1

The Red Eye

Dr Joseph Reich
The 'whites' of our eyes are the result of the opaque sclera being seen through the semi
transparent overlying conjunctival layer. The conjunctiva extends from where the cornea
joins the sclera ~
(the limbus) across the front third of the eyeball to then fold back to line the eyelids. The
fold is known as the fornix and can at times hide a foreign body such as an eyelash.

Seen up close, with a slit lamp or magnifying loupe, the normal conjunctiva can be
seen to have a vasculature. This is most evident during inflammation by the redness of
the eye. These vessels can be more prominent in some persons and patients often use
vasoconstrictors to blanch or whiten their eyes. While this can be of transient assistance
continued use of these agents can lead to continued redness due to rebound
vasodilatation.

..
The normal conjunctiva may develop lipid deposits and thickening in sun-exposed areas
(between the eyelids). Such changes are known as pingueculae and can be a minor
irritant, but rarely require excision. Less commonly sun exposure will stimulate the growth
of conjunctival tissue onto the cornea ( a pterygium ). This is seen more frequently in
northern Australia, and though benign, excision may be followed by recurrence.

The conjunctiva at the limbus is closest to the internal eye and therefore the sign of
ciliary injection where the vessels around the limbus are maximally inflamed is an
indicator of deeper inflammation.

Conjunctivitis is an inflammation primarily involving the conjunctiva lining the eyelid and
over the eye itself. Typically such inflammation is diffuse but may be more prominent
inside the eyelids than towards the limbus.
The conjuntiva lining the eyelids develops lymphoid follicles particularly with viral
infection and cobblestone like papillae with chronic allergic reactions.
2

Red Eye Diagnosis.

Is it unilateral or bilateral?

Bilateral red eyes

Most bilateral red eyes are due to conjunctivitis ( bacterial, viral, chlamydial or
allergic) and are therefore relatively benign and not sight threatening in most instances
(exceptions include herpetic infection, gonococcal conjunctivitis)
\

Other causes include flash burns (welding ), overuse of vasoconstrictor eye drops,
overwearing of contact lenses, dry eye syndrome.

Unilateral red eye

1. Injury

Vary from a trivial, but painful, corneal abrasion through to a blinding penetrating injury.
Seek history of injury as may be discounted when other injuries, may seem irrelevant to
patient. If no history examine for possible injury. Test and record visual acuity. If eye
penetrated do not instill any drops or ointment. Apply a gentle sterile eye pad and arrange
emergency
care.
A subtarsal foreign body will ab~,ade the corneal epithelium which then stains with
Flourescein dye. Usually found by everting the upper lid. There may be a small
associated lid haemorrhage to help find the foreign body. Lift off with moist sterile cotton
bud. If no local anaesthetic is-used then expect immediate relief.
Corneal foreign body. Will need local anaesthetic drops to remove. Can use cotton bud
but if deeper or associated rust remove with sterile disposable needle with magnification
to assist.
After antibiotic ointment, firm pad and review in one day.

2. Iritis

Acute iritis is an intraocular inflammation of the iris. The patient has pain, photophobia
and may have blurred vision. The red eye typically has ciliary injection. The pupil may be
small and adhesions develop between the iris and lens (synaechia). Deposits on the inner
cornea may be seen with the slit lamp ( keratin precipitates) as well as cells in the
normally clear aqueous humour. In severe cases the cells can form a pus layer
(hypopyon). The inflammation can also extend into the posterior segment of the eye and
involve vitreous opacity and retinal oedema. There may be a secondary glaucoma and in
the long term cataract and band keratopathy may develop.
3

Iritis is seen in juvenile rheumatoid arthritis, intraocular infection, sarcoidosis,

ankylosing spondylitis, and other inflammatory arthritic conditions but in many
instances is ideopathic.
Treatment involves steroid drops or systemically if severe. Pupil dilation with atropine or
homatropine can break synaechiae. Treatment should be 'undertaken by an
ophthalmologist.

3. corneal ulcer
\

Infection of the cornea with herpes simplex virus leads to recurrent infections
characterised by epithelial ulceration with a typical dendritic pattern or deeper scarring
corneal stromal disease. Treatment is with antiviral agents such as a cyclovir ointment 5
times a day. The use of steroid drops may cause the epithelial ulcer to spread and
deepen with corneal perforation.
Bacterial and fungal keratitis can occur following a corneal foreign body, contact lens
misuse or in the immune compromised. '

4. acute angle closure glaucoma

Rare. Older patient with predisposing shallow anterior chamber develops severe pain,
blurred vision with haloes around lights. The eye pressure is high and the pupil is seen
through a clQudy cornea to be fixed and dilated. Emergency treatment is required to lower
pressure. Laser iridotomy will prevent such an attack.

