OPHTHALMOLOGY COURSE FOR MED V

Adigrat University, School of Medicine

Tesfalem H.(MD)

 Credit hours: 3 hours

Course category: Minor
Course objective;
To know theoretical and practical aspects of common
eye diseases
To facilitate early referral system to ophthalmologists

INTRODUCTION

Terms
Visual impairment: VA of < 6/18- 3/60
Blindness: visual acuity of <3/60 with the better eye
with best correction

EPIDEMIOLOGY OF BLINDNESS
According to the WHOs 2010 global data on
VI ,
285 million visually impaired
39 million blind

80 % of the total global burden was due to

preventable causes

WHO,2010.

 The burden of total blindness, and VI in Africa

was 15%, 9.2% of the above global figures
respectively.
1.2% of the entire population of Africa is
blind, and cataract causes 36% of this
blindness

 According to 2006 National Blindness and

Low Vision Survey in Ethiopia,
National prevalence of blindness was 1.6% and
that of low vision was 3.7%.
1.2 million blind people, 2.8 million people with
low vision

Causes of Low Vision, National Blindness and Low Vision Survey of

Ethiopia, 2005-6.

Causes of Blindness. National Blindness and Low Vision Survey of

Ethiopia, 2005-6.

ANATOMY OF THE EYE AND

ADNEXA

 THE EYE IS THE MIRROR OF THE

BODY

Choroid
Retina

Zonular fibers
Lens

Sclera
Cornea

Central retinal vessels

A/C

Optic nerve

Iris
P/C
Ciliary body
Vitreous

ORBIT
It's an anatomic space bounded by orbital bone
Pear shaped, tapering posteriorlly to apex
Has a volume of 30ml
Contains
- Eye ball
- Extraocular muscle
- Nerves
- Blood vessels
- Connective tissue

 Bony Orbit made of seven bones

1.Frontal bone
2.Maxillary bone
3. Zygoamatic bone
4. Ethmoid bone
5. Sphenoid bone
6. Lacrimal bone
7.Palatine bone

Palatine
bone
Spheno
id bone

EYE LID
-Has the following parts

Skin
Orbicularis oculi muscle
Orbital septum
Orbital fat
Levator palpebrae muscle and aponeurosis
Muller muscle
Tarsus
Conjunctiva

Inferior tarsal

 Anterior lamella..skin and orbicularis oculi muscle

Posterior lamella..levator , Muller , tarsus, and
conjunctiva.
Anterior and posterior lamella are separated by a gray line,
which is an avascular zone .
Land marks on the lid
-Gray line
-Eye lashes
-Opening of the meibomian glands
-Punctum

 The lid skin is the thinnest,mobile,with little /no subcutaneous tissue

Orbicularis oculli muscle
Has two parts
- Orbital and palpebral (preseptal and pretarsal)
Function..lid closure(blink)
Innervated by facial nerve
Orbital septum
Is an extension of the periostium from the superior and inferior
orbital margin
Limits anterior or posterior extension of blood, edema or
inflammation

10/30/16

27

Levator muscle
Originates from a tendon that blends with superior rectus and
superior oblique in the orbital apex
Levator aponuerosis inserts in to lower 2/3rd of the tarsus and
Muller at the upper tarsal boarder
Fibrous element of the muscle passes through the orbicularis
and inserts subcutaneously to form the superior eye lid
fold/crease.
Function..major elevator of the eye lid
Innervated by superior division of the oculomotor nerve.

Muller muscle
Elevates the eye lid minimally
Innervated by sympathetic fibers.
Tarsus
A dense connective tissue which gives firmness and rigidity to
the eyelids

Meibomian glands

Upper lid..30-40, and lower lid..20-30 in number

Produce oily secretion over the lid margin
**Arterial supply of the eyelid
By the facial and ophthalmic artery which are branches of
external and internal carotid.
** Venous drainage
To internal and external jugular veins, cavernous sinus.
** Lymphatic drainage
Medial 1/3rd drains to submandibular lymphnods, lateral 2/3 rd to
perioricular lymphnodes

LACRYMAL GLAND
- Produces 90% of the tear
- Has 2 parts.. Larger orbital and palpebral parts
ACCESSORY LACRYMAL GLANDS
-Glands of Krause and wolfring
-Located at the proximal lid border and conjunctival fornix
- Accounts for 10% of the total tear secretion.

LACHRYMAL DRAINAGE SYSTEM

-Lacrimal puncta..measures 2mm long
-Lacrimal canaliculi..measures 8-10 mm long, 90% of the cases
the upper and lower canaliculi join to form common canaliculi
-Lacrimal sac..measures 12mm long, found in the lachrymal fosa
-Nasolacrimal duct.. Measures 18mm long, connects the lower
end of the sac with middle meatus of the nose, in 30% of the
cases NLD is closed at birth by a membrane up to 6 months of
age.

 Tear produced to keep the eye moist is produced by the

accessory lachrymal gland, but excess production as in crying
is mainly from the main lachrymal gland. The tear produced
enters the conjunctival fornix then through the punctum,
canaliculi ,common canaliculi, lachrymal sac, nasolachrymal
duct and finally gets evaporated by movement of air in the
nose.
TEAR FILM
-Has three layers..outer oily layer, middle watery layer and inner
mucin layer

 Oily layer..is

produced mainly by meibomian gland but also

by glands of zies and moll.
- Function is to prevent evaporation of the watery layer.
Watery/aqueous layer..is produced by accessory lachrymal
glands and main lacrymal gland
- Function 1.Supplies oxygen to the avascular cornea
2.Provides antibacterial and antiviral activity
3.Washes away debris
4.Smothens minute corneal irregularities

 Mucin layer..is produced by conjunctival goblet cells.

- Function..makes the corneal epithelium hydrophilic which is
important for even distribution of the tear film over the cornea.

THE EYE BALL

-Has an AP diameter of 23.6 mm

CONJUNCTIVA
-Is a mucous membrane that covers the eye lid and the eye ball
-Has 3 parts..palpebral, bulbar and fornicial.

Tenons capsule
- Is a facial sheath that lies under the conjunctiva
- Helps to position and support the eye ball within the orbital
cavity.
- It is fused to the sclera posteriorly at the optic nerve. Anteriorly
it ends beneath the conjunctiva. It is separated from the sclera
primarily by the episcleral space.

SCLERA
-Forms the posterior 5/6th of the eye ball
-Thinnest at the insertion of the extraocular muscles and thick at
the posterior pole.
-The sclera is pierced at three sites
1. Anteriorly ..anterior ciliary arteries at the level of rectus
muscle insertion.
2. Middle ..by the vortex veins, 4mm posterior to the equator
3. Posterior.. Fibers of the optic nerve, ciliary nerves, central
retinal vessels

 Episclera..is a loose connective tissue and the most superficial

part of the sclera which has a vascular plexus formed by the
branches of the anterior ciliary artery.
Blood supply..sclera is an avascular structure but anterior to the
insertion of the recti muscle anterior ciliary arteries form
episcleral plexus and posterior sclera gets its blood supply from
long and short posterior ciliary arteries.

**Nerve supply..is from the long and short ciliary

nerves
** Function
1. Protection of the intraocular structures
2. Gives the eye ball its shape
3. Provides a rigid insertion for the extraocular
muscles

CORNEA
Forms the anterior 1/6th of the eye ball
Convex and elliptical in shape.
Dimensions
- Vertical..10.6mm in diameter
- Horizontal..11.7mm in diameter
- Thickness at center..0.5mm and periphery..1mm
- Diopteric power 43D

 Has six layers

- Epithelial layer
- Bowmans membrane
- Stromal layer
- Duaes layer
- Descemets membrane
- Endothelial layer

 Epithelial layer is formed of a superficial non keratinized

squamous epithelium and basal columnar epithelium.
-Running between epithelial cells there are naked nerve
endings which are sensitive mainly to pain.
Bowmans layer is cellular formed of collagen fibers
Stroma..forms 90% of the corneal thickness
Descemets membrane is a basement membrane of the
endothelial cells
Endothelial cells..are single layer of hexagonal shaped cells
forming the inner layer of the cornea.

