Eye diseases & disorders

DISORDERS AND CONDITIONS OF THE EYE
Dr. Pallavi Pathania
Ph.D. MSN

CONDITIONS OF THE EYELIDS AND CONJUNCTIVA
• The eyelids are the outermost defense mechanisms of the eyes, functioning as a
physical barrier as well as to maintain moisture and dispersement of tears. The
palpebral conjunctiva lines the upper and lower lids, and the bulbar conjunctiva
forms a protective coating over the sclera. The conjunctiva responds to
infections, inflammatory disorders, and environmental irritants. Blood vessels in
the conjunctiva dilate readily causing redness, and pain receptors respond to
inflammatory changes. Inflammatory disorders are outlined
– Blepharitis
– Hordeolum (stye)/Chalazion
– Entropion : inward turning of the eyelid margin
– Ectropion: outward turning of the eyelid margin
– Ptosis: drooping of the upper eyelid
– Conjunctivitis

DISORDERS OF THE CORNEA AND UVEAL
TRACT
• The cornea is the outermost tissue that functions in vision. It must
remain clear and smooth to admit light to the retina. Epithelial layers
of the cornea repair rapidly, but if they are penetrated, infection can
rapidly spread inward and vision may be lost.
• The uveal tract is made up of the iris, which controls pupil size; ciliary
body, which secretes aqueous humor and controls accommodation;
and choroid layer, which provides vasculature to the anterior uveal
tract.
– Corneal Abrasion and Ulceration (Keratitis)
– Iritis/ Uveitis

ERROR OF REFREACTION
• MYOPIA { SHORT-SIGHTEDNESS}
• HYPERMETROPIA { LONG- SIGHTEDNESS}
• ASTIGMATISM

OTHER EYE DISORDERS
• CATARACT { DISEASE OF LENS}
• ACUTE (ANGLE-CLOSURE) GLAUCOMA
• CHRONIC (OPEN-ANGLE) GLAUCOMA
• RETINAL DETACHMENT
• Vitreous Haemorrhage
• Central Retinal Artery Occlusion
• Central Retinal Vein Occlusion
• Macular Degeneration
• Retinitis
• Diabetic Retinopathy
• EYE TRAUMA

BLEPHARITIS
An inflammatory reaction of the eyelid
margin caused by bacteria (usually
Staphylococcus aureus) or seborrheic
skin condition, resulting in flaking,
redness, irritation, and possibly recurrent
styes of the upper or lower lid, or both.

*It is Inflammation of the margins of the eye lids.
• ETIOLOGY
* Ulcerative: Staphy infection
* Nonulcerative: Allergies, smoke, dust,
chemicals, seborrhea, stye, chalazions
• SYMPTOMS AND SIGNS
– * Persistent redness & crusting on eyelids
* Itching / burning sensation
* feeling something in the eye
* Ulcers can cause eye lashes to fall out
* Scales can get into eye causing conjunctivitis

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• DIAGNOSIS
* visual examination
* Culture (confirm staphy infection)
• TREATMENT
– Salt & water cleansing for 2 weeks
– If unsuccessful - local antibiotics or sulfonamide
– If S. aureus is likely, antibiotic ointment is prescribed 1
to 4 times per day to eyelid margin. Teach patient to
scrub eyelid margin with cotton swab to remove flaking
and then apply ointment with cotton swab as directed.

HORDEOLUM (STYE)
The term stye refers to an inflammation
or infection of the glands and follicles
of the eyelid margin.

• It is Inflammatory infection of the hair follicle of the eye lid.
• ETIOLOGY
-staphylococcal infection usually associated with Blepharitis
-occurs on the outside
-Pain/swelling/redness/pus
-patient feels something in the eye

• DIAGNOSIS
– * Visual exam
* culture if needed
• TREATMENT
– * Hot compress to alleviate pain
* Topical or systemic antibiotics
– Treatment usually consists of warm soaks to help promote
drainage, good hand washing and eyelid hygiene, and
possible application of antibiotic ointment. In some cases,
incision and drainage in the office with local anesthetic may
be necessary. Teach patient how to clean eyelid margins and
not to squeeze the stye.

CHALAZION (MEIBOMIAN CYST)
It is Collection of fluid or soft mass cyst.
• ETIOLOGY
Blockage of meibomian gland
-Pea size cyst
-painless slow swelling of the inner part of eye lid
-Could become infected

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• DIAGNOSIS
– * Visual Examination
• TREATMENT
* small ones usually disappear spontaneously after
a month or two
* large ones usually need surgical removal

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ENTROPION
• MECHANISM
– * Inversion of eye lid into eye
• ETIOLOGY
– * aging (course fibrous tissue)
– * Foreign body sensation
* Tearing / itching / redness
* Continuous rubbing causes conjunctivitis or
corneal ulcers
Decreased visual acuity if not corrected

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• DIAGNOSIS
– * visual examination
• TREATMENT
– * clean up on its own
* if not, minor surgery

