proliferative diabetic retinopathy

punctum,

(see retinopathy)

vascular,

Proptosis (exophthalmos),

22, 26,

Ocular hypertensives,

32, 93

Onchocerciasis,

Pterygium,

37, 46

Opacity, cornea,

3, 7, 8, 10, 33,

Ptosis,

24, 30

36, 39, 40, 49 -50

acquired,

Ophthalmoscope,

7, 16, 68

congenital,

direct,

7, 15, 70, 72

in myasthenia gravis,

105,

indirect,

10, 20, 70

111

Opportunistic pathogens,

senile,

Optic atrophy,

101, 103, 109-110

Pupil,

6, 103

Optic chiasma (see lesions)

dilated,

43, 62

Optic cup,

54, 61

in diabetes,

in papilloedema,

96, 100,

in glaucoma,

43, 62

107

in iritis,

43, 65

pseudo,

96, 108

normal,

in retrobulbar neuritis,

102

oedema,

100, 107

irregular,

103

pallor of,

102, 109

large,

103

Optic nerve atrophy,

102, 109

reaction,

6, 104

Orbit, injuries,

132, 139

small,

8, 43, 103

Figures in bold refer to illustrations

159

Scan,

Radiotherapy,

CT,

11, 21, 87, 103

Red eyes,

Nuclear Magnetic Resonance,

bilateral,

33, 41

103

unilateral,

35, 42

Scar,

Reflex,

chorioretinal,

corneal light,

6, 14

corneal,

red,

7, 15, 70

Scleral necrosis,

white,

5, 118

Scleritis,

89, 99

Refractive changes,

Sclerosis, disseminated,

101

astigmatism,

141, 142

Scleromalacia,

hypermetropia,

141

Scotoma,

54, 60, 101

in diabetes,

Scotometer,

9, 18

in myopia,

140, 141

Sebaceous adenoma,

126

in presbyopia,

142

Sickle-celled anaemia,

86, 97

Refractive errors,

140, 142

Siderosis bulbi,

135

Retina,

Slit-lamp microscopy,

9, 20, 40

arteriosclerosis of,

68, 84

Squint,

114-116

detachment of,

69, 80, 114

convergent,

104, 111, 115,

exudative,

68, 70

123

traction,

70, 92

divergent,

111, 115

haemorrhage of,

69, 75, 79,

head tilt in,

111, 115

management of,

115

tears (holes),

67, 70, 80

non-paralytic or concomitant,

Retinal artery occlusion,

68, 75,

113-115

109

paralytic,

104, 112, 114, 116

Retinal haemorrhages,

75, 97

pseudo,

116

Retinal vein occlusion,

68, 75

vertical

114

Retinitis pigmentosa,

73, 109

Steroids,

Retinoblastoma,

113, 115, 120,

contraindication of,

148-149

122

dangers of,

148-149

Retinopathy,

indications for,

148-149

central serous,

72, 79

Staphylococcal antigens,

diabetic, background,

82, 91

Stevens-Johnson’s disease,

35, 90

hypertensive,

85, 96

Still’s disease,

hyperviscosity,

86, 97

Sturge-Weber syndrome,

119, 126

maculopathy,

77, 82

Stye,

23, 29

proliferative,

82, 83, 92, 93,

Subconjunctival haemorrhage,

36,

139

sickle-celled,

86, 97

Subconjunctival injections,

39,

vascular,

149

Retrolental fibroplasia,

113, 121

Subretinal fluid drainage,

Rheumatoid disease,

89, 90, 99

Subretinal neovascularisation,

Rodent ulcer,

25, 31

Synechiae, posterior,

58, 65, 103

Syphilis,

66, 89, 103

Systemic conditions,

Sarcoidosis,

Sjogrens syndrome,

Figures in bold refer to illustrations

160

severe loss of,

1, 44, 55

Tarsorrhaphy,

27, 98

sudden,

1, 51, 53, 65,

Tearing,

117

67, 69, 71, 73, 101

Thyroid disease,

27, 87, 98

telescopic central,

exophthalmos in,

Visual acuity, assessment (see

Tonometer,

examination)

Goldman applanation,

9, 20

Visual field,

non-contact,

chart,

Schiotz indentation,

9, 20

defect, hemianopic

Toxocarioxis,

bitemporal,

102, 110

Toxoplasma gandii,

homonymous,

103, 110

Toxoplasmosis,

76, 66

examination of

5, 18

congenital,

120

in glaucoma (see glaucoma)

Trabeculectomy,

56, 64

loss of,

51, 54, 60, 101

Trachoma,

36, 45

Vitamin A, deficiency,

TRIC (Trachoma inclusion

Vitreous,

conjunctivitis),

conditions,

Trichiasis,

24, 30

detachment,

Tuberculosis,

66, 89

haemorrhage,

73, 86

Tuberous sclerosis,

118, 126

Vitrectomy,

73, 86, 70

Tumour,

Von Hippel-Lindau disease,

118,

choroidal,

66, 77

126

eyelid,

25, 31

Von Recklinghausen’s disease,

pituitary,

119

Ulcer,

Watering of eyes,

corneal,

38, 39, 47

White pupil,

113

dendritic,

38, 44

congenital,

120

Ultrasonic disintegration,

retinoblastoma,

113, 123

Ultrasonography,

10, 21

management of,

113

Unilateral red eye,

35, 42

squint due to,

114, 123

Uveitis,

World Cataract Surgeons Society,

Vascular occlusion,

Vasculitis,

Xanthelasma,

25, 31

Vision,

X-ray, in intraocular foreign body,

loss in quiet eyes,

135

gradual,

2, 51, 67, 70

Figures in bold refer to illustrations

161