 Blood supply..cornea is avascular , it is nourished by diffusion

from the aqueous humour and tear film.
Nerve supply.. By the long cilliary nerve.
Function ..it is the main refractive media.
The corneal epithelium is capable of regeneration after
damage but other layers dont.
The corneal epithelium and endothelium maintains the normal
fluid content of the cornea; any damage causes corneal edema.

 Transparency of the cornea results from

-Uniform spacing of collagen fibers in the stroma
- Avascularity of the cornea
- Homogeneous corneal epithelial arrangement
- Corneal epithelial and endothelial barrier function
- Corneal endothelial active pump function

Limbus
-Is a 1.5mm-2mm wide ring found between the cornea and sclera.
** Surgical limbus marks the point of entry for all anterior
segment surgeries.

UVEAL TRACT
Is the main vascular component of the eye.
Consists of three parts
-Iris, ciliary body and choroid
The uveal tract is firmly attached to the sclera at the scleral spur,
exit of the vortex veins, and optic nerve.

IRIS
-Is made up of pigmented cells, blood vessels, and connective
tissue.
-The iris diaphragm divide the anterior segment in to anterior and
posterior chamber.

 Has a dilator and sphincter muscles

Dilator muscle is innervated by the sympathetic
fibers and helps for pupilary dilation
Sphincter muscle upon innervation by the
parasympathetic fibers causes pupilary constriction.

CILIARY BODY
Is triangular in cross section, bridges the anterior and
posterior segment.
Function..aqueous secretion and accommodation.
Has two parts..pars plana and pars plicata.
Pars plana..is 4mm wide , avascular extends from the oraserata to ciliary process.
- Is the safest area for posterior surgical
space i.e vitreous
- Located 3-4 mm posterior to the limbus

 Pars plicata has folds on which the zonular fibers of the lens
attach
Ciliary body is lined by pigmented and nonpigmented
epithelium , along the lateral intercellular space near the apical
boarder of the non pigmented epithelium are tight
junction(zonula occludenties) that maintains the blood
aqueous barrier.
Ciliary body has 3 layers of muscles longitudinal, radial, and
circular, when innervated by the parasympathetic fibers it
initiates accommodation.

LENS
Is biconvex and transparent
Is one of the refractive media of the eye like the cornea , aqueous
& vitreous.
10mm in diameter , 4mm in thickness, has a diopteric power of
15D.
Parts..capsule, cortex, epinucleus, nucleus.
Zonules of the lens attach to the ciliary body and keeps it in place.
The lens accommodates and changes its shape to a more globular
form to see an object at near.
The lens grows through out life.

 Anterior chamber..0.2ml aqueous in volume, 3mm in AP diameter

Posterior chamber..0.06mL in volume.

AQUEOUS HUMOR
-Produced by the ciliary body
-Rate of formation 2-6 micro liter/min
- Turns over every 1-2 hr
- Out flow 90% through posterior chamber-pupil-anterior chambertrabecular meshwork-canal of shlem-collector canal-scleral vein
- 10% passes anterior to the ciliary body suprachoroidal space- vortex
vein
- Function of the aqueous..supplies the cornea and lens with nutrients and
oxygen, and maintains the shape of the eye ball

VITREOUS BODY
- Is a transparent gel which occupies a space between the lens and retina,
- Forms 80% of the volume of the eye
- Contents - 90% water
- 10% Salt , soluble proteins, hyaluronic acid, fine collagen
fibers, macrophages.
- It is bound by anterior and posterior hyaloid membrane.
- Is attached to the retina at the ora serata, margin of the optic disc, blood
vessels,macula and to the ciliary body at the pars plana.
- Function..optical media, maintains the shape of the eye, supports the
lens, keeps the RPE and neurosensory retina attached.
- The vitrous undergoes degeneration and liquefaction with aging.

CHOROID
-Is the posterior part of the uveal tract.
-Consists of three layers of blood vessels
*Inner choriocapillaries
* Middle layer of small vessels
* Outer layer of large vessels
- Perfusion of the choroid comes from long and short posterior
cilliary arteries and from perforating anterior ciliary arteries.
- Venous blood drains through the vortex vein
- Blood flow through the choroid is high as compared to other
tissues.

Bruches membrane
-Is formed from fusion of the basal lamina of the RPE and
choriocapilaries.
- Extends from ora-serata to optic disc.
- Any defect in bruches membrane causes subretinal neovascular
membrane.

RETINA
Is a purple red,transparent nervous coat of the eye which is in
contact with the vitrous and bruches membrane at its inner
and outer surface respectively.
Two major layers: the outer pigmented layer and inner
neurosensory retina.

 Has 10 microscopic layers

1. Retinal pigment epithelium
2. Rods and cons
3. External limiting membrane
4. Outer nuclear layer
5. Outer plexiform layer
6. Inner nuclear layer
7. Inner plexiform layer
8. Ganglionic cell layer
9. Nerve fiber layer
10.Inner limiting membrane

Outer

Neuro-sensory retina
Inner

 A center of the posterior part of the retina which is oval and

yellow colored called macula lutea with its center fovea
centralis.
Macula and fovea centralis has the most distinct vision
RPE cells have tight junction which forms the blood retinal
barrier.

Functions of RPE
Absorbs light
Maintains the subretinal space
Phagocytoses rod and cone outer segments
Participates in retinal and polyunsaturated fatty acid
metabolism
Forms the outer blood- ocular barrier
Heals and forms scar tissue

 Rods..are responsible for vision in a dim light

.. 120 million in number
Cons ..Are responsible for vision in a bright light
.. 6.5 million in number
.. Detect colors
.. Detailed resolution

OPTIC DISC
-Lies 3mm medial to the macula
-Pale pink in color,circular, well demarcated
-1.5mm in diameter.
- Depressed at the center where CRA & CRV passes
- Optic disc fibers forms the optic nerve after passing the lamina cribrosa
- Devoid of rods and cons , this area is non seeing forming blind spot.
** Blood supply
-Choriocapilaries supply RPE,rods and cons, outer nuclear layer
-CRA(central retina artery) supplies from outer plexiform layer inwards.

OPTIC NERVE
It represents peripherally extended nerve tract of the
brain
Parts of optic nerve and its course
- Intra ocular
-1mm
- Intra orbital
-25mm
- Intra canalicular - 5-9mm
- Intra cranial
-16m

Extraocular muscles
- Four rectus muscles and two oblique muscles
- Origin.. Four rectus muscles from the annulus of zin, superior
oblique from trochlia, inferior oblique from the lachrymal crest
- Insertion..5.5mm, 6.5mm, 6.9mm, 7.7mm from the limbus in the
sclera for medial, inferior, lateral and superior rectus respectively.
- Superior oblique..superior posterior and lateral part of the sclera.
- Inferior oblique.. Inferior posterior, and lateral part of the sclera, at
the level of the macula.

- The lateral rectus muscle is supplied by a single

artery but all others by two anterior ciliary arteries .
- Oculomotor nerve..innervates SR,MR,IR,IO,
trochlear nerve innervates the superior oblique, and
abducence nerve innervates the LR.
Function..ocular motility.

HISTORY
Obtaining a thorough history from the patient is an important first step
in an ophthalmic evaluation.
In general the history includes
-Demographic data: name, sex, race and occupation
-Chief compliant: the main problem that prompted the visit
-History of present illness: more detailed description of the chief
compliant.
-Present status of vision, visual needs, and any ocular symptoms.
-Past ocular history: prior eye disease, injuries, surgery, medication, and
use of glasses.
-Past/ present systemic allergies, systemic illness like DM, HTN
-Family history of poor vision, known ocular or systemic illness.

PHYSICAL EXAMINATION

Visual acuity examination (both distance and near, with and

with out pinhole)

Tonometry to determine intraocular pressure.
Pupillary light reflex
Ocular alignment and motility tests
Examination of the external eye and ocular adnexa.
Examination of the anterior segment.
Examination of the posterior segment

Diseases of the eyelids

Infections & inflammation of the eyelids

Chronic Marginal blepharitis

Blepharitis is an inflammation of the eyelids causing red,

irritated, itchy eyelids and the formation of dandruff-like
scales on eyelashes.
It is the most frequently encountered ocular disease
Caused by either bacterial or a skin condition such as
dandruff of the scalp or acne rosacea.
It affects people of all ages.

