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The eyeball is a bilateral and spherical organ, which houses the structures responsible for vision. It lies in
a bony cavity within the facial skeleton – known as the bony orbit.

Anatomically, the eyeball can be divided into three parts – the fibrous, vascular (Uveal tract)
and inner layers.


The eyeball can be divided into the fibrous, vascular and inner layers. These layers have different
structures and functions. We shall now look at these layers in further detail.

1. Fibrous Layer

The fibrous layer of the eye is the outermost layer. It consists of the sclera and cornea, which are
continuous with each other. Their main functions are to provide shape to the eye and support the
deeper structures.

 The sclera
comprises the majority of the fibrous layer (approximately 85%). It provides attachment to
the extraocular muscles – these muscles are responsible for the movement of the eye. It is
visible as the white part of the eye.
 The cornea
is transparent and positioned centrally at the front of the eye and is the first surface that light
hits on the way to the retina. The cornea has several functions but the most important is the
cornea refracts or bends light entering the eye toward the lens of the eye which then focuses on
the retina. The cornea is also where a contact lenses rest and where LASIK is performed.
2. Vascular Layer (UVEA)

The vascular layer of the eye lies underneath the fibrous layer. It consists of the choroid, ciliary body and

 Choroid – layer of connective tissue and blood vessels. It provides nourishment to the outer
layers of the retina.

 Ciliary body – comprised of two parts – the ciliary muscle and ciliary processes. The ciliary
muscle consists of a collection of smooth muscles fibres. These are attached to the lens of the
eye by the ciliary processes. The ciliary body controls the shape of the lens, and contributes to
the formation of aqueous humor

 Iris – circular structure, with an aperture in the centre (the pupil) and is what gives the eyes
their color . The diameter of the pupil is altered by smooth muscle fibres within the iris, which
are innervated by the autonomic nervous system. It is situated between the lens and the

3. Inner Layer

The inner layer of the eye consists of the retina, the light detecting part of the eye. The retina itself is
composed of two cellular layers:

 Neural layer – the innermost layer of the retina. It consists of photoreceptors; the light
detecting cells of the retina. It is located posteriorly and laterally in the eye.

 Pigmented layer – the outer layer of the retina. It is attached to the choroid layer and acts to
support the neural layer. It continues around the whole inner surface of the eye.

Anteriorly, the pigmented layer continues but the neural layer does not – this is part is known as
the non-visual retina. Posteriorly and laterally, both layers of the retina are present. This is
the optic part of the retina.

The optic part of the retina can be viewed during ophthalmoscopy. The centre of the retina is marked by
an area known as the macula. It is yellowish in colour, and highly pigmented. The macula contains a
depression called the fovea, which has a high concentration of light detecting cells. It is the area
responsible for high acuity vision. The area that the optic nerve enters the retina is known as the optic
disc – it contains no light detecting cells.

Other Structures in the Eyeball

Within the eyeball, there are structures that are not located in the three layers. These are the lens and
the chambers of the eye.

 Lens
The lens of the eye is located anteriorly, between the vitreous humor and the pupil of the iris.
The shape of the lens is altered by the ciliary body, altering its refractive power. In old age, the
lens can become opaque – a condition known as a cataract.
 Pupil
Not so much an actual structure, the pupil is simply a hole in the middle of the iris that allows
light to enter the eye. The size of this hole is controlled by muscles in the iris and enlarges under
dim illumination (like driving at night) and gets smaller or constricts under strong illumination
(like bright sunlight). Malfunction of the pupil and iris are often signs of neurological problems.
Additionally, it is through this hole that doctors assess the health of the interior of the eye, often
putting pharmacological or “dilating” drops in to force the pupil open and allow clearer viewing
of internal structures.
 Conjunctiva
This is a tissue that lines the inside of the eyelids and covers the sclera (the white of the eye). It
is composed of unkeratinized, stratified squamous epithelium with goblet cells, and stratified
columnar epithelium. The conjunctiva is highly vascularized, with many micro vessels easily
accessible for imaging studies. When the eye gets “red” it is the conjunctival vessels that are
enlarging with the goal of bringing more blood cells to the area to fight off a potential infection.
When this happens, the inflammation or infection of the conjunctiva is called conjunctivitis
 Trabecular Meshwork
This meshwork of connection tissue is located where the iris meets the cornea and functions by
draining the aqueous fluid from the front of the eye and through the Schlemm’s canal, back into
the blood stream. Very commonly, the trabecular meshwork does not function properly in
patients with glaucoma which cause a backup in fluid and increased pressure in the eye. Several
very effective medications and surgical treatment exist to the increase the fluid outflow through
this structure.