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ECTROPON
• MECHANISM
– * Outurned eye lids
• ETIOLOGY
– * elderly (weakness of eye lid muscles)
– * dryness of the exposed part of the eye
* tears run down the cheeks
* if not treated can cause ulcers and permanent
damage to cornea

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• DIAGNOSIS
• TREATMENT
– * minor surgery if doesn’t disappear

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BLEPHAROPTOSIS (PTOSIS)
• MECHANISM
– * weakness of eye muscle that raises eyelid
(superior rectus, superior oblique)
• ETIOLOGY
– * familial
– * trauma
* diabetes mellitus
– * muscular dystrophy
* myasthenia gravis
– * brain tumors

– * “drooping eye”
* Blocks vision
• DIAGNOSIS
– * ophthalmic examination
* blood work to rule out underlying disease
• TREATMENT
– * Surgery (strengthen muscles)
* eye glasses with raised eyelid support
* treat underlying disease

Conjunctivitis
ANATOMY
• It is the mucous membrane covering the under
surface of the lids and anterior part of the eyeball up
to the cornea.
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• Palpebral; covering the
lids—firmly adherent.
• Forniceal; covering the
fornices—loose—thrown
into folds.
• Bulbar; covering the
eyeball—loosely attached
except at limbus.
• Also marginal and limbal
parts and plica semilunaris.

Nerve supply – Sensory:
• Ophthalmic division of trigeminal
• Blood supply:
– Posterior conjunctival arteries derived from arterial
arcade of lids which is formed by palpebral branches of
nasal and lacrimal arteries of the lids.
– Anterior conjunctival arteries derived from the anterior
ciliary arteries – muscular br. of ophthalmic artery to
rectus muscles.
Venous drainage;
• Palpebral and Ophthalmic veins.

physiology :
• Smooth surface.
• Secretes mucin and aqueous component of tear
film.
• Highly vascular: supplies nutrition to the
peripheral cornea.
• Aqueous veins drains from anterior chamber
maintenance of IOP.
• Lymphoid tissue helps in combating infections.
• Basic secretion—reflex secretion.
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CONJUNCTIVITIS
(PINK EYE)
Inflammation or infection of the bulbar (covering the sclera and
cornea) or palpebral (covering inside lids) conjunctiva. May be
allergic, bacterial (S. aureus, Streptococcus pneumoniae, Haemophilus
influenzae, and others), gonococcal, viral (adenovirus, herpes simplex,
coxsackievirus, and others), or irritative (topical medication,
chemicals, wind, smoke, contact lenses, ultraviolet light) causes.
Trachoma is caused by Chlamydia trachomatis and is a major cause of
blindness worldwide, but is rare in North America. Symptoms of
conjunctivitis vary from mild pruritus and tearing to severe drainage,
burning, hyperemia, and chemosis (edema). The term pink eye usually
refers to infectious conjunctivitis.

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CONJUNCTIVITIS (PINK EYE)
* Inflammation of the
conjunctiva.
• ETIOLOGY
– * Viral / bacterial
* irritants (allergies,
chemicals, UV light)

Acute Bacterial Conjunctivitis
Mucopurulant conjunctivitis
– Caused by:
Staph epidermidis and Staph aureus –usually. Strep
pneumonae, H influensae and Morexella lucanatae
occasionally
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Symptoms:
*Acute onset of redness, grittiness, burning and
discharge.
*Photophobia may be present (corneal
involvement)
*Stickiness of the eyelids
*Usually bilateral disease
Signs:
*Conjunctival hyperaema
*Mild papillary reaction
*Mucopurulant discharge
*Lid crusting

Purulant cojunctivitis (Adult gonococcal)
– Symptoms:
*Hyperacute condition
*Extremely profuse, thick, creamy puss
from the eye or eyes

• Signs:
*Severe conjunctival chemosis
*May be membrane formation
*Periocular edema
*Ocular tenderness
*Gaze restriction
*Lamphadenopathy
*Corneal involvement
• Treatment
Systemic and topical antibiotics
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VIRAL CONJUNCTIVITIS
• The leading cause of a red, inflamed eye is viral
infection. A number of different viruses can be
responsible.
•

Signs & symptoms:
– Vary from moderate to severe.
– Eye redness (hyperemia) is a common
– Swollen, red eyelids
– More tear production in the eyes than usual
– Make you feel as though there is something in
the eye
– Creamy white or thick yellow drainage.
– Sensitivity to light (photophobia)

Allergic Conjunctivitides
Allergy is an altered or exaggerated susceptibility to
various foreign substances or physical agents which are
harmless to the great majority of individuals. It is due
to an antigen antibody reaction.
Allergens is an agent capable of producing a state or
manifestation of allergy.
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Symptoms:
Itching, lacrimation, photophobia, FB sensation,
burning.
Signs:
Giant papilla, ptosis, hyperemia, mucus, trantas dots,
punctate keratopathy, corneal ulcer.