Classification:
1. Anterior blepharitis inflamation of eyelid skin, lash roots & glands
along eyelid margin
a. Staphylococal
b. Seborrhoeic
c. Mixed

2.Posterior blepharitis inflamation of the tarsal plate and

meibomian glands,characterized by meibomian gland
dysfunction(MGD), which may lead to ocular surface
disease as well.
3.Mixed anterior & posterior

Anterior blepharitis
Commonly caused by bacteria (staphylococcal blepharits) or
dandruff of the scalp and eyebrows (seborrhoeic blepharitis).
Less commonly due to allergies or infestation of the eyelashes
(lice, mite)

Posterior blepharitis
Caused by irregular oil production by the glands of the eyelids
(meibomian blepharitis)
Creates a favorable environment for bacterial growth.
It can also develop as a result of other skin conditions such as
acne rosacea and scalp dandruff.

Diagnosis
Patient history to determine any symptoms the patient is experiencing
and the presence of any general health problems that may be
contributing to the eye problem.
External examination of the eye, including lid structure, skin texture
and eyelash appearance.
Evaluation of the lid margins, base of the eyelashes and meibomian
gland openings using bright light and magnification.
Evaluation of the quantity and quality of tears for any abnormalities.

Staphylococal blepharitis

Signs
Hyperemia of lid margin with hard
scales around base of the
lashes( collarettes), mild sticking
together of the lids
Notching, scaring,poliosis &
madarosis in severe long standing
cases.
Treatment
Lid hygiene with diluted baby
shampoo
Topical antibiotic ointment in severe
cases

Seborrhoeic blepharitis

Signs
Hyperaemic anterior lid
margin ,oily/greasy debris & soft
scales clinging to sticky lashes

Treatment
Similar to staph. blepharitis

Meibomian Gland Dysfunction(MGD)

Meibomian blepharitis is evident by blockage of the oil
glands in the eyelids, poor quality of tears, and redness of the
lining of the eyelids and ocular surface irritation.
Lipase-producing bacteria alter the glandular secretion

 Most patients have nonspecific complaints inconsistent with

the degree of disease clinically evident on examination.

Lid margins have

Focal or diffuse inflammation
With telangiectasia around the meibomian gland orifices.
The orifices are pouting, obstructed, displaced, or reduced
in number.

Meibomian gland dysfunction

Meibomian gland dysfunction

Management
Patient education and lid hygiene with warm
compresses and expression of glands every day to
alleviate symptoms.
Oral tetracycline (250 mg PO Qid)or doxycycline
(100 mg po Bid), for weeks to months.
These medications decrease production of bacterial
lipases and thus decrease fatty acid levels.

How is blepharitis treated?

The key to treat most types of blepharitis is keeping the lids
clean and free of crusts.
Warm compresses can be applied to loosen the crusts, followed
by gentle scrubbing of the eyelids with a mixture of water and
baby shampoo.
If the glands in the eyelids are blocked, the eyelids may need to
be massaged to clean out oil accumulated in the eyelid glands.

 Artificial tear solutions or lubricating ointments may be

prescribed in some cases.
Use of an anti-dandruff shampoo on the scalp can help.
Limiting or stopping the use of eye makeup is often
recommended, as its use will make lid hygiene more difficult.
Blepharitis seldom disappears completely even with successful
treatment, relapses may occur

Diseases of the eyelids

External hordeolum( stye)

It is a staphylococcal infection of eyelash follicle or

sebaceous glands of eyelash roots
Signs
Tender,erythematous nodule in the lid margin pointing
through the skin which may be associated with cellulitis
Treatment
Hot compression
Epilation of lash associated with infected follicle
Antibiotic ointment
Systemic antibiotics such as cloxacillin if preseptal
cellulitis develops

Diseases of the eyelids

Internal hordeolum
Staphylococal infection of the meibomian glands
Acute tender and red swelling on the internal part of eyelid
Treatment
- As external hordeolum

Diseases of the eyelids

Chalazion
A chalazion is a slowly enlarging and painless nodule on the
eyelid that is formed by inflammation and obstruction of a
sebaceous gland.
Lipogranulomatous reaction to sebaceous secretions
Categorized into superficial or deep
Inflammation of the meibomian glands leads to deep
chalazia, whereas inflammation of Zeis sebaceous glands
leads to superficial chalazia.
Chalazia can reoccur, and those that do should be evaluated
for malignancy

Diseases of the eyelids

Predisposition
Chronic posterior blepharitis
Acne rosacea
Seborrhoeic dermatitis
Chalazia are more common in adults than in children.

Chalazion

Work-up
1. History: previous chalazion excision?
2. Palpate the involved eyelid, feeling for a
nodule
3. Slit-lamp exam: Evaluate the meibomian
glands and evert the involved eyelid

DDx
1. Hordeolum
2. Sebaceous cell carcinoma( should be
suspected in recurrent chalazion)
3. Pyogenic granuloma

Signs of chalazion (meibomian cyst)

Painless, roundish, firm lesion

within tarsal plate

May rupture through conjunctiva

and cause granuloma

Diseases of the eyelids

Chalazion

Treatment
1. Conservative management
. More than 50% of chalazia resolve with conservative
treatment.
- Warm compresses for 15-20 minutes qid
- Lid hygiene with baby shampoo
2. Topical or systemic antibiotics usually are not necessary
because chalazia are secondary to sterile inflammation.

3. Surgical Incision & curretage if chalazion does not

disappear after 3-4 weeks of appropriate therapy.

Surgical treatment of chalazion

njection of local anaesthetic

Insertion of Incision and curettage

clamp

Diseases of the eyelids

MOLLUSCUM CONTAGIOSUM
DNA poxvirus causes multiple, round, waxy umbilicated skin
papules.
Lid margin skin papules may be associated with a toxic
follicular conjunctivitis , superior micropannus and fine
epithelial keratitis
Severe disseminated disease may occur in patients with AIDS.
The diagnosis is based on recognition of the characteristic
lesions.
Incision with scalpel blade, followed by expression of the viral
bead

Molluscum contagiosum

Multiple, dome-shaped, waxy papules are

situated along the lid margin

POSITIONAL DEFECTS OF THE LID

ENTROPION
ECTROPION
TRICHIASIS

Diseases of the eyelids

Entropion
Sign
Inward turning of the eyelid margin

Other signs

Superficial punctate keratitis (SPK) (from eye

lash contacting the globe), conjunctival
injection
Symptom

Ocular irritation, foreign-body sensation,tearing,red eye

Etiology
Involutional ( aging)
Cicatricial ( Due to conjunctival scarring )
Spastic (Due to surgical trauma, ocular
irritation, or blepharospasm)
Congenital

Involutional entropion

ffects lower lid because upper lid If longstanding may result

as wider tarsus and is more stablein corneal
ulceration

Cicatricial entropion

Severe scarring of palpebral conjunctiva

which pulls lid margin towards globe
May affect lower or upper eyelid
Causes include cicatrizing conjunctivitis,
trachoma and chemical burns

Congenital entropion

Very rare - not to be confused with epiblepharon

Inturning of entire lower eyelid and lashes
Absence of lower lid crease
When skin is pulled down lid also pulls
away from globe Does not resolve
spontaneously

Diseases of the eyelids

Treatment
Antibiotic ointment for SPK
Everting the eyelid margin away from globe & taping it in place
with adhesive tape may be a temporizing measure.
Surgery for permanent correction.

Diseases of the eyelids

ECTROPION

Sign

Outward turning of the eyelid margin

Other signs

SPK (may result from exposure keratopathy),

conjunctival injection & eventually keratinization
( from conjunctival drying)

Symptom

Tearing eye or eyelid irritation ; may be asymptomatic

Etiology

Congenital
Paralytic( 7th nerve palsy)
Involutional( aging)
Cicatricial (due to chemical burn,
surgery,trauma scar, others)
Mechanical (Due to herniated orbital fat, eyelid
tumor)

Involutional

Affects lower lid of elderly patients

May cause chronic conjunctival inflammation
and thickening

Causes of cicatricial ectropion

Contracture of skin pulling lid away from globe
Unilateral or bilateral, depending on cause

Unilateral ectropion due to

traumatic scarring

Bilateral ectropion due to severe

dermatitis

Paralytic ectropion
Caused by facial nerve palsy which,
If severe, may give rise to the following:

Epiphora
Exposure keratopathy caused
by caused by combination of:
lagophthalmos
Failure of lacrimal pump
mechanism
Increase in tear production
resulting from corneal exposure

Diseases of the eyelids

ECTROPION
Treatment

Treat exposure keratopathy with lubricating agents

Treat an inflammed , exposed eyelid margin with warm compresses
and antibiotic ointment
Definitive treatment usually requires surgery.