The eyeball is divided into two segments, each of which is filled with fluid. The pressure generated by
these fluids fills out the eyeball and helps maintain its shape.

 Anterior segment (anterior and posterior chambers)

 Posterior segment

Anterior segment

The anterior segment) extends from the inside of the cornea to the front surface of the lens. It is filled
with a fluid called the aqueous humor, which nourishes the internal structures. The anterior segment is
divided into two chambers. The anterior chamber extends from the cornea to the iris. The posterior
chamber extends from the iris to the lens. Normally, the aqueous humor is produced in the posterior
chamber, flows slowly through the pupil into the anterior chamber, and then drains out of the eyeball
through outflow channels located where the iris meets the cornea.

Posterior segment

The posterior segment extends from the back surface of the lens to the retina. The posterior segment
includes the retina, choroid and optic nerve head as well as the vitreous compartment filled with a
jellylike fluid called the vitreous humor.
DEFINITION: Glaucoma is a group of eye diseases which result in damage to the optic nerve and cause
vision loss. It represents a final common pathway for a number of conditions, for most of which raised
intraocular pressure is the most important risk factor


There are two main types of glaucoma

 Open angle glaucoma

 Closed angle glaucoma

Open angle glaucoma

There are a variety of different types of glaucoma. The most common forms are:
 Primary Open-Angle Glaucoma
 Most common in SL
 It occurs mainly in the over 40 age group.
 There are usually no symptoms associated with POAG.
 The pressure in the eye slowly rises and the cornea adapts without swelling. If the cornea were
to swell, which is usually a signal that something is wrong, symptoms would be present. But
because this is not the case, this disease often goes undetected.
 It is painless, and the patient often does not realize that he or she is slowly losing vision until
the later stages of the disease.
 However, by the time the vision is impaired, the damage is irreversible.
 It may be hereditary

 Normal Tension Glaucoma

also known as low-tension glaucoma

characterized by progressive optic nerve damage and visual field loss with a statistically
normal intraocular pressure.
 NTG is generally regarded as a subcategory of POAG, although some have suggested a
distinct pathogenesis, such as vascular anomalies, systemic hypotension, and inherited
abnormalities of the optic nerve.
 It is present in 0.1% of the population.
 Pigmentary Glaucoma
 Pigmentary glaucoma is a type of inherited open-angle glaucoma that develops more
frequently in men than in women.
 Nearsighted patients are more typically afflicted. The anatomy of the eyes of these
patients appears to play a key role in the development of this type of glaucoma.
 Myopic (nearsighted) eyes have a concave-shaped iris which creates an unusually wide
angle. This causes the pigment layer of the eye to rub on the lens.

This rubbing action causes the iris pigment to shed into the aqueous humor and onto
neighboring structures, such as the trabecular meshwork. Pigment may plug the pores of
the trabecular meshwork, causing it to clog, and thereby increasing the IOP.
 Exfoliation Syndrome
 most common among people of European descent.
 whitish material which upon slit-lamp examination looks somewhat like tiny flakes of
dandruff, builds up on the lens of the eye.
 This exfoliation material is rubbed off the lens by movement of the iris and at the same time,
pigment is rubbed off the iris. Both pigment and exfoliation material clog the trabecular
meshwork, leading to IOP elevation, sometimes to very high levels.
 Trauma-Related Glaucoma
 A blow to the eye, chemical burn, or penetrating injury may all lead to the development of
glaucoma, either acute or chronic.
 This can be due to a mechanical disruption or physical change within the eye´s drainage
 It is therefore crucial for anyone who has suffered eye trauma to have check-ups at regular

Closed angle glaucoma

 A condition of elevated IOP resulting from partial or complete occlusion of the angle by the
 It is present in around 0.1% of the general population over 40yrs old, but up to 1.5% of the
Chinese population over 50.