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DIAGNOSIS
– Ophthalmic examination
– Culture discharge
– Slit lamp examination
TREATMENT
– Warm compress 3-4 times daily (10-15 min.)
– If bacterial (antibiotics)
– If viral- self limiting

Prevention:
– Highly contagious
– Spread by direct contact with infected people
– Proper washing and disinfecting can help prevent the spread
– Wash your hands frequently, particularly after applying medications
to the area
– Avoid touching the eye area
– Never share towels or hankies
– Change bed linen and towels daily if possible
– Disinfect all surfaces, including worktops, sinks and doorknobs
– To reduce pain from conjunctivitis use a cold or warm compress on
the eyes
•
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Applying Eye Drop
Medicine• STEP ONE:
Tilt your head back. Using your middle finger,
gently press the corner of the eye
by the side of the nose.
• STEP TWO:
Use your index finger to
pull down the lower lid.
Then apply the eye drop medicine.
• STEP THREE:
After applying the eye drop, let go of your lower lid.
Close the eye and keep the middle finger in place for at
least two minutes. If you’re applying more than one
type of drop, wait at least 15 minutes for the next
application. Use a facial tissue to wipe away excess
drops on eyelids.

Ptregium
• A pterygium is a fleshy growth that invades the cornea. It
is an abnormal process in which the conjunctiva grows into
the cornea.
OR
• It is a fibro vascular, triangular and degenerative condition
of conjunctiva.

Types of Pterygium: two types.
1. Progressive Pterygium: These types of
pterygium are those which progress day by
day.
2. Non Progressive Pterygium: Those
which after limited growth has been occur
than stop their generation.
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Etiology:
– The exact cause is not known.
The probable causes are:
i. Commonly occurs in people living in hot & dry
climate.
ii. Dusty atmosphere.
iii. Common in outdoor workers.
iv. Common in males.
v. It may occur nasal than temporal side.
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Symptoms:
– Redness
– Irritation
– Dryness
– Tearing
– May cause decreased vision ( when it reaches the visual
axis of cornea)
Sign:
-Visible triangular fold of conjunctiva.
- Triangular shape with the apex, or head, extending onto
the cornea.
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Treatment
1. Local:
i. Lubricant eye drops.
ii. Topical steroids for inflammation.
2. Surgical:
i. Surgical excision when the pterygium progressive towards the
cornea.
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Precautions:
-Use sun glasses.
-Protect from sunlight
-Use eye goggles when working.
-(laborers, welders) Wash eye with water after work in
sunlight.
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Trachoma:
• Trachoma is the world’s leading cause of
preventable blindness
• Trachoma is a contagious bacterial infection in the
eye which causes blindness after multiple
reinfections.
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– Trachoma is caused by the bacterium Chlamydia
trachomatis
– Chlamydia trachomatis is spread through direct
contact with an infected person.
– Flies also play a major role in the spread of the
disease.
– Poor sanitation, dirty water, and lack of hygiene
are causes of trachoma.
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Intervention:
– Surgery for trichiasis.
– Antibiotics .
– Facial cleanliness to prevent transmission.
– Environmental change to prevent transmission.
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DISORDERS
OF
THE CORNEA AND UVEAL TRACT
– Corneal Abrasion and Ulceration (Keratitis)
– Iritis/ Uveitis

KERATITIS
Loss of epithelial layers of cornea due to some type of
trauma contact with fingernail, tree branch, spark or other
projectile, or overwearing contact lens. May lead to
corneal ulceration and secondary infection into cornea
(keratitis), which may lead to blindness. Symptoms are
pain, redness, foreign body sensation, photophobia,
increased tearing, and difficulty opening eye.

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KERATITIS
It is inflammation and ulceration of the cornea.
• ETIOLOGY
– * herpes simplex virus (cold sores)
* other bacteria & fungi
* trauma
* dry air or intense light (welding)

• Bacterial keratitis.
• Viral keratitis
• Fungal keratitis
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– * pain or numbness of the cornea
* decreased visual acuity
* irritation
– * tearing
* photophobia
* mild conjunctivitis

• DIAGNOSIS
– * Examination of cornea using slit lamp
* Medical history
* Previous upper respiratory tract infection
• TREATMENT
– Treatment is urgent.
– Fluorescein staining and examination with Woods lamp or slit
lamp to identify the abrasion or ulceration.
– Antibiotic ointment may be instilled and eye patched for 24 hours.
– Cycloplegic drops may also be used in large abrasions or ulcers.
Abrasion heals in 24 to 48 hours. Ulceration should be followed
by an ophthalmologist.
– Teach patient to use topical antibiotic after patch is removed, and
follow up as directed such as wearing protective eye shields, not
rubbing eyes, using contact lenses properly, and washing hands
frequently.