Diseases of the eyelids

Trichiasis
Sign

Posterior misdirection of
normal lashes rubbing
against the globe

Symptoms

Ocular iritattion, foreignbody sensation, tearing,

red eye

Diseases of the eyelids

Causes:

Idiopathic
Secondary: - Chronic anterior blepharitis
- Herpes zoster ophthalmicus
- Trachoma

Treatment
1. Remove the misdirected lashes
A. If few misdirected lashes:
- Remove them at slit lamp with fine forceps (recurrence is common)
B. Diffuse, severe, or recurrent trichiasis:
- Definitive Rx, generally requires electrolysis, cryotherapy, or surgery
2. Treat SPK with antibiotic ointment

Diseases of the eyelids

PTOSIS &
PSEUDOPTOSIS
Defn.:
Ptosis is the drooping
of the upper eyelid due
to innervation or
myopthy of levator
musle or aponeurosis

Evaluation
Pseudoptosis
True ptosis

Causes of pseudoptosis

Lack of lid support Contralateral lid retraction

Ipsilateral hypotropiaBrow ptosis - excessive

Dermatochalasis - excessive
eyebrow skin
eyelid skin

CLASSIFICATION OF PTOSIS
1. Neurogenic

Third nerve palsy

Third nerve misdirection
Horner syndrome

2. Myogenic
Myasthenia gravis
Myotonic dystrophy
Ocular myopathies
Simple congenital

3. Aponeurotic
4. Mechanical

Mechanical ptosis
Causes

Dermatochalasis

Severe lid oedema

Large tumours

Anterior orbital lesions

Evaluation of ptossis
History: congenital/acquired, family Hx,
Variability in degree of ptosis during day &
night time
Physical exam: 4 clinical measurements
Vertical interpalpebral fissure height
Marginal- reflex distance
Upper eyelid crease position
Levator function( upper eyelid excursion)

 Treatment
Surgical correction

TUMORS OF THE EYELIDS

Benign tumors
Malignant tumors

BENIGN EYELID LESIONS

1. Cysts

Cyst of Moll
Cyst of Zeiss
Sebaceous cyst
Hidrocystoma

2.
Viral wart
Tumours

Keratoacanthoma
Capillary
haemangioma
Naevus
Port-wine stain
Pyogenic granuloma
Cutaneous horn

MALIGNANT EYELID TUMOURS

1. Basal cell carcinoma
2. Squamous cell carcinoma
3. Meibomian gland
carcinoma
4. Melanoma
5. Kaposi sarcoma

Basal Cell Carcinoma

. Most common human malignancy
. Usually affects the elderly
. Slow-growing, locally invasive
. Does not metastasize
. 90% occur on head and neck
. Of these 10% involve eyelids

. Accounts for 90% of eyelid malignancies

quency of location of basal cell carcinom

Lower lid - 70%

Medial canthus - 15%

Upper lid - 10%

Lateral canthus - 5%

Squamous cell carcinoma

Less common but more aggressive than BCC
May arise de novo or from actinic keratosis
Predilection for lower lid

Nodula
r

Hard, hyperkeratotic
nodule
May develop crusting
fissures
No surface

Ulcerative

Red base
Borders sharply defined, indurated
and elevated

Meibomian gland carcinoma

Very rare aggressive tumour with 10% mortality

Predilection for upper lid
Nodular

Hard nodule; may Very large tumour

mimic a chalazion

Spreading

Diffuse thickening of lid Conjunctival invasion;

margin and loss of lashes
may

Melanoma
Nodular

Superficial spreading From lentigo maligna

(Hutchinson freckle)

Plaque with irregular

Affects elderly
Blue-black nodule with
normal surrounding outline
skin
Slowly expanding
May be non-pigmented
Variable pigmentation
pigmented macule

Kaposi sarcoma
Vascular tumour occurring in patients with AIDS
Usually associated with advanced disease
Very sensitive to radiotherapy

Early

Pink, red-violet lesion

Advanced

May ulcerate and bleed

Treatment Options
1. Surgical excision

Method of choice

2. Radiotherapy

Small BCC not involving medial

canthus

Kaposi sarcoma

3. Cryotherapy

Small and superficial BCC

irrespective of location

Adjunct to surgery in selected cases

DISEASES OF THE CONJUNCTIVA

Conjunctivitis
Trachoma
Degenerations (Pterygium, pinguecula)
Tumors of conjunctiva
Xerophthalmia

Conjunctivitis
Definition: a general term for any infection or inflammation of
conjunctiva
Classification
Usually is based on cause, including viral, bacterial, fungal,
parasitic, toxic, chlamydial, chemical, and allergic agents.
It also can be based on age of occurrence or course of disease.
Etiology often can be distinguished on clinical grounds.

Epidemiology
Conjunctivitis is extremely common
The vast majority of pediatric cases are bacterial, while in adults
bacterial and viral causes are equally common
Conjunctivitis occurs in all ages.

Conjunctivitis
Symptoms:
Eye discomfort in the eye ( conjunctivitis does not cause any real pain )
Vision should be normal
Signs vary much according to type
Vasodilatation of superficial vessels(redness)
Increased secretion the character of secretions helps to diagnose the cause
Purulent or mucopurulent acute bacterial infection
Watery( serous) typical of viral infection
Thick sticky mucus allergic conjunctivitis
Edema of conjunctiva (chemosis)
Follicles (enlarged nodules of lymphoid tissue)
Papillae (central core of hypermic blood vessels surrounded by edema &
inflammatory cells)
Membrane formation
Scarring

Follicle

Papilla
e

Membrane

Bacterial conjunctivitis
Commonly caused by staphylococcus aureus, streptococcus
pneumonia, Hemophilic influenza, and moraxella catarrhalis
S. aureus is common in adults
Highly contagious from secretions or with contaminated
objects and surfaces

Bacterial conjunctivitis
Symptoms:
Patients typically complain of redness and discharge in
one eye; although it can also be bilateral.
The affected eye often is stuck shut in the morning
Purulent discharge continues throughout the day.
The discharge is thick; it may be yellow, white or green.
No real pain as the conjunctiva has few sensory nerve
supplies but complain of irritation, itching and
discomfort
Vision is almost always normal.

Bacterial conjunctivitis
Signs:
Purulent discharge at the lid margins and in the
corners of the eye. More purulent discharge appears
within minutes of wiping the lids
Red eye
Edema of the conjunctiva (chemosis) and eyelid
swelling
Cornea is mostly clear; but if it is involved, there
will be different degree of corneal opacity it is
common especially in untreated and delayed patients

Bacterial conjunctivitis
Diagnosis: -Mostly clinical
- Gram stains

may be sometimes used.

Course : It lasts for 1 - 2 weeks and then it usually

resolves spontaneously.
Treatment
Chloramphenicol eye drop or ointment QID
Ciprofloxacillin eye drop QID
Clean any discharge or dried secretions
Normally resolves after 3 or 4 days of treatment
N.B. Dont use steroid or steroid containing antibiotic as they will
reduce local immunity and encourage micro organism to
multiply

Neonatal Conjunctivitis
(Ophthalmia Neonatorum)
Definition:
Conjunctivitis occurring in the first 28 days of life
caused by a number of agents ( bacterial, viral,
chemical)
It remains significant source of ocular morbidity and
blindness.
Infection typically occurs by direct contact during
vaginal delivery

Neonatal Conjunctivitis (Ophthalmia Neonatorum)

Etiology: The most important causes are:

Chlamydia trachomatis
Neisseria gonorrhoeae
Herpes simplex
Chemical conjunctivitis
C. trachomatis is the most common cause.
N.gonorrhoeae is the most serious form of ophthalmia
neonatorum(can progress to corneal perforation
within 24 hr.)