Risk factors
 Age: increasing age (uncommon <40yrs)
 Race: African-Caribbean: more frequent, younger onset, more severe
 FH: first degree relative confers 1 in 8 risk; higher in siblings
 Steroid-induced IOP elevation: more common in POAG and those with FH of POAG
 People who have:
 Diabetes
 Myopia (nearsightedness)
 Regular, long-term Steroid/Cortisone use
 A previous eye injury
 high intraocular pressure (IOP).
High IOP is the most important risk factor for glaucomatous damage
Clinical features
 Usually asymptomatic; (rarely eye ache and haloes—transient corneal edema if rapid increase in
 IOP>21mmHg, often with high diurnal variability.
 Disc changes: C/D asymmetry, high C/D for disc size, vertical elongation of the cup
 Visual field defects:
 focal defects respecting the horizontal meridian including nasal step, baring of the blind
spot, arcuate defects, and altitudinal defects
 generalized depression.

The patient might complain of the following

 Blurry vision
 Seeing haloes
 Bumping into stationary objects
 Loss of peripheral vision
 Redness
 Pain
 Corneal edema


Visual symptoms -Asymptomatic; haloes, ache, precipitants (dim light, exercise); subjective loss of

POH -Previous surgery/trauma; concurrent eye disease; refractive error

PMH- Diabetes, hypertension, smoking; migraine, Raynaud’s phenomenon; vascular disease;

asthma/COPD, renal disease

FH- Family members with glaucoma and their outcome

Dx-Current/previous topical medications, current drugs (interactions), systemic beta blockers,

current/previous use of steroids (any route)

Ax -Allergies or relevant drug contraindications

Diagnosing Glaucoma
Your eye doctor has a variety of diagnostic tools that aid in determining whether or not you have
glaucoma -- even before you have any symptoms. Let us explore these tools and what they do.

The Tonometer
The Tonometer measures the pressure in the eye. If your doctor were to use applanation tonometry,
your eye would be anesthetized with drops. Then, you would sit at the slit lamp, and a plastic prism
would lightly push against your eye in order to measure your IOP. In air tonometry a puff of air is sent
onto the cornea to take the measurement. Since this instrument does not come in direct contact with
your eye, no anesthetic eye drops are required.

Visual Field Test

Testing your visual field lets your doctor know if and how your field of vision has been affected by
glaucoma. The visual field is an important measure of the extent of damage to your optic nerve from
increased IOP. There are several methods of examination available to your doctor. In computerized
visual field testing you will be asked to place your chin on a stand that appears before a computerized
screen. Whenever you see a flash of light appear, you will be asked to press a button. At the end of this
test, your doctor will receive a printout of your field of vision. Another test that is similar is the
Goldmann perimeter. However, in this test, no computer is used. The examiner records your answers
whenever you indicate that the light is in view.

Ophthalmoscopy (fundoscopy)
Using an instrument called an ophthalmoscope, your eye doctor can look directly through the pupil at
the optic nerve. Its color and appearance can indicate whether or not damage from glaucoma is present
and how extensive it is. (Chorioretinal scarring, retinoschisis, retinal detachment)

Visual acuity
Visual acuity is a measurement of central vision only. Assessment of total visual system from cornea to
occipital cortex. Visual acuity can be tested for both distance and near vision. Distance visual acuity is
the most common test. Measured with the use of either a Snellen chart or an E-chart.

Cup:Disc Ratio
Normal 0.3-0.5
Abnormal values are higher and are associated with glaucoma.

Treating Glaucoma
Glaucoma can be treated with eyedrops, pills, laser surgery, eye operations, or a
combination of methods. The whole purpose of treatment is to prevent further loss of vision.
This is imperative as loss of vision due to glaucoma is irreversible. Keeping the IOP under
control is the key to preventing loss of vision from glaucoma.