5. subconjunctival hemorrhage

The most spectacular, yet most benign cause of a red eye. Not associated with internal
eye disease it usually occurs spontaneously, perhaps after rubbing the eye. No treatment
is required. Also seen with facial trauma in which case a hemorrhage extending into the
fornix may iJldicate an orbital wall fracture.

THE LOCAL ANAESTHETIC TEST

To assist in diagnosis when there is pain associated with the red eye a drop of local
anaesthetic~ ( benoxinate or amethocaine from a single dose Minum) can be instilled. If
the pain is relieved then the cause is superficial i.e. foreign body, corneal ulcer,
abrasion. Deep pain from causes such as acute glaucoma, acute iritis will not be relieved.

Never allow the patient to use local anaesthetic drops to control their pain. They will
prevent epithelial healing resulting in a persistent painful ulceration. A better option is a
firm eye pad, eye ointment and sedation. Most ulcers will heal within a day.
4

Conjunctivitis

1.

Bacterial

Usually bilateral. Typically purulent discharge. May have associated eyelid margin
infection (blepharitis). If recurrent or chronic check that there is not a blocked tear duct
with mucocoele of the lacrimal sac. Is the commonest cause of conjunctivitis in infants.
Other possibilities include trichiasis, entropion, ectropion.
Treatment involves bathing crusting off eyelids, use of antibiotic drops frequently (i.e.
chloramphenicol or tobramycin hourly) initially and ointment at night. Should resolve in
days.

2. Viral

Adenoviral conjunctivitis is common, usually unilateral at the beginning but may spread
to the fellow eye. Typically watery discharge, with follicles, subconjunctival haemorrhage
and a tender preparotid lymph node. Treatment is symptomatic and care should be
taken to prevent spread. Avoid steroids as may be mimicked by herpes simplex infection.
May develop a keratitis that can blur the vision after the acute stage.

3. Allergic

Acute allergy typified by itch and redness with watery discharge. Chronic allergy reaction
develop cobblestone papillae inside lids.
Respond well to steroid drops. Risk that patient may continue to use unsupervised with
attendant danger of secondary glaucoma, cataract and infection. Alternatives include
sodium cromoglycate drops which may need prolonged use but are relatively risk free.
John L Colvin, AM; FRACO, FRACS
Simon W G Permezel, FRACO, FRACS, FRCOphth (UK)

BASIC OCULAR ANATOMY

Embryology

Surface Ectodenn -lens, epithelium of cornea an,d conjunctiva lacrimal gland and drainage \

Neural Ectoderm -retina, vitreous, epithelium of iris, ciliary body, pupil muscles & optic nerve

Mesoderm

-sclera, corneal stroma, conjunctiva, iris, choroid, extra-ocular muscles, lids, optic nerve sheath, CT
and blood supply, and bony orbit

Major Ocular Structures

General Information

- age
- past medical history including current medications
- past ocular history including accidents, operations and spectacles
- family history of eye disease such as glaucoma, squint, cataracts and retinal detatchment

The Ocular Complaint

Modes of presentation
1) Subnormal vision
2) Pain or discomfort
3) Change of appearance of lids, eye, or orbit 4) Diplopia or dizziness
5) Discharge or increased conjunctival secretion

1) Subnormal Vision Duration

Unilateral or bilateral
Disturbances ,;c~
-distortion(metmorphopsia) in macular lesions or astigmatism -photophobia in corneal inflamni~tion and
iritis
-colour change as in washed oufreds in optic neuritis and yellow vision of digitalis toxicity
-halos are seen in raised lOP and more commonly with early cataract
-floaters and spots if unilateral and seen against light coloured background then likely to represent benign
vitreous opacities whereas if bilateral, simultaneous and present even with eyes closed likely to be
vertebrobasilar insufficiency
-visual field defects can be due to pathology in cornea, media, retina or brain e.g. scintillating scotomas of
migraine
-night blindness is a rare symptom seen in retinitis pigmentosa but also occasionally with ageing
degeneration of the eye and cataract
-momentary loss of vision in one eye(amaurosis fugax) is seen with emboli or spasm of the central retinal
artery or carotid disease