Neonatal Conjunctivitis (Ophthalmia Neonatorum)

Symptoms:- Profuse purulent eye discharge

Sign:
Purulent eye discharge, eye lids are swollen
If cornea is involved: ulcer, scarring, perforation
Diagnosis
Gram stain & culture of conjunctival discharge

Neonatal Conjunctivitis (Ophthalmia Neonatorum)

Treatment:
It is sight threatening condition that needs systemic
antibiotic and close follow up in better
ophthalmic center
Admit and start iv Ceftriaxone 50mg/kg for 1 week
Ciprofloxacillin eye drop q 2hrs
Clean any discharge frequently

Neonatal Conjunctivitis (Ophthalmia Neonatorum)

Prevention
The eye lids should be cleaned with saline swabs as
soon as the head was born and before the infants eyes
opened
Then apply TTC eye ointment
Other options:
Erythromycin o.5% oint.
1% silver nitrate ( used in the past, not effective for
Chlamydia, causes chemical conjunctivitis)
Most recently ,5% povidone-iodine has been recommended

Viral conjunctivitis
Viruses are a common cause of conjunctivitis in
patients of all ages.
Adenovirus is by far the most common cause, and herpes
simplex virus(HSV) is the most problematic.
Less common causes include varicella-zoster virus(VZV),
picornavirus, poxvirus and HIV.

It is highly contagious, spread by direct contact with

secretions or with contaminated objects

Viral conjunctivitis
Diagnosis
Typical signs & symptoms:
Acute onset , often bilateral ,watering (not
purulent),redness , discomfort and photophobia
There may be follicles or papillarry reaction
Mostly associated with upper respiratory tract
infection

Viral conjunctivitis
Treatment
Usually self limiting
Cold compresses and lubricants, such as artificial
tears, for comfort.
Prophylaxis antibiotic eye drops may be given as
necessary to prevent bacterial super infection.

Never use steroid or steroid containing

antibiotics.

Allergic conjunctivitis
It is caused by air borne allergen contacting the eye.
Pathogenesis:
Common airborne antigens, including pollen,
grass, and weeds, may provoke the symptoms
Reaction of antigens with specific IgE antibody,
causes local mast cell degranulation and the
release of chemical mediators including
histamines, eosinophil chemotactic factors and
platelet activating factors.

Allergic conjunctivitis
Types of allergic conjunctivitis

Seasonal allergic conjunctivitis (SAC)

Perennial allergic conjunctivitis (PAC)
Vernal keratoconjunctivitis (VKC)
Atopic keratoconjunctivitis(AKC)
Giant papillary conjunctivitis(GPC)

Allergic conjunctivitis
Symptoms
Red eye
Severe and persistent itching of both eyes
Mucoid eye discharge
Tearing ,photophobia

Visual reduction depends on type

History of atopy, seasonal allergy, or specific allergy

Signs
Visual acuity is normal/abnormal
Papillary reaction to hypertrophy on tarsal conjunctiva

Allergic conjunctivitis
Treatment

Mast cell stabilizers like cromolyn sodium

Vasoconstrictor-antihistamine
Topical steroid Terracortril eye suspension
NSAIDs
Cold compresses and periodic instillation of artificial
tears, may provide temporary relief.

Maintenance of an air-conditioned environment

and control of dust particles at home and work also
may be helpful.

TRACHOMA
Definition: Trachoma is a chronic keratoconjunctivitis caused by
the obligate intracellular bacterium - Chlamydia trachomatis
The second most common cause of blindness in developing
countries.
Trachoma is the leading infectious cause of blindness in the world.
Caused by serovars A, B, Ba, and C of C. trachomatis

TRACHOMA
Pathophysiology:
Infection causes inflammation (lymphocytic,monocytic infiltrate, plasma cells and macrophages in follicles).
Repeated episodes of reinfection
Chronic follicular or intense conjunctival inflammation (active trachoma)
Tarsal conjunctival scarring (distorts the upper tarsal plate)

Entropion and trichiasis (cicatricial trachoma)

Corneal abrasions, corneal scarring and opacification

Blindness.

TRACHOMA
Epidemiology
Trachoma is endemic in parts of Africa, Asia, the Middle East,
Latin America
Worldwide, an estimated 84 million people in 55 endemic
countries have active trachoma.
In hyperendemic areas, most members of nearly all families may
have active disease.
WHO estimates about 15% of world blindness is caused by
trachoma
It is the leading cause of preventable blindness
10 million have TT
6 million are blind

 The main carriers of infection are children below

the age of 10, & especially preschool children
The disease spreads from person to person by
direct contact on fingers & on clothes
,handkerchiefs & pillows( fomite)
Disease transmission occurs primarily between
children and the women who care for them.
Overcrowding ,poor hygiene & large no of flies all
help disease to spread

TRACHOMA

Epidemiology
Race
Has no racial preponderance.
Trachoma persists in areas with poor personal and community hygiene, for
example, communities with inadequate access to water and sanitation in hot,
dry, dusty climates.
Trachoma typically affects the most marginalized, deprived members of a
community.

Sex
Active disease most commonly occurs in preschool children of both sexes and
their care providers (usually female).
Trichiasis and blindness may be 2-4 times more common in women than men.

 Age
Active disease most commonly occurs in preschool
children, with the highest prevalence in children aged
3-5 years.
Cicatricial disease is most common in middle-aged
adults. The age group in which cicatricial disease
begins to appear depends on the intensity of
transmission in the community. In areas of extremely
high endemicity, rare cases of trichiasis occur in
children younger than 10 years.

TRACHOMA
Clinical presentation
History
Two phases: the active phase and the scarring (cicatricial)
phase
1.The active phase
Follicular conjunctivitis is a feature.
Most patients with active trachoma are relatively
asymptomatic.
Some have a mucopurulent discharge,redness,tearing,eye
discomfort
A screening program is generally required to establish the
diagnosis

2.The cicatricial phase has unique clinical features, which

lead to definitive diagnosis in most cases.
Conjunctival scarring alone -asymptomatic
Associated disturbance of the architecture of the tear
filmdry eye.
Trichiasis foreign body sensation, as well as
blepharospasm. Ultimately, it leads to corneal scarring.
Many patients self-epilate before their presentation.
Corneal opacities or scars- impair the patient's vision.

TRACHOMA
Physical examination
Eyelids: Trichiasis, entropion
Conjunctiva: follicles over upper tarsal
conjunctiva, tarsal conjunctval scarring( Arlts line)
Cornea: limbal follicles (Herberts pit), superior
corneal neovascularization (pannus), and punctate
keratitis, corneal opacity

Follicles,scaring, Herberts pit,panus

TRACHOMA
Diagnosis
Clinical Dx of trachoma requires at least 2 of the
following:
1. Conjunctival follicles on the upper tarsal
conjunctiva
2. Typical tarsal conjunctival scarring( Arlts line)
3. Limbal follicles & their sequelae (Herberts pit)
4. Vascular pannus most marked on the superior
limbus

 Findings of active trachoma TF, TI &

Herbert's pits are largely observed in
children. Older individuals often do not
display a follicular response but may develop a
papillary reaction, particularly if there is
secondary bacterial infection.

TRACHOMA
WHO simplified trachoma grading scheme
TF : > 5 follicles ,each >0.5mm,in the upper tarsal
conjunctiva

TI : Pronounced inflammatory thickening of upper tarsal

conjunctiva that obscures more than half of normal deep vessels

TS : Presence of scarring in the upper tarsal conjunctiva

TT : At least one eyelash touching the cornea or history of
previous epilation

CO : Easily visible corneal opacity over the pupil

TF
Trachomatous
inflammation
follicular
The follicles are white
or pale yellow foci of
inflammatory material
with a diameter of 0.5
to 2 mm

TI

Trachomatous inflammationintense

TS

Trachomatous scarring

TT

Trachomatous trichiasis

CO

Corneal opacity

Treatment
The key to the treatment of trachoma is the
SAFE strategy developed by the WHO.
The SAFE strategy

S Surgery for trichiasis,entropion and Co

A Antibiotics for active trachoma
F Facial cleanliness
E Environmental hygiene improvement

The SAFE strategy

Surgery for TT
Eyelid surgery to correct entropion and/or trichiasis may
prevent blindness in individuals at immediate risk
Eyelid rotation limits the progression of corneal scarring
PKP for CO
Epilation is considered an alternative for refusal to have
surgery

The SAFE strategy

Antibiotic for active trachoma( TF or/&TI):
Management of trachoma should be community
based.
If prevalence of TF in children aged 1-9 yr in the community is 10% or
more Rx: mass treatment

The following antibiotic treatment is recommended by

the WHO:
Single dose azithromycin: 20mg/kg (maximum dose 1g); in
Topical 1% tetracycline eye ointment bid for 6 wks
Add Doxycycline 100mg po Bid for 3 weeks

The SAFE strategy

Facial cleanliness:
- Promote regular face-washing with clean water

The SAFE strategy

Environmental improvement
- Improving water supply, latrine provision and fly
control

SUMMARY
Conjunctivitis is a clinical diagnosis of exclusion.
R/O serious diseases; keratitis, iritis, or angle closure
glaucoma.