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CORNEAL ABRASION OR
ULCER
• ETIOLOGY
– * foreign bodies
* trauma (fingernail, contact lenses)
– * pain / redness & tearing
* something constantly in eye
* vision impairment

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• DIAGNOSIS
* fluorescien (stain)
• TREATMENT
– * remove foreign bodies
* eye wear for protection.
* eye dressing to reduce movement

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SCLERITIS
– * Inflammation of sclera
• ETIOLOGY
* rheumatoid arthritis
* digestive disorders (Crohn’s)
• * Dull pain
• * Intense redness
* loss of vision (posterior sclera inflammation)
* if untreated can lead to perforation or loss of eye

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• DIAGNOSIS
– * ophthalmic examination
* Blood work to uncover underlying cause
• TREATMENT
– * MILD: eye drops (antibiotics)
* SEVERE: Immunosuppressive drugs
* PERFORATION: surgery

UVEITIS
Uveitis is an inflammation of the intraocular structures.
It is classified by involved structures
(1)anterior uveitis iris (iritis) or iris and ciliary body (iridocyclitis),
(2)Intermediate uveitis structures posterior to the lens (pars plantis or
peripheral uveitis),
(3)Posterior uveitis choroid (choroiditis), retina (retinitis), or vitreous
near the optic nerve and macula. Anterior uveitis is most common
and is usually unilateral. Posterior uveitis is usually bilateral.

• Causes of uveitis are infections;
– Immune-mediated disorders, such as ankylosing spondylitis,
Crohn's disease, Reiter's syndrome, lupus; trauma;
– It may be idiopathic.
– Onset is acute with deep eye pain, photophobia, conjunctival
redness, small pupil that does not react briskly, ciliary flush
(redness around limbus), and decreased visual acuity

TREATMENT
• Urgent ophthalmology evaluation is needed.
• Inflammation is treated with a topical corticosteroid and a
cycloplegic agent.
• Teach patient how to instill medications and adhere to
dosing schedule to prevent permanent eye damage.
• Suggest sunglasses to decrease pain from photophobia.
Encourage follow-up for intraocular pressure (IOP)
measurements because corticosteroids can increase IOP.

ERROR OF REFREACTION DISORDERS
• MYOPIA { SHORT-SIGHTEDNESS}
• HYPERMETROPIA { LONG- SIGHTEDNESS}
• ASTIGMATISM

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MYOPIA (NEAR SIGHTEDNESS)
• MECHANISM
– * object focuses in front of the retina
* able to see only close objects
• ETIOLOGY
– * genetic link
– * blurred vision
* squinting
* eye rubbing
– * headaches

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• DIAGNOSIS
– * Snellen visual acuity test
* opthalmoscope
• TREATMENT
– * concave lens
* radical keratotomy - shallow incision in
the cornea causing it to flatten in desired area
(could have significant complications)

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HYPEROPIA (FAR SIGHTEDNESS)
• MECHANISM
– * object focuses behind the retina
* able to see only far objects
• ETIOLOGY
– * genetic link

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* squinting
* eye rubbing
* headaches
• DIAGNOSIS
– * ophthalmoscope
• TREATMENT
– * Convex lens

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ASTIGMATISM
• MECHANISM
– * Abnormal shaped cornea
(egg shape instead of spherical)
* object is partially clear & other blurred
• ETIOLOGY
– * genetic link

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* squinting
* eye rubbing
* headaches
• DIAGNOSIS
* opthalmoscope
• TREATMENT
– * artificial lens transplant
* radial keratotomy

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PRESBYOPIA
• MECHANISM
– * Rigidity of the lens (old age)
* unable to focus
• ETIOLOGY
– * genetic link
– Old age (< 40 year)
* squinting
* eye rubbing
* headaches

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• DIAGNOSIS
* opthalmoscope
• TREATMENT
– * lens transplant

The lens:
• The crystalline lens is the only structure continuously growing
throughout the life.
• Changeable refractive media.
• Capsule, epithelium and lens fibers.
• Congenital anomalies and effect of systemic diseases.
• Cataract.

Anatomy of lenses:
• Location
-Posterior to iris
-Anterior to vitreous
• Shape: Biconvex
• Structure
• lens capsule
• lens cortex
• lens nucleus

Physiology of lens:
– No vessel, nerve and transparent.
– Derive nutrients from the aqueous humor
– Significant refractive medium
– Accommodative function
– No immediate relation with adjacent tissues
– Complex metabolism
– Simple disorders: transparency and location change
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CATARACT
Clouding or opacity of the crystalline
lens that impairs vision.

CATARACT
Definition:
– Gradual deterioration of lens.
– Opacification of the lens
ETIOLOGY
– Any factors that change the intraocular
environment to affect lens metabolism.
• Such as: ageing, mechanical, chemical,
operation, inflammation, metabolic
– Malformation
– Congenital factors

TYPES
• Senile cataract commonly occurs with aging
• Congenital cataract occurs at birth
• Traumatic cataract occurs after injury
• Aphakia absence of crystalline lens
• Additional risk factors for cataract formation include
diabetes; ultraviolet light exposure; high-dose radiation;
and drugs, such as corticosteroids, phenothiazines, and
some chemotherapy agents.