2) Pain and Discomfort

- headache
- eye ache
- burning
- gritty
- itchy

3) Change in Appearance
i. discolouration
-red eye in inflammation and subconjunctival haemorrhage -yellow eye injaundice and
hypercarotinaemia .
-blue eyes in osteogenesis imperfecta
ii. swelling mass displacement
iii. mass
iv. displacement

4) Diplopia

- monocular as in ghosting of vision with on axis lens opacities

- binocular diplopia of true extraocular muscle imbalance
- is the diplopia horizontal or vertical
5) Discharge

- purulent in bacterial conjunctivitis

- watery and red in viral conjunctivitis
- watery and white with a blocked tear dainage system

Routine Ocular Examination

GOLDENRULE

MORE MISTAKES IN MEDICINE ARE MADE BY NOT LOOKING THAN NOT

KNOWING
STANDARD PROCEDURE

1. Visual Acuity +/- Colour

2. General Observation
3. Local Examination
4. Pupils
5. Eye movements
6. Fields to Confrontation
7. Front of Eye Examination
8. Fundal Examination

1. Visual Acuity and Colour Vision

REQUIREMENTS

Snellen Chart
Kay Picture Test
Pin-hole occluder
Ishihara colour plates

.METHOD

Visual acuity testing is a medico-legal necessity in anyc:»ne presenting with an eye related problem The
Snellen Chart is placed 6 meters from the patient. Always test one eye at a time. Record uncorrected
vision R and L. If they have distance spectacles record corrected distance acuity R and L. If no spectacles
and uncorrected vision is worse than 6/9 then test each eye using the pin-hole which will overcome most
refractive errors. Normal vision is 6/6. Ask the patient to read as far down the chart as possible. If able to
read the "6" line this is recorded a 6/6 where the numerator is the dj;:.tance of the chart and the
denominator is the line seen.

Distance from chart Line seen

If unable to read even the large "60" letter at the top of the chart, the patient should be moved
progressively closer until able to read it. If this letter is seen at 3 meters this is then recorded as 3/60. If
they are still unable to see the top letter at I meter attempt finger_counting at 1 meter i.e. CF at 1m. If no
success try hand movements (HM), followed by light perception(LP) and if unable to see light this is
recorded as no perception of light(NLP).

With children and illiterate adults the Kay Picture test is used following an identical format. It is u'f;ually
possible to get an acuity measurement from 3 years and sometimes earlier.

2. General Examination

Remember to examine the whole person. How old are they and what is there general condition and are
there any specific findings such as Marfan' s syndrome, t"heumatoid arthritis, acromegaly etc. which are
very relevant to the eye.

3. Local Examination

Look at the face, eyelids and skin. Note any BCC's, acne rosacea, ectropion, entropion, ptosis and
exophthalmos.

Tarsal section of lid

Medial canthus
4. Pupil Examination

Pupils -They should be inspected for:

Equality
Size
Shape
Reaction to stimulation -(light reflex, accommodation reflex, and consensual light response).

Inquiry should be made as to the use of any drug that might cause mydriatic or miotic effect. Never use
eyedrops to dilate the pupil prior to examination of the pupil.
Normal pupils are equal in size. The pupil is larger in childhood and gets progressively smaller with age. A
slight difference in size of the pupils (anisocoria) is' quite often observed and is a normal variation.
Unequal pupils may suggest previous eye disease or neurological disorder.
Pupils that are smaller than 4rm in diameter are called "miosis" or "miotic" pupils. This can be observed in
cases of inflammation in the anterior segment of the eye. Morphine causes miosis. Physiologically, the
pupil is miotic in sleep.
Enlarged pupils, larger than 7mm are called "mydriatic pupils". The pupil is large in cases of ocular injury,
systemic poisoning, and many neurological diseases of the mid-brain.
Irregular pupils are almost always pathological. The shape can be affected by congenital abnormalities,
and other diseases such as iritis, syphilis or trauma.