 Warning signs of a more serious problem

1. Reduction of visual acuity
2. Ciliary flush: A pattern of injection in which the redness is
most pronounced in a ring at the limbus
3. Photophobia
4. Severe foreign body sensation that prevents the patient
from keeping the eye open
5. Corneal opacity
6. Fixed pupil
7. Severe headache with nausea and vomiting

Degenerations of the conjunctiva

Pinguecula
Pterygium

Pinguecula
A pinguecula (Latin, pingueculus meaning fatty) is a yellowish,
raised growth located on the bulbar conjunctiva in the palpebral
fissure.
It is commonly thought to be the precursor of pterygium .
Common in in the interpalpebral zone
Common in warmer areas with high levels of sunlight and dust
Excision is indicated - If it causes a cosmetic problem,
- Chronically inflamed or interferes with
contact lens wear.

Pterygium

Fleshy growth of the conjunctiva that encroaches the cornea

and cover cornea (Pterygium means wing)
It usually starts nasally, but occasionally temporally at
the 3 o'clock or 9 o'clock.
More common in dry, hot and dusty environment
The main risk factor for the development of pterygium is
exposure to UV light.
If it grows into the pupil, it will cause blurring of vision to
blindness

Pterygium
Treatment
Protection from sun with eye glass or hat
If irritated, topical steroid-Terracotril eye suspension
BID
Surgical excision

CONJUNCTIVAL TUMOURS

1. Benign

Naevus
Papilloma
Epibulbar
dermoid
Lipodermoid

2. Pre-malignant

Primary acquired melanosis ( PAM )

Intraepithelial neoplasia (carcinoma in sit

3. Malignant
Melanoma
Kaposi
sarcoma

Squamous cell carcinoma

Lymphom
a
Melanom
a

Naevus

Most frequently juxtalimbal

Presents in first two decades
Sharply demarcated and slightly
30% are almost non-pigmented
elevated

Papilloma
Pedunculat
ed

Sessil
e

Presents in childhood or Presents in middle age

early adulthood
Infection with papilloma virus
May be multiple and bilateral Single and unilateral

Epibulbar dermoid
Signs

Presents in childhood
Smooth, soft mass,dome shaped
Usually juxtalimbal

Lipodermoid

Presents in adulthood
Soft, movable, subconjunctival mass

Most frequently at outer canthus

Intraepithelial neoplasia
(carcinoma in situ)

Signs

Progression

May become vascular and extend ont

Presents in late adulthood
cornea
Juxtalimbal fleshy mass Malignant transformation may occur

Primary acquired melanosis (PAM)

Signs

Presents in late adulthood

Types

PAM without atypia is benign

PAM with atypia is pre-malignan

Unilateral, irregular areas of flat,
brown pigmentation
May involve any part of conjunctiva

Conjunctival melanoma

rom PAM with atypia From naevus

Most common type

Very rare

Primary

Solitary
nodule
Sudden
Sudden appearance
of
Frequently
juxtalimba
increase in size
nodules in PAM
but may be anywhere
or pigmentation

Squamous cell carcinoma

Signs

Progression

Arises from intraepithelial Slow-growing

neoplasia or de novo
May spread extensively
Presents in late adulthood
Rarely metastasizes
Frequently juxtalimbal

Kaposi sarcoma

Affects patients with AIDS

Vascular, slow-growing tumour of low malignancy
Very sensitive to radiotherapy
Most frequently in inferior fornix

Lymphoma

Usually presents in adulthood

Benign or malignant
Salmon-coloured, subconjunctival infiltrate

Xerophthalmia
Definition:
Xerophthalmia (from the Greek xeros, dry, and ophthalmia,
inflamed eye)
Keratomalacia: is commonly described as liquefactive or
colliquative corneal necrosis.
It also occurs in other conditions, such as severe measles
Nutritional blindness refers especifically to these two
interrelated conditions.

Etiology and Pathogenesis

Vitamin A is a fat-soluble substance that is essential for immunity, growth,

maintenance of mucosal surfaces, cell differentiation, reproduction, and vision.

Rich sources of preformed vitamin A include liver, cod liver oil, butter, eggs,
and cheese.

Provitamin A carotenoids, such as -carotene, are found in dark green leafy

vegetables, carrots, and certain orange and yellow fruits and vegetables. carotene is converted in the gut to vitamin A.

Vitamin A is largely transported in to the liver, which stores about 90% of the
vitamin A in the body

Etiology and Pathogenesis

Retinol is required:
For the elaboration of rhodopsin or visual purple by the
rods,
For maintenance of normal differentiation of the epithelial
lining of several structures throughout the body, and
For a full competency immune response

Etiology and Pathogenesis

Changes in vitamin A deficiency :

Keratinization of the epithelium of mucous membranes harder &

resist wetting
Loss of goblet cells which secrete mucusdry eye
Rhodopsin is not formed night blindness
Thus, vitamin A deficiency can affect the tear layer, the conjunctiva, the
cornea, and the ability to see at night

Many factors can contribute to vitamin A deficiency

Decreased intake
Impaired absorption, altered storage
Decreased circulation
Increased utilization and uptake by tissues
Increased metabolic losses of vitamin A

Epidemiology

Nutritional blindness is primarily a problem of developing countries

250 million pre-school-age children are subclinically vitamin A deficient
3 million have clinical xerophthalmia
300,000 are blind from xerophthalmia (about 10% of all blind children)
Nutritional blindness can occur at any age, but particularly among young
children and pregnant women.

Epidemiology
Xerophthalmia is most common among 1- to 6-year-old
children, although severe, blinding forms are concentrated in
those 6 months to 3 years of age.
At least four factors account for this pediatric age distribution:
1. Children often are born to vitamin A-deficient mothers
2. Childhood is a period of rapid growth, placing heavy demands
on vitamin A stores
3. The young child is in the dangerous weaning period.
4. Childhood also is the age of greatest morbidity (and mortality)
from measles, chickenpox, pertussis, respiratory infections,
and especially gastroenteritis.

CLINICAL CLASSIFICATION

XN: Night blindness

X1A:Conjunctival xerosis
X1B:Bitot's spots
X2:Corneal xerosis
X3A:Corneal ulceration/keratomalacia involving less than
one third of the corneal surface
X3B:Corneal ulceration/keratomalacia involving one third or
more of the corneal surface
XF: Xerophthalmic fundus
XS: Corneal scars presumed secondary to xerophthalmia

Conjunctival & corneal xerosis

Bitots spot

Corneal xerosis and corneal ulcer

keratomalacia

Corneal scar

Diagnosis
Diagnosis requires a high degree of suspicion
Treatment is most practical way to confirm the diagnosis.
Xerophthalmia is a clinical diagnosis.
For children, serum or plasma vitamin A levels less than 0.35
mol/L are considered to indicate vitamin A deficiency
Histologic examination of the conjunctival epithelium for
squamous metaplasia and loss of goblet cells has been used

Treatment
Xerophthalmia is a medical emergency that should be treated

promptly with vitamin A therapy.

Individuals with xerophthalmia are at increased risk of blindness, and

because of the effects of vitamin A deficiency on the immune system,

they are also at increased risk of infections and death.
Night blindness usually improves within 24 hours, and corneal and

conjunctival xerosis responds within days.