Decrease the production of aqueous humour
Increase the outflow of aqueous humour
Drugs (medical approach)

Note: beta blockers are contraindicated in

 Asthmatic
 HF
 Heart blocks

Surgical interventions (1st line in children)

When medication does not achieve the desired results, or when it has intolerable side effects, your
ophthalmologist may suggest surgery.

 Laser Surgery
Laser surgery has become increasingly popular as an intermediate step between drugs and
traditional surgery. The most common type performed for open-angle glaucoma is called
This procedure takes between ten and twenty minutes, is painless, and can be performed in
either a doctor´s office or in an outpatient facility. The laser beam (a high energy light beam) is
focused upon the eye´s drain. Contrary to what most people think, the laser does not burn a
hole through the eye. Instead, its intense heat causes some areas of the eye´s drain to shrink,
resulting in adjacent areas stretching open and permitting the fluid to drain more easily.
 Traditional Surgery (preferred method for children)
The most common of these operations is called a trabeculectomy. In this procedure, the
surgeon removes a small section of the trabecular meshwork -- the eye´s drain. This allows the
aqueous humor to drain more easily, reducing the pressure in the eye. It is important to note
that your eyes may not have their normal visual acuity for several weeks following this
procedure. Although trabeculectomy is a relatively safe surgical procedure, about one-third of
patients develop cataracts within five years of surgery. After trabeculectomy, most patients are
able to discontinue all anti-glaucoma medications. Perhaps ten to fifteen percent of patients
require additional surgery.

 Glaucoma drainage tube implants

 Ciliary body ablation

Complications of glaucoma surgery

1. Cataract
2. Decreased vision
3. Hypotony (IOP <5mmHg)
4. Infections
5. Wound leak
6. Excessive filtration
7. Pupillary block
8. Retinal detachment

A cataract is a clouding of the lens in the eye that affects vision. Most cataracts are related to aging.
Cataracts often develop slowly and can affect one or both eyes.

What is the lens?

 A biconvex structure attached to the ciliary process by the zonular fibre, between iris & vitreous
 Non-vascular, colorless and transparent
 Index of refraction 1.336
 Consists of stiff elongated, prismatic cells known as lens fibre, very tightly packed together
 Divided into nucleus, cortex and capsule
 The whole lens enclosed within an elastic capsule
 Helps to refract incoming light and focus it onto the retina



There are three primary types of cataracts:
1. nuclear sclerotic
2. cortical
3. posterior subcapsular
Nuclear Sclerotic Cataracts
A nuclear cataract is the most common type of cataract, beginning with a gradual hardening and
yellowing of the central zone of the lens also known as the nucleus. Over time, this hardening and
yellowing will expand to the other layers of the lens. A nuclear sclerotic cataract progresses slowly and
may take several years of gradual development before it begins to affect vision.

Cortical Cataracts
A cortical cataract forms in the shell layer of the lens known as the cortex and gradually extends its
“spokes” from the outside of the lens to the center. These fissures can cause the light that enters the
eye to scatter, creating problems with blurred vision, glare, contrast and depth perception. People with
diabetes are at risk for developing cortical cataracts.

Posterior Subcapsular Cataracts

Primarily affecting one’s reading and night vision, this type of cataract begins as a small opaque or
cloudy area on the posterior (back surface) of the lens. It is called subcapsular because it forms beneath
the lens capsule which is a small sac or membrane that encloses the lens and holds it in place.
People who use steroids or have diabetes, extreme nearsightedness, and/or retinitis pigmentosa may
develop this type of cataract. Subcapsular cataracts can develop rapidly and symptoms can become
noticeable within months.


Maturity of cataract
 Immature: opacification is incomplete (the lens is partially opaque)
 Mature: opacification is total (the lens is completely opaque)
 Hypermature: lysis of cortex results in shrinkage, seen clinically as wrinkling of the capsule.
 Morgagnian: liquefaction of cortex allows the harder nucleus to drop inferiorly (but still within
the capsule).