METHOD
Examination for reaction to light is best performed in a semi-dark room. The light should be brought from
the side. The pupils contract to direct light. Constriction of the pupil of the opposite side is called
"consensual pupil reaction" to light. ::'.
,"
The reaction to accommodation is tested by holding one fmger, or a pencil, in front of the eye being
tested, and about 10 centimeters away from the eye. The patient is requested to look alternately at the
pencil and then at the far wall directly beyond the pencil. The pupil constricts looking at the near object
and dilates looking at the far object. In general, if the pupil reacts to light, it reacts to accommodation as
well. "Argyll-Robertson Pupil" is a pathological condition due to central nervous system syphilis in which
there is a failure of direct and consensual light response, but there is a normal reaction to accommodation.
" Adie's pupil" or tonic pupil, responds to stimulation, but very, very slowly.
The afferent pupillary defect as seen in acute retrobulbar neuritis and central retinal artery occlusion is
demonstrated by the pupil on the affected side reacting slowly to direct light, and the contraction being
poorly sustained whilst on the other hand, contraction of the pupil to consensual stimulation is intact. This
is best seen with the swinging light test.

PUPILLARY PATHOLOGIC STATES

Dilation: Pharmacological, Adie's syndrome, peripheral 3rd nerve injury Constriction: Argyll-Robertson
pupil (syphilis), Homer's syndrome. Irregularity: Previous iritis, ocular trauma or surgery
Squint (or strabismus) means a deviation of the eyes so that their axes are no longer parallel, but excluding the
normal convergence that accompanies near vision.
Infants do not develop binocular co-ordination until about 6 weeks of age, and since this, is well established by 6
n1onths of age, an infant's eyes should move together in a normal fashion at this time.
Deviations may be in any direction, but are most commonly horizontal (convergent or divergent) and occasionally -
vertical. Such a deviation of the visual axes is obvious if the squint is gross, but small degrees of squint can be
recognized from the asymmetrical positions of the bright comeallight reflections relative to their respective pupil
margins. This is confirmed by covering each eye in turn, and noting whether a perceptible movement is made by
either eye to assume fixation, when its fellow eye is occluded
I
(The Cover Test).

DIAGNOSIS
a. Apparent Squint -There are certain conditions which give rise to the appearance of squint, though the visual
axes are actually parallel. The commonest cause of this phenomenon is epicanthus, when the bridge of the nose
is very broad and an abnormal fold of skin hides the medial angle of the eye. The comeae then seem to be closer
to the midline than they actually are and convergent squint is mistakenly thought to be present. The true state of
affairs will be disclosed by the application of the cover test (see below).
b. True Squint -In large degrees of deformity, and particularly in those squints that are uniocular, there is usually
no doubt as to the diagnosis. Common Types: -congenital esotropia (convergent), acquired accommodative
esotropia, exottopias (divergent squints) and paralytic strabismus (e.g. IIIrd nerve palsy).
.METHOD ,;;:",
, ,..
The Application of the Cover Test -The child t~ persuaded to fixate object (a light, doll or brightly coloured toy).
Whilst fixation is being maintained, the eyes are covered in turn, either by the hand or a card. If each eye remains
stationary when its fellow eye is covered, no squint is present. If, however, on covering one eye the opposite eye
moves in order to take up fIXatiOn, this eye was originally squinting. When the cover is removed, the originally
squinting eye may maintain fIxation whilst it will be found that the covered eye is now squinting (alternating squint),
or it will revert to its original position and the eye which has been covered will take up fixation once more (uniocular
squint). In older children, the cover test should be carried out while the child is first looking at a distant object and
then at something held a foot or so from the eyes. This additional measure may disclose a squint that varies with
distances of gaze.
GOLDEN RULE
SQUINT -ALWAYS REFER WHEN FIRST SEEN. DO NOT DELAY CORRECTABLE.