High-dose vitamin A therapy is recommended by WHO for children

with measles

Treatment schedule for xerophthalmia or

measles
Timing of dose
On diagnosis

Age
Dose in IU
< 6 months
50, 000
6 12 months
100, 000
>12 months
200, 000

Following day

same age-specific dose

2-4 weeks later

same age-specific dose

Treatment indications
All children with any active corneal ulceration
All children with signs of xerophthalmia
All children with measles
All severely ill or malnouished children from areas
where xerophthalmia occurs, even if there is no clinical
evidence of xerophthalmia

Prevention
Distribution of massive dose of vit A
Fortification of food with Vit.A
Horticulture and agriculture to grow & eat the
right sort of food
Nutrition and health education
Immunization especially for measles

Periodic oral vitamin A supplementation

Infants <6 months

50,000 IU

Non-breast-fed infants, breast-fed infants

whose mothers have not received supplemental vitamin A

Infants 6-12 months

100,000 IU

Every 4-6 months

Children >12 months

200,000 IU

Every 4-6 months

Mothers
Within 8 weeks of delivery

200,000 IU

Diseases of the lacrimal apparatus

Infections of the Lacrimal apparatus
Obstructions of lacrimal drainage system

NFECTIONS OF LACRIMAL PASSAGES

1. Canaliculitis
2. Acute Dacryocystitis
3. Chronic Dacryocystitis

Canaliculitis

Symptoms
Tearing or discharge, red eye, mild tenderness over
the nasal aspect of the lower or upper eyelid.

Signs
Erythmatous pouting punctum,erythema of skin
surrounding the punctum.
Mucopurulent discharge or concretions may be
expressed from the punctum when pressure is
applied over the nasal corner of lower eyelid
(lacrimal sac).
Recurrent conjunctivitis confined to nasal aspect of
the eye, gritty sensation on probing of the
canaliculus.

 Etiology

Actinomyces israeli (most common cause)

Fungal ( e.g. candida, fusarium, Aspergillus)
Viral ( e.g HSV & VZV)
Other bacteria( e.g Nocardia)

Chronic canaliculitis
Frequently caused by Actinomyces
Unilateral epiphora and chronic mucopurulent discharge

Oedema of canaliculus and pouting

punctum

Expressed concretions consisting of

sulphur granules

Treatment - Simple curettage or canaliculotomy

Canaliculitis
DDx
Dacryocystitis
NLD obstruction
Conjunctivitis

Work-up
Apply gentle pressure over lacrimal sac with cotton-tipped
swab & rolled it toward the punctum; observe for a punctal
discharge
Smears and cultures of the material expressed

Treatment
1. Remove obstructing concretions, surgical canaliculotomy
2. After removing irrigate with penicilin G soln. or 1%
iodine solution
3. Warm compresses to the punctal area qid.

Acute dacryocystitis
Pathogenesis
Acute bacterial infection of the lacrimal sac
secondary to nasolacrimal duct obstruction(NLDO)
Symptoms
Pain, redness, and swelling over the innermost aspect
of the lower eyelid (over lacrimal sac); tearing;
discharge; fever; may be recurrent.

Signs
Tender, red, tense swelling at the medial canthus which may be
associated with preseptal cellulitis( extending around periorbital
area nasally)

Acute dacryocystitis

Usually secondary to nasolacrimal duct obstruction

May develop into abscess

Tender canthal swelling
Mild preseptal cellulitis

Acute dacryocystitis
Treatment
1. Systemic antibiotic
- Amoxicilin /clavulante( Augmentin), TID for 10-14
days
2. Topical antibiotic drops
3. Warm compresses and gentle massage to inner canthal
region qid
4. Antipain
5. Consider incision and drainage of pointing absess
6. Consider surgical correction ( DCR) once acute episode
has resolved, particularly with chronic dacryocystitis.

Chronic dacryocystitis

Pathogenesis

Chronic bacterial infection of lacrimal sac secondary

to NLDO

Signs

Painless swelling at the inner canthus(mucocele)

with reflux of mucopurulent material on pressure
over the sac

Chronic dacryocystitis
Epiphora and chronic or recurrent unilateral conjunctivitis

Painless swelling at inner canthus

Expressed mucopurulent material
Treatment - DCR

Obstruction of lacrimal apparatus

Obstruction can occur at the level of
punctum, canaliculi,or nasolacrimal duct.

Congenital nasolacrimal duct obstruction

Caused by delayed canalization near valve of Hasner
On pressure reflux of purulent material from punctum

Epiphora and matting

Infrequently acute dacryocystitis

Treatment of congenital nasolacrimal

duct obstruction
Massage of nasolacrimal duct and antibiotic drops 4 times daily
Improvement by age 12 months in 95% of cases

If no improvement - probe at 12-18 months

Results - 90% cure by first probing and 6% by seco

Congenital dacryocele

Distension of lacrimal sac by trapped amniotic fluid (amniont

aused by imperforate valve of Hasner

Bluish cystic swelling at or below medial canth

May become secondarily infected

Treatment
Initially massage
Probing if massage fails

Evaluation of acquired tearing

Causes of tearing:
1. Hypersecretion of tears(Lacrimation)
2. Impairment of drainage(Epiphora)

 Diagnostic tests:
Dye disappearance test (DDT): useful for assessing
presence or absence of adequate lacrimal outflow.
Diagnostic irrigation and probing

Treatment of NLDO
Dacryocystorhinostomy( DCR)

DISEASES OF THE ORBIT

 Evaluation of orbital diseases

7 Ps
Pain
Proptosis
Progression
Palpation
Pulsation
Periorbital changes
Past medical history

 Infectious and inflammatory orbital diseases

Infections: preseptal cellulitis, orbital cellulitis
Inflammations: Graves ophthalmopathy, pseudotumor of
orbit

Space-occupying orbital lesions

Infections
Cellulitis
Acute infection of the orbit/ periorbital tissues with
pyogenic bacteria

Bacterial infections of the orbit or cellulitis occur

from 3 primary sources:
Direct spread from an adjacent sinusitis (the large
majority of cases )
Direct inoculation following trauma or skin infections
Bacteremic spread from a distant focus (otitis media,
pneumonia)

 Classification
Two clinical types
Preseptal cellulitis
Orbital cellulitis

Preseptal cellulitis

Definition
Infection & inflammation confined to eyelids or
periorbital structures anterior to orbital septum.

Etiology & Pathogenesis

Staph. aureus or strept. Pyogenes most
common but H. influenzae in children < 5
years.
In adults usually caused by penetrating trauma
or cutaneous source of infection
In children the most common cause is
underlying sinusitis

Preseptal cellulitis
Symptoms:-Tenderness and redness of the
eyelid, mild fever, irritability
Signs
Eyelid erythema, edema, warmth, tenderness
No proptosis, no restriction of extraocular
motility, no pain with eye movement, usually
the globe is not involved (unlike orbital
cellulitis).
The patient may not be able to open the eye
because of eyelid edema.

Preseptal cellulitis
Work-up
1. History: pain with eye movement? Prior trauma or cancer?
2. Complete ocular exam:
Restriction of ocular motility or proptosis.
Eyelid speculum or Desmarres eyelid retractor

3. Check facial sensation in the distribution of first and second

division of trigeminal nerve(CN V).
4. Check vital signs
5. Gram stain and culture of any open wound or drainage
6. CBC with diff. and blood culture in severe cases or when a
fever is present

Preseptal cellulitis
Treatment
1.Systemic Antibiotic therapy
2.Warm compresses to the inflamed area tid prn
3. Antibiotic ointment to eye if secondary conjunctivitis is
present
4. Exploration and debridement of lesion if a fluctuant mass or
abscess is present

Orbital cellulitis

Definition: A life threatening infection of soft tissues behind

the orbital septum
Pathogenesis
Infection with strep. Pneumoniae, s.aureus, strep. Pyogenes &
H. influenza, bacteroides, gram-negative rods associated with
the following conditions:
Sinusitis, most commonly ethmoidal
Extension of preseptal cellulitis
Local spread from dacryocystitis
Hematogenous spread
Post-traumatic
Post-surgical

Orbital cellulitis
Symptoms
Red eye, pain, blurred vision, fever, headache,
double vision

Signs
Eyelid edema, erythema, warmth, tenderness,
conjunctival chemosis , and injection, proptosis
and restricted ocular motility with pain on
attempted eye movement are usually present.