Visual symptoms: Blur at distance/near, glare, distortion, colour perception, ‘second sight’ (myopic

POH: Previous acuity, previous surgery, trauma; concurrent eye disease;

PMH: Diabetes, hypertension, intrauterine disease; ability to lie flat and still for 30min;

anaesthetic history: (if GA considered)

FH: history of 1st degree relative with cataract

DH: steriods

SH: Occupation, driving, hobbies, daily tasks


Your ophthalmologist will examine and test your eyes to make a cataract diagnosis. This comprehensive
eye exam will include dilation. This means eye drops will widen your pupils (tropicamide,
Cyclopentolate, Phenylephrine)

Slit-lamp exam
Your ophthalmologist will examine your cornea, iris, lens and the other areas at the front of the eye.
The special slit-lamp microscope makes it easier to spot abnormalities.

Retinal exam
When your eye is dilated, the pupils are wide open so the doctor can more clearly see the back of the
eye. Using the slit lamp, an ophthalmoscope or both, the doctor looks for signs of cataract

Refraction and visual acuity test

This test assesses the sharpness and clarity of your vision.


 Cataracts can be removed only with surgery.

 If your cataract symptoms are not bothering you very much, you don’t have to remove a
cataract. You might just need a new eyeglass prescription to help you see better.
 You should consider surgery when cataracts keep you from doing things you want or need to

How does cataract surgery work?

During cataract surgery, your eye surgeon will remove your eye’s cloudy natural lens. Then he or she
will replace it with an artificial lens. This new lens is called an intraocular lens (or IOL)

Presbyopia-correcting IOLs potentially help you see at all distances, not just one. In most cases, unless
you choose presbyopia-correcting IOLs, you will still need reading glasses after cataract surgery.


 Corneal edema (most common)

 Patient can go blind
 Raised IOP
 Infection (endoophthalmitis)
 Retinal detachment
 Hyphema (Bleeding in the front of the eye)
 cystoid macular edema (Swelling and fluid in the center of the nerve layer)
Inflammation of the uveal tract with associated inflammation of the adjacent structures such as cornea,
sclera, vitreous and retina. Uvea consists of middle layer of pigmented vascular structures of the eye
which Includes the iris, ciliary body, and choroid.

Types (anatomically)
1. anterior uveitis (most common uveitis) - localized to anterior segment - iritis and iridocyclitis.
 Includes iridocyclitis and iritis.
 Iritis is inflammation of the anterior chamber and iris.
 Iridocyclitis presents the same symptoms as iritis, but also includes inflammation in the
ciliary body

2. intermediate uveitis
 -centered immediately behind iris and lens in region of ciliary body and pars plana -
cyclitis and pars planitis.
 Consists of vitritis -inflammation of cells in vitreous cavity.
 Deposition of inflammatory material on the pars plana.
 "Snowballs”, Inflammatory cells in the vitreous.
3. posterior uveitis
 inflammation of choroid (chorioiditis)
 and or associated inflammation of retina (chorioretinitis)
4. Panuveitis (diffuse, Endophthalmitis) – the whole uvea is involved

1. Noninfectious Causes Behcet disease.
 Crohn's disease
 HLA-B27 related uveitis
 Sarcoidosis
 Spondyloarthritis
 Sympathetic ophthalmia.
2. Infectious causes
 Brucellosis  Tuberculosis
 Leptospirosis  Zika Fever.
 Lyme disease
 Syphilis

3. Associated with systemic diseases

 Inflammatory Bowel  Kawasaki's Disease
Disease  Multiple Sclerosis
 Reactive Arthritis  Whipple's Disease.
 Sarcoidosis
4. Drug related side effects
 Rifabutin, a derivative of Rifampin has been shown to cause uveitis.
 Quinolones especially Moxifloxacin may lead to uveitis.
 All of the widely administered vaccines have been reported to cause uveitis.

Anterior uveitis

 Burning.  Eye pain.