CLASSIFICATION:
by cause: congenital, senile(age-related),
complicated, metabolitic, drug-induced, toxic,
traumatic, secondary
by age: congenital, acquired
by location: cortical, nuclear, subcapsular
by shape: dot-like, coronary, lamellar
by degree: immature, intumescent, mature,
hypermature
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Risk factors:
• UV
• Diarrhea
• Malnutrition
• Diabetes
• Smoking
• Drinking alcohol
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Mechanism:
many factors lens capsular damage
osmosis increase, loss of protective
screen,metabolic disorders protein
degeneration, cell apoptosis lens
opacify cataract
84

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– * Cloudy / white opaque area of the lens
* reduce visual acuity
* Blurring of vision
* photosensitivity
• DIAGNOSIS
– * Visual examination
* pen light of slit lamp confers the presence of a
cataract
– Direct and indirect ophthalmoscopy to rule out retinal
disease

TREATMENT
– * Intra-capsular phacoemulsification (involves breakage of cataract then aspiration)
* Extra-capsular phacoemulsification: (artificial lens replacement)
• Surgical removal of the lens is indicated.
– A patient with one cataract can usually manage without surgery.
– If cataract occurs in both eyes, surgery is recommended when vision in the better
eye causes problems in daily activities. Surgery is done on only one eye at a time.
• Cataract surgery is usually done under local anesthesia. Preoperative eye
drops produce decreased response to pain and lessened motor activity
(neuroleptanalgesia). Oral medications may be given to reduce IOP.
• IOL implants are usually implanted at the time of cataract extraction,
replacing thick glasses that may provide suboptimal refraction.
• If intraocular lens implant is not used, the patient will be fitted with
appropriate eyeglasses or a contact lens to correct refraction after the healing
process.

SURGICAL PROCEDURES
Two types of extractions:
• Intracapsular extraction The lens as well as the capsule are removed through a small
incision.
• Extracapsular extraction the lens capsule is incised, and the nucleus, cortex, and anterior
capsule are extracted.
– The posterior capsule is left in place and is usually the base to which an IOL is implanted.
– A conservative procedure of choice, simple to perform, is usually done under local anesthesia.
Two types of procedures for extraction are:
– Cryosurgery a special technique in which a pencil-like instrument with a metal tip is
supercooled (-35Â° C), then touched to the exposed lens, freezing to it so the lens is
easily lifted out.
– Phacoemulsification the mechanical breaking up (emulsifying) of the lens by a
hollow needle vibrating at ultrasonic speed. This action is coupled with irrigation
and aspiration of the emulsified particles from the anterior chamber.
– Intraocular Lens Implantation

GLAUCOMA
What is it?
A disease of progressive optic
neuropathy with loss of
retinal neurons and their
axons (nerve fiber layer)
resulting in blindness if left
untreated.

GLAUCOMA
“Glaucoma describes a group of diseases that
kill retinal ganglion cells.”
“High IOP is the strongest known risk factor for
glaucoma but it is neither necessary nor
sufficient to induce the neuropathy.”

GLAUCOMA
Angle AnatomyAngle Anatomy

GLAUCOMA
How do we measure IOP?
•ApplanationApplanation
•TonopenTonopen
•SchiotzSchiotz
•AirAir
•Non-contactNon-contact

GLAUCOMA
TonometryTonometry
ApplanationApplanation
SchiotzSchiotz

Glaucoma: what is
happening
Either:
the drain
blocks here
Or poor
blood supply
here
Damages the optic
nerve..looks ‘caved
in’, called ‘cupped’

Characteristic pattern to loss of visual field
Rim of optic nerve
becomes thinner as disc
caves in and becomes
more cupped

Acute glaucoma
• Emergency
• Can be more gradual
• Red eye
• Achy, abdominal pain
• Misty vision
• Go from light into dark
• Small eye, shallow anterior
chamber, pupil mid dilated,
• Iris lens contact
• Push the iris forward
• Eye feels hard

Chronic glaucoma
• Painless, common in elderly
• Don’t notice anything wrong
• detected by optometrist
• Screening vital
• field, pressure, disc

ACUTE (ANGLE-CLOSURE)
GLAUCOMA
• A condition in which an obstruction occurs at the access to
the trabecular meshwork and the canal of Schlemm. IOP is
normal when the anterior chamber angle is open, and
glaucoma occurs when a significant portion of that angle is
closed. Glaucoma is associated with progressive visual
field loss and eventual blindness if allowed to progress.
This is most commonly an acute painful condition not to
be confused with chronic open-angle glaucoma.