MOST CASES ARE

c. Convergence Insufficiency -While not strictly a state of ocular imbalance this quite common condition deserves
consideration here. There is an inability to sustain convergence and this is manifest clinically ~ blurring of print
while reading, "running together" of words, and a sensation of eye strain. The patients are usually young or middle-
aged, often admit to not being very fit, and are sometimes convalescent after an illness. The condition is also seen
as a manifestation of anxiety states. Convergence insufficiency is one condition in which orthoptic treatment is an
almost certain means of relieving symptoms. A short course of training ii combined with exercises to be used at
home. Improvement of convergence takes place in a short time. The normal convergence reflex should be able to
be sustained to a point of 10cm or less, irrespective of the age of the patient.
d. Nystagmus -Rhythmical involuntary oscillation of the eyes, which is nearly always bilateral. May be ocular or
labyrinthine-cerebellar in origin. The ocular nystagmus has regular pendulum-like movements, which are
exaggerated on looking to either side; the movements are generally horizontal, but may have a vertical or rotatory
component. It occurs usually as a congenital abnormality accompanying poor vision, as in ocular albinism. The
labyrinthine-cerebellar nystagmus has movements that show a slow drift in one direction and a fast correction jerk
back again; the direction of the nystagmus is conveniently labeled according to the direction of the fast (correcting)
phase. The slower drift is generally towards the side of the lesion (e.g. middle ear damage, acoustic neuroma),
and the movements are usually exaggerated on looking in the opposite direction. A rather indefinite "wobbling"
nystagmus is particularly common in multiple sclerosis.
d. Ptosis -Drooping of the upper lid occurs in paralysis or weakness of the levator of the lid as part of a 3rd nerve
lesion, and as such, may be see~ as a manifestation of some generalized neurological cause, such as vascular
lesions, head injuries, intracranial tumours, --etc. It is not uncommonly seen as a manifestation of some localized
neurological disorder, particularly myasthenia gravis. The diagnostic feature of ptosis in myasthenia is that it tends
to be worse at the end of the day and may be provoked during examination by making the patient gaze steadily at
the examiner's finger held in front of the patient's face and above the horizontal plane. Of greater importance from
the ophthalmic point of view is congenital ptosis, which may be unilateral or bilateral, complete or partial, and
which may be associated with a weakness of elevation of the affected eye, due to paralysis of the superior rectus
muscle. It is impossible to mistake a child suffering from bilateral congenital ptosis, for he has a characteristic
"head back" attitude in an attempt to see through this reduced palpebral aperture. Treatment is a matter of urgency
only if the cornea is completely covered by the upper lid and the eye is, therefore, not being used and likely to
become amblyopic. This is more likely to occur in a unilateral case. In other cases, where there is full vision in
each eye, correction is best left until the child is 7y.o. or so, when any operation is easier on account of the greater
size of the parts, and a degree of spontaneous improvement may well occur before this time. This is particularly
true with regard to the epicanthus that often goes with congenital ptosis. As the child's nasal bones develop, so the
epicanthus fold is drawn forward and becomes less prominent while a reduction in the amount of ptosis also takes
place.

6 Fields of Confrontation

Assessment of visual fields is a very important part of an ophthalmological examination. Generally only fairly crude
bedside testing can be carried out without modern sophisticated computerised field testing. Finger counting in four
quadrants is however sufficient for detecting most neurological and many ocular field defects.

METHOD
Sit directly in front of the patient and ask the patient to look directly at your nose. Initially test both eyes together
and then one at a time. Hold up fingers in each of the four quadrants and ask can they tell you how many fingers
you are holding up. Make sure they are not cheating and are fixed on your nose. To look for neglect present
fingers in two quadrants on different sides of the mid-line.

TYPES OF FIELD LOSS

1 Bilateral – homonymous hemianopias of stroke

bitemporal hemianopia of pituitary tumour compression of optic chiasm
2 Unilateral – Glaucoma acruate defects
Altitudinal lesions of vascular events of retina or optic nerve
 7 Front of Eye Examination

REQUIREMENTS

Pencil torch with cobalt blue filter

Magnifying loupes, slit-lamp if available
Cotton buds
Local anaesthetic drops
Flurescein strips
Tonometer (optional)
Algerbrush rust ring remover

METHOD

• Eyelashes
-look for trichiasis, which can be missed unless the lid is examined before being pulled away from
the eye

• Evert lower lid (conjunctival sac, FB's lower fornix and tarsal conjunctivae).

• Evert upper lid -necessary to instruct patient to put his chin up and to look down at all times -and to
observe same as for lower lid, with special reference to subtarsal FB's and muco-pus. No eye
examination is complete until the upper eyelid is everted and closely inspected.

• Bulbar conjunctiva -Is there a pinguecula or a pterygium; are there dilated vessels (note if ciliary or
conjunctival type injection)

• Sclera – redness and swelling overthe sclera is known as episcleritis. It is usually a localized
unilateralcondition occurring in one quadrant and exhibits local tenderness when the eye is pressed
through the closed eye lid. There is no associated discharge.

• Cornea -Proper illumination and magnification are mandatory. Sterile local anaesthetic drops
instilled prior to examination of a painful lesion will assist greatly: a)look for foreign bodies b) stain
with sterile fluroscein for ulcers and be especially alert for the branching pattern of a dendritic ulcer

• Anterior Chamber -Is it of normal depth compared with other eye; are there blood or pus fluid levels,
flare, keratic precipitates.