 Redness  Photophobia or sensitivity to light
 Blurred vision  Floaters, which are dark spots that float
 Headaches in the visual field
 Irregular pupil

Intermediate uveitis Posterior uveitis

Most common  Floaters

 Blurred vision
 Floaters
 Photopsia or seeing flashing lights
 Blurred vision


 Diagnosis includes dilated fundus examination to rule out posterior uveitis which
presents with white spots across the retina along with retinitis and vasculitis.
 Laboratory testing is usually used to diagnose specific underlying diseases, including
rheumatologic tests (e.g. antinuclear antibody, rheumatoid factor, angiotensin
converting enzyme inhibitor) Serology for infectious diseases (e.g. Syphilis,
Toxoplasmosis, Tuberculosis).

What should treatment achieve?

1. Relieve pain and discomfort

2. Prevent sight loss due to the disease or its complications
3. Treat the cause of the disease where possible, that is, treat the inflammation.

The drugs used to treat uveitis fall into 3 main groups

1. Steroids
2. Immunosuppressant
3. Mydriatics.


Steroids have wide ranging effects but their action may be looked on as being anti-inflammatory and
immunosuppressant". They are used in different forms:

 Eye drops.
 Periocular injections.
 By oral (tablets).
 Intra-venous infusion (drip).
 Eye Drops: Used for Anterior Uveitis. Drops can penetrate the part of the eye in front of the lens,
where anterior uveitis occurs

 Periocular Injections: Use of injections around the eye to deliver the steroid treatment.

 In certain situations, injections offer a better way than either tablets or drops. They are used along with
other forms of treatment.

 Oral Steroids E.g. Prednisolone Tablet.

 The use of systemic steroids is more serious than, steroid drops because in this form there are
potentially significant side effects.
 Many different situations in which oral steroids are considered
• If anterior uveitis is resistant to treatment with drops and injections then systemic steroids
• The main use of oral steroids is to treat posterior uveitis, panuveitis
• when rapid control of inflammation is needed high dosage of steroid needs to be delivered
Side effects of steroids
Delay wound

Activation of

May produce profound and irreversible vision loss!

1. Cataract
2. Glaucoma
3. Retinal detachment
4. Neovascularization of retina, optic nerve, iris
5. Cystoid macular edema (most common cause of decreased vision from uveitis).

Common Ocular Drugs

 Antimicrobials  Anti-inflammatory (NSAIDS,
 Antivirals Corticosteroids)
 Antifungals  Local anesthetics
 Mydriatics and cycloplegics  Ocular diagnostic drugs
 Antiglaucoma

I. Antibacterials (antibiotics)
 Penicillins  Fluoroquinolones (ciprofloxacin,
 Cephalosporins moxifloxacin, levofloxacin)
 Sulfonamides  Vancomycin
 Tetracyclines  macrolides (Topical ophthalmic
 Chloramphenicol azithromycin, erythromycin)
 Aminoglycosides (gentamycin,
neomycin, tobranycin)
Uses Of Antibiotics
 Used topically in prophylaxis (pre and postoperatively) and treatment of ocular bacterial
 Used orally for the treatment of preseptal cellulitis e.g. amoxycillin with clavulonate, cefaclor
 Used intravenously for the treatment of orbital cellulitis e.g. gentamicin, cephalosporin,
vancomycin, flagyl
 Can be injected intravitrally for the treatment of endophthalmitis

II. Ocular diagnostic drugs

 Fluorescein dye Available as drops or strips
USES: stain corneal abrasions, applanation tonometry, detecting wound leak, NLD obstruction,
fluorescein angiography
 Rose bengal
USES: stain devitalized epithelium so severe dry eye, herpetic keratitis
III. Local anesthetics
1. Topical e.g. propacaine, tetracaine
Uses :
 applanation tonometry,  removal of sutures,
 goniscopy,  examination of patients who
 removal of corneal foreign cannot open eyes because of
bodies, pain
adverse effects :
 toxic to corneal epithelium
 allergic reaction rarely
2. Local anesthetics e.g. lidocaine, bupivacaine
 cause anesthesia and akinesia for intraocular surgery
IV. Antivirals (INDICATIONS HZ keratitis Viral uveitis)
 Acyclovir  Cytarabine
 Idoxuridine  Triflurothymidine
 Vidarabine  Gancyclovir