Types of glaucoma
• Congenital
• Secondary
• Juvenile
• Chronic open angle
• Acute closed angle
• Many different
types

PATHOPHYSIOLOGY AND ETIOLOGY
– Mechanical blockage of anterior chamber angle results in accumulation of
aqueous humor (fluid).
– Anterior chamber is anatomically shallow in most cases.
– The shallow chamber with narrow anterior angles is more prone to
physiologic events that result in closure.
– Angle closure occurs because of pupillary dilation or forward displacement
of the iris.
– Angle closure can occur in subacute, acute, or chronic forms.
– Episodes of subacute closure may precede an acute attack and cause
transient blurred vision and pain but no increased IOP.
– Acute angle closure causes a dramatic response with sudden elevation of
IOP and permanent eye damage within several hours if not treated.
– Within several days, scar tissue forms between the iris and cornea, closing
the angle. The iris and ciliary body begin to atrophy, the cornea degenerates
because of edema, and the optic nerve begins to atrophy.

CLINICAL MANIFESTATIONS
• Pain in and around eyes due to increased ocular pressure; may be
transitory attacks.
• Rainbow of color (halos) around lights.
• Vision becomes cloudy and blurred.
• Pupil mid-dilated and fixed
• Nausea and vomiting may occur.
• Hazy-appearing cornea due to corneal edema.
• Although onset may have initial subclinical symptoms, severity of
symptoms may progress to cause acute symptoms of increased IOP
nausea and vomiting, sudden onset of blurred vision, severe pain,
profuse lacrimation, and ciliary injection.

DIAGNOSTIC EVALUATION
– Tonometry elevated IOP, usually greater than 50 mm
Hg.
– Ocular examination may reveal a pale optic disk.
– Gonioscopy (using special instrument called
gonioscope) to study the angle of the anterior chamber
of the eye
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MANAGEMENT
• Emergency pharmacotherapy is initiated to decrease eye pressure
before surgery.
• Medications are prescribed at the discretion of the ophthalmologist
according to the patient's condition and needs.
• Medication classifications prescribed include:
– Parasympathomimetic drugs used as miotic drugs pupil contracts; iris is
drawn away from cornea; aqueous .
– humor may drain through lymph spaces (meshwork) into canal of
Schlemm.
– Carbonic anhydrase inhibitor restricts action of enzyme that is necessary
to produce aqueous humor.
– Beta-adrenergic blockers nonselective may reduce production of aqueous
humor or may facilitate outflow of aqueous humor.
– Hyperosmotic agents to reduce IOP by promoting diuresis.

SURGERY
• Surgery is indicated if:
– IOP is not maintained within normal limits by medical regimen.
– There is progressive visual field loss with optic nerve damage.
• Types of surgery include:
– Peripheral iridectomy excision of a small portion of the iris whereby
aqueous humor can bypass pupil; treatment of choice. Typically a laser
procedure.
– Trabeculectomy partial-thickness scleral resection with small part of
trabecular meshwork removed and iridectomy. Necessary if peripheral
anterior adhesions (synechiae) have developed due to repeated glaucoma
attacks.
– Laser iridotomy multiple tiny laser incisions to iris to create openings for
aqueous flow; may be repeated.
• Other eye is usually operated on eventually as a preventive measure.

CHRONIC OPEN-ANGLE GLAUCOMA
Glaucoma is characterized as a disorder of
increased IOP, degeneration of the optic nerve,
and visual field loss. Open-angle glaucoma makes
up 90% of primary glaucoma cases (angle-closure
glaucoma makes up the other 10%), and its
incidence increases with age. Incidence with
chronic open-angle glaucoma 2% at age 40, 7% at
age 70, 8% at age 80.

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GLAUCOMA
Chronic Open-Angle
Glaucoma
• Increased intraocular pressure due to a
malfunction in eyes aqueous humor drainage
system - can lead to optic nerve damage
– ETIOLOGY
• * trauma
* overuse of steroids

PATHOPHYSIOLOGY AND ETIOLOGY
– Degenerative changes occur in the trabecular meshwork and canal
of Schlemm, causing microscopic obstruction.
– Aqueous fluid cannot be emptied from the anterior chamber,
increasing IOP.
– IOP varies with activity, and some people tolerate elevated IOP
without optic damage (ocular hypertension), whereas others
exhibit visual field defects and optic damage with minimal or
transient IOP elevation.
– The risk of eye damage increases with age, family history of
glaucoma, diabetes, and hypertension.

SYMPTOMS AND SIGNS
– Mild, bilateral discomfort (tired feeling in eyes, foggy vision).
– Slowly developing impairment of peripheral vision central vision unimpaired.
– Progressive loss of visual field.
– Halos may be present around lights with increased ocular pressure
• DIAGNOSIS
* Ophthalmic examination
* tonometry (pressure measure)

MANAGEMENT
• Treated with a combination of topical miotic agents (increase the outflow of aqueous
humor by enlarging the area around trabecular meshwork) and oral carbonic anhydrase
inhibitors and beta-adrenergic blockers (decrease aqueous production).
• If medical treatment is not successful, surgery may be required, but is delayed as long as
possible.
• Types of surgery include:
– Laser trabeculoplasty
– Iridencleisis an opening is created between anterior chamber and space beneath the
conjunctiva; this bypasses the blocked meshwork, and aqueous humor is absorbed
into conjunctival tissues.
– Cyclodiathermy or cyclocryotherapy the ciliary body's function of secreting aqueous
humor is decreased by damaging the body with high-frequency electrical current or
supercooled probe applied to the surface of the eye over the ciliary body.
– Corneoscleral trephine (rarely done) a permanent opening at the junction of the cornea
and sclera is made through the anterior chamber so aqueous humor can drain