• Iris – Colour each, texture. Tremulousness of the iris indicates a dislocated lens or aphakia. Look
for the peripheral or sector iridotomy indicating previous intra-ocular surgery. Coloboma of the iris in
typical position of infronasal is congenital.

• Lens - In correct position or dislocated, or absent; are there lens opacities.

• Palpation -Sinuses, lacrimal sac and gland, lymph nodes, temporal arteries, carotids. Digital
tonometry is useless and should not be relied on as an accurate estimation of the intra-ocular
pressure. Ausculation – carotid bruit, bruit over eye in carotico-cavernous fistula.

• Tonometry - Schiotz, Perkins or Tonopen done at any age with a family history of glaucoma, over
age 35 years in all patients except in the presence of conjunctival discharge or corneal damage.
CONDITIONS REQUIRING URGENT REFERRAL TO AN Ol!HTHALMOLOGIST

Trauma (including all chemical burns) * Hyphaema * Corneal Ulcer * Severe Conjunctivitis * Acute Iritis *
Glaucoma * Vitreous Haemorrhage * Recent Unilateral Exophthalmos * Acute Dacryocystitis * Orbital
Cellulitis * Optic Nerve Pathology * Ocular Tumours * Strabismus (squint) * All cases of sudden loss of
Vision
a. Painless (occlusion of central retinal artery or vein, retinal detachment). b. Painful (cranial arteritis,
acute angle closure glaucoma).

IF YOU DON'T KNOW -ASK!

8. Fundal Examination and the Ophthalmoscope

JOHN L. COLVIN; AM. FRACO, FRACS JOSEPH A. REICH; FRACO, FRACS;

SIMON WG. PERMEZEL, FRACO, FRACS, FRCOphth(UK)

MECHANICAL DIFFICULTIES
Make sure you have a suitable instrument -The Keeler, Welch Allyn and Heine ophthalmoscopes are
satisfactory, especially the pocket types now available.
Small Pupil -Dilate with 1% Mydriacyl (Tropicami~e) drops, unless anterior chamber is shallow. Always
reverse the dilated pupil by using 1 % Pilocarpinc drops to prevent closed angle glaucoma.

ABSOLUTE CONTRA-INDICATIONS TO PUPIL DILATION IS HEAD INJURY OBSERVATION

GOLDENRULE
NEVER GIVE A FUNDAL OPINION THROUGH AN UNDILATED PUPIL. WHAT PASSES UNSEEN
REMAINS UNSUSPECTED.

Too Much Light in the Examination Room -Always try to examine fundi in the dark.
Poor Position -Many medical patients are examined lying in a bed. This is quite unsuitable; sit patients up
in a chair in order to examine the eyes properly.

PHYSIOLOGICAL DIFFICULTIES '

Myopia -shortsightedness of more than about 6 or 7 diopters makes it very difficult to see the fundus
clearly by direct ophthalmoscopy. To overcome this, examine the patient's fundus while he is wearing his
glasses.

Poor Appreciation of the Normal -the fundus varies in colour with the complexion. In a brunette it is dark
red and mottled, and in a blonde light red, while an albino is very pale. A tigroid' or tessellated appearance
is seen in people of Mediterranean origin, and chocolate colour in the black races.
-the disc also varies to a similar extent, so that in dark people a very prominent ring of pigment may be
seen around the optic disc, and in fair people the temporal half of the disc looks almost pathologically pale.
NOTE: Children have brighter retinal light reflexes than an adult.

Normal Abnormalities -These are conditions of little or no significance, but startling appearance. They are
frequently mistaken for much more serious conditions.

1. A physiological cup, which although it does not extend to the edge of the optic disc, is often mistaken for
glaucomatous cupping of the disc and nerve head. If the cupping of the optic nerve head is greater than
30% of the total disc area, then that patient should be referred to an ophthalmologist to exclude glaucoma.

2. Opaque nerve fibres, which look rather like white flames running out from the edge of the disc, and
which have a feathery edge, are frequently mistaken -for papilloedema. This appearance is due to
medullation of the optic nerve fibres; medullation usually stops behind the disc. It is developmental and not
congenital. No associated headache and effect on vision.

3. Myopic scleral crescent, which produces a white area round the optic nerve head, is frequently mistaken
for optic atrophy. Seen in people with high myopia. If one looks c.arefu1ly, the normal pink disc can be
seen in the centre of this large white area. .