 Polyenes (amphotericin B, natamycin, nystatin)
 Imidazoles (miconazole, ketoconazole,fluconazile )
VI. Mydriatics and cycloplegics (Dilate the pupil, ciliary muscle paralysis)
 Short acting- Tropicamide (4-6 hours)
 Intermediate- homatropine (24 hours)
 Long acting- atropine (2 weeks)
 corneal ulcer
 uveitis
 cycloplegic refraction

VII. Anti-inflammatory (corticosteroid, NSAID)

1. Corticosteroids
 Short acting: hydrocortisone, cortisone, prednisolone
 Intermediate acting Trimcinolone, Fluprednisolone
 Long acting Dexamethasone, betamethasone

 Topical
(allergic conjunctivitis, scleritis, uveitis, allergic keratitis, after intraocular and extra ocular surgeries)
 Systemic (pathology behind the LENS)
(uveitis Optic neuritis corneal graft rejection)
Complications of topical administration
 Mechanical injury from the bottle e.g. corneal abrasion
 Pigmentation: epinephrine- adrenochrome
 Ocular damage: e.g. topical anesthetics, benzylkonium
 Hypersensitivity: e.g. atropine, neomycin, gentamicin
 Systemic effect: topical phenylephrine can increase BP

Visual acuity is a measurement of central vision. The test for visual acuity can be used to diagnose
refractive errors.

Normal Vision 6/6

Normal vision relies on the following:

• Both eyes in alignment (extraocular muscles functioning)
• Clear cornea
• Clear lens of the eye
• Clear ocular media (aqueous and vitreous)
• Intact retina, optic nerve, visual pathway

Patient Requirements
• Patient’s co-operation
• Patient’s comprehension of what is required
• Ability to recognise images used on the various charts (letters, numbers or pictures)
• Distance correction (glasses or contact lenses)

Why do a visual acuity test?

• Diagnostic tool
• Baseline data
• Measures progression of disease
• Evaluates treatment

Vision Testing Tools

 The Snellen Chart is used in most facilities for testing distance vision. They are designed to be
read at 6 metres or 3 metres (usually indicated on chart)
 E chart is used in NESB (non-English speaking background) or illiterate patients. Patient matches
direction of E with fingers
 Sheridan Gardiner. For use with children, illiterate, aphasic patients. Patients match letter seen
with letter on handheld card Often used by Community / Rural nurses
Using the Snellen Chart
 Place patient 3 or 6 metres from chart
(depending on the chart)
 Use adequate illumination
 Cover left eye with occluder / pad or
cupped hand
 Ask patient to read from the top letter
 Keep going until they cannot read the
line clearly and start to make multiple
errors. The previous line is the line you
 Encourage patient to keep going as
some give up easily
 Encourage patient to relax and blink
 If the 6/6 line is not reached, use
pinholes to see if vision improves
 If yes, continue testing vision until the
patient is unable to clearly identify
further letters/ numbers


Expressed as a ratio recorded as X / Y. Where X is the testing distance and Y refers to the line containing
the smallest letter that the patient identifies. For example, a patient has a visual acuity of 6/9

Record visual acuity (VA) for each eye
Include pinhole (PH) if used
If wearing glasses or contact lenses please document
Artificial eyes need to be noted too

Examples: RVA 6/9 LVA 6/6 (with glasses)

PH 6/6

RVA 6/60 LVA prosthesis

PH no improvement
 If the patient cannot see the top line of the chart, walk patient towards the chart so they are at
3 metres.
 Still can’t read the chart? Ask patient to count how many fingers you are holding up at 1 metre.
Keep fingers still. Recorded as Count Fingers (CF @1m)
 If they cannot count fingers see if they can see a moving hand. Recorded as Hand Movements
(HM @1m)
 Still no result: can they see a pen torch light: Light perception (LP)
 Unable to perceive light: No Light Perception (NLP)

E chart