Acute Angle-Closure
Glaucoma
It is complete blockage of aqueous humor drainage
system.
ETIOLOGY
• * trauma

– * Blurred vision
– * severe eye pain
* redness of the eye
– * nausea & vomiting
* photophobia (sees “halo” around light)
* hazy cornea (elevated pressure)
* if untreated --> blindness
• DIAGNOSIS
– * goniolens (special lens to view the opening)
• TREATMENT
– * LASER IRIDOTOMY (creation of a hole in the iris
between the anterior and posterior chamber)
* medications to reduce pressure

RETINA:
• light-sensitive
layer of tissue
• sends visual
messages
through the optic
nerve

RETINAL DETACHMENT
Detachment of the sensory area of the
retina (rods and cones) from the
pigmented epithelium of the retina. A
break in the continuity of the retina
may first occur from small
degenerative holes and tears, which
may lead to detachment.

Retinal detachment
The separation of neurosensory retina (NSR) from
the retinal pigment epithelium (RPE) by subretinal
fluid (SRF).
113

PATHOPHYSIOLOGY
• pulled away from the underlying choroid
• small areas of the retina torn =>
retinal tears or retinal breaks
• retinal cells deprived of oxygen
• if not promptly treated => permanent
vision loss
114

Types of RD
• Rhegmatogenous RD (RRD)
• Tractional RD
• Exudative RD
• Combined tractional-rhegmatogenous
RD
115

Rhegmatogenous RD (RRD)
• Affect about 1 in 10,000 of the population each year.
• Both eyes may eventually involved in about % of cases.
Acute PVD (Posterior Vitreous Detachment):
• A separation of the cortical vitreous from the internal
limiting membrane (ILM) of the sensory retina posterior
to the vitreous base.
Myopia:
Over 40% of all RDs occur in myopic eyes.
Trauma:
Responsible for about 10% of all cases of RD and is most
common cause in children.
116

Tractional Retinal detachment
• 1. PDR ( proliferative diabetic retinopathy )
• 2. ROP ( retinopathy of prematurity )
• 3. Penetrating posterior segment trauma
117

Exudative Retinal detachment
1. Choroidal tumor:
Melanomas, metastases
2. Inflammation:
Posterior scleritis
118

SYMPTOMS
• floaters - bits of debris in field of vision
that look like spots, hairs or strings

SYMPTOMS:
• floaters
• light flashes
• shadow or curtain over a portion of
visual field
• blur in vision

Can occur as a result of:
• trauma
• advanced diabetes
• an inflammatory disorder, such as
sarcoidosis
• shrinkage of the jelly-like vitreous that
fills the inside of the eye

• vitreous liquid leaks through retinal tear and
accumulates underneath retina
• retina can peel away from underlying layer of
blood vessels

Factors that may increase risk of retinal
detachment:
• aging - more common in people older than
40
• previous retinal detachment in one eye
• family history of retinal detachment
• extreme nearsightedness
• previous eye surgery
• previous severe eye injury or trauma

Diagnostic Evaluation
– Indirect ophthalmoscopy shows gray or opaque
retina. The retina is normally transparent. Slit-
lamp examination and three-mirror gonioscopy
magnify the lesion.
11/1/2011 125

TREATMENTS
Retinal tears:
• laser surgery (photocoagulation)
• freezing (cryopexy)
Retinal detachment:
• pneumatic retinopexy
• scleral buckling
• vitrectomy

MANAGEMENT
• Sedation, bed rest, and eye patch may be used to restrict eye
movements.
• Surgical intervention may be indicated.
• Return of visual acuity with a reattached retina depends on:
– Amount of retina detached before surgery
– Whether the macula (area of central vision) was detached
– Length of time the retina was detached
– Amount of external distortion caused by the scleral buckle
– Possible macular damage as a result of diathermy of cryocoagulation
• Surgical reattachment is successful approximately 90% to 95% of the
time. If retina remains attached 2 months postoperatively, condition
likely to be corrected and unlikely to reoccur

Nursing care:
• Asses visual status and functional vision in the unaffected eye to
determine self care needs.
• Prepare the client for surgery by explaining possible surgical
interventions and technique to alleviate some of the client's
anxiety.
• Discourage straining during defecation, bending down and hard
coughing, sneezing or vomiting to avoid activities that increase
intraocular pressure.
• Assist with ambulation, as needed, to help the client remain
independent.
• Approach the clients from the unaffected side to avoid startling
him.
• Provide assistance with activities of daily living to minimize
frustation adn strain.
• Orient the client to his environment to reduce the risk of injury.
• Posoperatively instruct the client to lie on his back or on his
unoperated side to reduce intraocular pressure in the affected
area.
133