4. Pseudopapilloedema Is due to heaping up of nerve fibres at the optic disc margin caused by buried
calcific nodules (drusen) within the nerve head. It gives the impression of papilloedema but there are no
haemorrhages or exudates, nor any oedema. The patient is physically quite well and there is no headache.
The aforementioned conditions can he a source of great confusion therefore it is VERY IMPORTANT
THAT ANY CASE IN WHICH YOU CANNOT CLEARLY SEE THE OPllC DISC EDGE, HOWEVER YOU
FOCUS YOUR OPHTHALMOSCOPE, SHOULD BE REFERRED TO AN OPHTHALMOLOGIST FOR
ASSESSMENT.

METHODS OF FUNDUS EXAMINATION .

Look through your ophthalmoscope into the patient's dilated pupil from an arms length away with no lens
(0 on scale) in position and in darkened surroundings. Seated position for patient preferred.
You will normally see the red fundus reflex (choroidal circulation). However, any opacities that are present
in the patient's ocular media, e.g. lens opacities will stand out as black silhouettes against this red reflex. ~
Rotate a +,12 lens into the aperture and bring the instrument close to the patient's eye. The magnified
details of the anterior segment of the eye (cornea, iris & lens) will be seen. Then, by gradually decreasing
the strength of the plus lenses, the point of focus gradually passes posteriorly through the vitreous until
finally the retinal details come into view, magnified 14x. Depending on one's own accommodation, it helps
to have a -1 to -4D lens in the peephole of the ophthalmoscope, t~ see the: retina clearly.
Aphakic eyes (i.e. without lenses) are examined with the + 10 lens in the aperture, to compensate for
absence of the patient's lens. The optic disc appears smaller as the normal lens acts as a magnifier.

ROUTINE
The optic disc itself is first inspected and accurately assessed.
Then each of the leashes of vessels is traced towards the periphery, using same focus as for the optic
disc. Then the extreme periphery of the retina in each of the 4 meridia.
Then view the macular area -ask the patient to look directly at your light.
Finally, any areas of special interest in the individ~ case; you may have to change focus.
Note that in the normal {undue the retinal vessel~ are curvilinear with a regular calibre and have an
arteriole/venules calibre ratio of 2:3. The temporal arterioles and venules cross frequently. The nasal
vessels are straighter, slightly narrower and cross less frequently.
The presence -of any hemorrhages, exudates or oedema in tile retina is abnormal. The cause must be
speedily determined as the vision may well be threatened. ALWAYS COMPARE DISCS on both sides.

GOLDEN RULE

OPHTHALMOSCOPY -MUST HA VB: GOOD OPHTHALMOSCOPE PATIENT S I1TIN G UP IN THE

DARK DILATED PUPIL

OPTIC DISC ABNORMALITIES 0

I.Papilloedema
Raised Intra-cranial pressure. (Not always so, as in malignant hypertension when may not have increasing
CSF pressure)
Signs are -a. Reddish discolouration of the disc.
b. Engorgement of the veins, leading in severe cases to small haemorrhages and exudates in the adjacent
retina (not generalized).
c. Blurring of the disc margins, which become traversed by grey streaks of oedema, usually starting
around the emergent vessels then at the nasal and finally the temporal margin.
d. Filling-IIi by oedema of the central (physiological) cup in the optic disc. This is NOT invariable. e.
Elevation of the disc. Three diopters of elevation as measured by the ophthalmoscope = Imm of swelling I
f.o Long standing papilloedema leaves elevated pale disc.
g. Vision usually good in early stages, but can be compromised.

2.0ptic Neuritis
Swollen disc similar to papilloedema, though often unilateral unlike papilloedema. Marked visual loss
unlike papilloedema in the early stages. Causes include demyelination (Multiple Sclerosis), drug toxicity,
and temporal arteritis.

3.0ptic Atrophy
Pale disc with often attenuated vessels on surface. Afferent pupil defect (pupil reacts to consensual from
other eye better than direct response). Vision usually poor. Optic atrophy may follow papilloedema or optic
neuritis. Other causes include trauma, vascular od'clusion in retinal or optic nerve, chronic simple
glaucoma, drug toxicity, compressive lesions (tumour or aneurysm).

4.Chronic Simple Glaucoma

Raised intra-ocular pressure increases size of physiologic cup. Cup deepens, temporal margin becomes
reduced and field is gradually irreversibly constricted. Depth of cup is pale. Often asymmetry between the
two eyes. Refer cupping greater than 30%.

5.Drusen of the Optic Disc

Uncommon familial cause of and pseudopapilloedema. Crystalline deposits in nerve head make disc
lumpy. No pathologic significance. Vision nonnal but may have irregular field defects.

VASCULAR ABNORMAUl1ES ;,;~

I.Normal
Retinal arterioles and venules divide on disc. ~al yessels make straight course to periphery while temporal
vessels curve around the macular region.~WV calibre ratio 2/3. In health vessel walls invisible so are
viewing blood column. Therefore, arterioles bright red and the venules darker.

2.Arteriolar Sclerosis '

Arteriole walls thicken with straightening of course. Obscure venule at crossing (Nipping) and lwnen may
appear irregular. See light reflex from vessel wall (Early copper wiring). Causes include normal aging
process, but when marked usually longstanding hypertension.

3. Artery Occlusion
May affect branch or central retinal artery.
Early -retinal oedema (milky white with cherry red spot at macula).
Late -attenuation of vessels and optic atrophy. Causes include arteriolar sclerosis, hypertension,
embolism.

4. Venous Occlusion
More common. Veins engorged with associated retinal haemorrhages and oedema. Causes include
arteriolar sclerosis, hypertension, increased blood viscosity.

5. Neovascularization
New vessels form in response to retinal hypoxia. Tufts of immature capillaries on optic disc or along major
vessels. Tend to bleed and may become gliotic leading to traction retinal detatchment. Causes include
diabetic retinopathy and after vein occlusion.

RETINAL ABNORMALITIES
I.Normal
Colour due to underlying rich choroidal circulation. Amount of pigmentation varies with complexion. Retinal
nerve fibres not myelinated but occasionally myelinated fibres are seen in the retina and appear as white
flame-shaped lesions with feathery edges close to the optic disc (opaque nerve fibres). In childhood the
retina has a brighter "wet looking" reflex. Macular area is avascular.
2.Retinopathy
Term used when there is a breakdown in the blood retinal barrier. May be manifest by haemorrhage,
exudates both soft and hard and occasionally by papilloedema. Seen in diabetes mellitus, hypertension,
venous occlusion and any cause of retinal circulatory disturbance. In diabetes mellitus there are. micro-
aneurysms of capillaries but with normal major retinal vessels compared with the vessel changes seen
with longstanding hypertension. The finding of any of the components of retinopathy is worthy of further
investigation..

3.Drusen
Sago-like whitish/yellow granules in the retina. Not is large as hard exudates and usually no other
evidence of retinopathy. May be familial and can be a precursor of senile macular degeneration in the
elderly.

4.Retinitis
Term indicating an inflammatory origin of retinal fmdings. Classic lesion is pale with irregular heavily
pigmented edge. Common cause is toxoplasmosis. Similar appearance after trauma to retina including
photocoagulation and cryotherapy for retinal detachment.

5.Retinitis Pigmentosa
Not inflammatory but a hereditary dystrophy. Bone corpuscular pigmentation of the peripheral retina
spreading centrally with vessel attenuation and optic atrophy. Night blindness due to rod degeneration in
the retina. Similar findings with Melleril toxicity, Quinine poisoning and syphilis. Less pigmentation with no
visual loss in congenital rubella.

6.Retinal Detachment
Grey mass focussed in front of adjacent retina. May involve entire retina. Vessels seen on folds and may
move with ocular movements. Due to retinal hole (trauma, degeneration, and high myopia). More "solid"
detachment may cover malignant melanoma. '

7.Macular Degeneration
Two types, both seen in the elderly.
i) Exudative type may have rapid central visual loss with elevated yellow mass. at macula. Can be
haemorrhagic also. Often drusen in other eye. Prognosis poor.
ii) Atrophic type have pigmentary disturbance at macula with more gradual visual loss. Commonest cause
of irreversible visual loss in elderly. Retain nonnal peripheral visual field so remain mobile though unable to
read.

METHOD OF DESCRIBING LESIONS IN ORALS AND CLINICALS

1. First give the precise anatomical position of lesion.
2. Then give its general pathology, e.g. vascular, traumatic, neoplastic, etc. Remember, if condition came
on-.
a. Suddenly -then likely to be vascular or traumatic.

b. Within 24-48 hours then likely to be inflammatory change

c. Very Gradually -then neoplastic or degenerative (occasionally chronic inflammatory change)

3. Finally, give its special pathology -if it is inflammatory then, toxoplasmosis, syphilis, tuberculosis, etc

REMEMBER -MORE MISTAKES MADE IN MEDICINE BY NOT LOOKING THAN NOT

KNOWING