134
MUSCULAR DISORDERS
• NYSTAGMUS
• STRABISMUS (CROSS EYED)

135
NYSTAGMUS
• MECHANISM
* repetitive involuntary movements of one
or both eyes
• ETIOLOGY
* Congenital
* Brain tumors
* CV lesions
* Ear lesions
* Alcohol/drug abuse

136
– * Eye Movements
*Horizontal, vertical, circular, or combination
* blurred vision
• DIAGNOSIS
* viewing of the eyes - involuntary movement
* complete neurological tests
• TREATMENT
* Treat the underlying condition
* Congenital stays for life

137
STRABISMUS (CROSS EYED)
• MECHANISM
– * Failure of eyes to look in the same direction
at the same time
* Weakness of muscles of one eye
(superior oblique, interior oblique, lateral)
• ETIOLOGY
– in childhood: associated with amblyopia
(decreased vision in one eye)
(reversible after 7 years of age)
in adults: Usually caused by disease:
i.e. diabetes, high blood pressure, brain
trauma

138
– * TYPES:
1. Esotropia (convergent-cross eye of one
eye)
2. Exotropia (divergent- one eye turns
outward)
3. Diplopia (adults strabismus)
4. Congenital (no strabismus exists)

139
• DIAGNOSIS
– * complete ophthalmic examination
* Diagnose underlying disease
• TREATMENT
– * Treat early
* Corrective glasses
* orthoptic training
* surgery to restore eye muscle balance
* treat underlying disorder

Blindness:
DEFINITIONS:
• blindness: visual acuity of less than 3/60
or its equivalent.
• low vision: visual acuity of less than 6/ 18
but ≥ 3/60 or corresponding to visual
field loss to less than 20° in the better
eye with best possible correction.
• avoidable blindness: blindness which
could be either treated or prevented by
known cost-effective means.
140

CAUSES OF BLINDNESS:
In Developed Countries: accidents, glaucoma,
diabetes, vascular diseases(hypertension),cataract and
degeneration of ocular tissues esp. of the retina and
hereditary conditions.
In Developing Countries:
cataract-62.6%
refractive errors-19.7%
glaucoma-5.8%
post. segment disorder-4.7%
surgical complication-1.2%
141

Causes Of Childhood Blindness:
refractive errors, trachoma, conjunctivitis,
xerophthalmia, congenital cataract ,
retinopathy of prematurity.
Causes Of Avoidable Blindness:
cataract, trachoma, childhood blindness,
refractive errors, glaucoma, diabetic
retinopathy
142

Reheblitation :
 Skills person with blindness or low
vision may need
– Compensatory skills
– Visual efficiency skills
– Literacy and Braille skills
– Listening skills
– Orientation and mobility skills
– Social interaction skills
– Independent living skills
– Recreation and leisure skills
– Career and transition skills
143

• In general, students with blindness and low
vision should learn the same information as
general education students although more
time and accommodations might be needed.
• Counseling to deal with reactions from others
• Possible teaching of care for prosthetic eye
• Adaptations for color or visual discrimination
problems
• Responding to traffic signals, etc.
• Provide a copy of teacher’s notes
• Read aloud
• Supply audio tapes/CDs of print materials
• Use hands-on models and manipulatives
144

• Assist through touch and sound, more than
sight, for those with little or no functional
vision.
• Use specialized equipment.
• Provide equal access to the core curriculum.
• Do not re-arrange the furniture or leave items
in the path.
• Determine the LRE based on student needs
and strengths, preferences, and related
services needs.
• In general, provide appropriate lighting, tactile
materials, necessary print size, and decrease
visual clutter.
145

• Use programs to magnify computer
screens.
• Scan materials for access.
• Provide Braille if the student uses it.
• Use of a guide dog may be needed.
• May scan in materials and use a
synthesizer that reads the text to the
student
• Voice recognition software applications
146

• Request large print materials in advance.
• Get training on the use of optical devices and
software.
• Encourage student relationships and interaction.
• Support emotional and learning needs.
• Provide daily cues.
• Consult with vision specialist regularly.
• Use tactile materials.
• Reduce glare on materials.
• Speak in normal tones.
• Tell the student when you are leaving the room.
• Maintain high expectations and give regular
feedback.
147

BASIC REHABILITATION
• The activities on the basic rehabilitation are
directed at rehabilitating the person’s social
functions with the purpose of optimum
accomplishing a self-dependent life.
• The following basic rehabilitation activities take
place at the NRCB:
148

Training in orientation and mobility
this training helps students to move in new
conditions -
149

Visual rehabilitation
the better usage of poor sight
150

Useful skills
rehabilitates the previous everyday skills and
assists the acquisition of new ones under the
conditions of bad damaged or missing sight
152

Braille training
assists the overcoming of the informational
deficit
153

Computer training for blind people, operating a
computer with synthetic speech or a Braille display
Computer training for visually impaired people,
operating a computer with a visual monitor
155

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