CT scan usually shows sinusitis ( typically

ethmoid sinusitis)

Orbital cellulitis
Work-up
History: trauma? Ear, nose, throat or systemic infections?
Stiff neck or mental status changes? Diabetes or an
immunosuppressive illness?
Complete ophthalmic evaluation: Look for afferent
papillary defect, limitation of or pain with eye movements,
proptosis, decreased skin sensation , or an optic nerve or
fundus abnormality.
Check vital signs, mental status, and neck flexibility
CT of orbits and sinuses
CBC with differential
Blood culture
Explore and debride wound, if present; obtain gram stain
and culture of any discharge
Obtain a lumbar puncture for suspected meningitis

Complications of orbital cellulitis

Raised intraocular pressure

Retinal vasculature occlusion

Optic neuropathy
Orbital
Intracranial

Orbital or subperiosteal Meningitis, brain abscess

Cavernous sinus
abscess

Management of orbital cellulitis

1. Hospital admission

2. Systemic antibiotic therapy

Pre-treatment 3. Monitoring of optic nerve

function

4. Indications for surgery

Resistance to antibiotics
Orbital or subperiosteal abscess
Optic neuropathy

Post-treatment

THYROID EYE DISEASE (GRAVES OPHTHALMOPATHY)

It is an autoimmune inflammatory disorder whose

underlying cause continues to be elucidated.
Characteristic clinical signs includes a combinations of
eyelid retraction, lid lag, proptosis, restrictive extraocular
myopathy and optic neuropathy
Although typically associated with hyperthyroidism,
Graves ophthalmopathy may accompany hypothyroidism
or Hashimoto thyroiditis.

Ocular symptoms:
Prominent eyes, eyelid swelling, double vision, foreignbody sensation, pain, photophobia, decreased vision in one
or both eyes.

THYROID EYE DISEASE (GRAVES

OPHTHALMOPATHY)

Critical ocular signs:

Retraction of eyelids, eyelid lag on downward
gaze, and often, unilateral or bilateral proptosis.
When EOMs are involved, elevation and outward
movements are commonly restricted.
Orbital CT scan shows thickening of the involved
EOM with sparing of the tendon.
Injection of blood vessels over the insertion sites of
involved EOMs, resistance to retropulsion, eyelid
edema, superficial punctate keratitis or ulceration
from exposure keratopathy

Soft tissue involvement

Periorbital and lid swelling
Conjunctival hyperaemia

Chemosis

Superior limbic
keratoconjunctivitis

Signs
of
eyelid
retraction

Occurs in about 50%

Bilateral lid retraction Bilateral lid retraction

No associated proptosis
Bilateral proptosis

Unilateral lid retraction Lid lag in downgaze

Unilateral proptosis

Proptosis
Occurs in about 50%
Uninfluenced by treatment of hyperthyroidism

Axial and permanent in about 70%

May be associated with choroidal fol
Treatment options

Systemic steroids
Radiotherapy
Surgical decompression

Optic neuropathy
Occurs in about 5%

Early defective colour vision

Usually normal disc appearance

Caused by optic nerve Often occurs in absence of significa

compression at
proptosis
orbital apex by enlarged

Restrictive myopathy
Occurs in about 40%
Due to fibrotic contracture

Elevation defect - most common

Abduction defect - less
common

Depression defect - uncommon

Adduction defect - rare

THYROID EYE DISEASE (GRAVES OPHTHALMOPATHY

Treatment
Refer the patient to medical internist or
endocrinologist for mgt of systemic thyroid
disease, if present.
Treat exposure keratopathy with artificial tears and
lubricating ointments or by taping eyelids closed at
night.
Options of Rx:
Systemic steroid( prednisolone)
Radiation therapy
Orbital decompression surgery

IDIOPATHIC ORBITAL INFLAMMATION

(ORBITAL PSEUDOTUMOR)

Definition: It is an idiopathic tumor like inflammation

made up of a pleomorphic inflammatory cellular
response and a fibrovascular tissue reaction.
Presentation - 20 to 50 years with abrupt painful onset
It occurs as a nonspecific idiopathic inflammatory
process
Un related to any other systemic or local disorders

Symptoms:
May be acute, recurrent or chronic
Pain, prominent red eye, double vision, or
decreased vision are common in acute disease
Asymptomatic proptosis may develop in chronic
disease

ORBITAL PSEUDOTUMOR

Critical signs
Proptosis or/and restriction of ocular motility, usually
unilateral.
Orbital CT scan shows a thickened posterior sclera,
orbital fat or lacrimal gland involvement, or thickening
of EOMs ( including tendon)

Other signs
Eyelid erythema and edema, lacrimal gland enlargement
or palpable orbital mass, decreased vision, uveitis,
elevated IOP, conjunctival chemosis and injection

Treatment options
Systemic steroid
Radiation therapy

ORBITAL PSEUDO TUMOUR

SPACE OCCUPYING ORBITAL LESIONS

The most common type of orbital disease
Causes :
-Tumors
- Cysts
- Inflammatory orbital masses
-Vascular lesions
Clinical features:
Proptosis (Exophthalmos)
Diplopia( double vision)
May affect vision

 Orbital tumors in children include the following:

Demoid and epidermoid cysts

Capillary hemangioma
Rhabdomyosarcoma
Lymphangioma
Optic nerve glioma
Leukemia
Metastatic neuroblastoma
Plexiform neurofibroma
Teratoma

 Orbital tumors in adults:

Metastatic tumors from breast, lung,prostate, GIT

Cavernous hemangioma
Mucocele
Lymphoid tumors
Optic-nerve-sheath meningioma
Localized neuro fibroma
Neurilemoma
Fibrous histiocytoma
Hemangiopericytoma

Treatment depends on the cause

Diseases of the cornea

- Infectious
- Immune mediated
- Trauma

Infectious causes
Bacteria/ Virus/ Fungus/ Acanthamoebal

Bacterial Keratitis
A common sight threatening condition
Onset can be Rapid (explosive) or Slow

Risk Factors

Contact lens wear

Trauma
Contaminated ocular drugs
Impaired defense mechanism (Corticosteroids,
malnutrition,)
Blepharoconjunctivitis

Etiologies
- S.aureus/ S.epidermidis/St.pneumonia
- Moraxella/Serratia/ P.aeruginosa
- Mycobacteria/Anaerobes
Clinical Presentation
Pain,Redness,Photophobia,Reduced vision,purulent eye
discharge
Corneal ulcer
-Has Sharp demarcation with underling suppuration

Diagnosis

Clinical
Identifying the causative agent by gram stain and culture
Treatment

First with broad spectrum antibiotics for both gram positives

and gram negatives and once the organism is identified with
culture, patient can be treated with monotherapy.
Route of administration
Topical/Sub conjunctival/Systemic

Drugs of choice
Vancomycin/ Bacitracin/ Cefuroxime for gram positives
Tobramycin/ Gentamicin/ Amikacin for gram negatives
Ciprofloxacin/ Levafloxacin/ Ofloxacin for monotherapy

Corticosteroids
Should be started once the organism is identified or once the patient has
shown response to antibiotic therapy
Surgery -- Penetrating keratoplasty
Indication--Progressive disease despite antibiotic therapy/Corneal perforation
Broad-spectrum antimicrobial therapy with topical cefazolin (50 mg/mL) and
tobramycin (14 mg/mL) or a fluoroquinolone should be instituted immediately
and given hourly around the clock after smears and cultures of the ulcer are
obtained.

Herpes simplex eye disease

Herpes simplex virus infection is ubiquitous in human.
Almost 100% of those older than 60 years of age harbor HSV
in their trigeminal ganglion.
HSV Causes recurrent infection
Two types --HSV1- Orofacial & ocular infection
HSV2 Genital infection
Route of transmission=direct contact with infected lesion or
secretion

Primary infection
Lid Vesicles /Follicular conjunctivitis
Epithelial keratitis
Recurrent ocular infection
From reactivation of virus in latently infected sensory
ganglion
Patient with HIV are at increased risk of recurrence.

Clinical manifestation
Belepharo conjunctivitis
Epithelial keratitis (Dendritic or Geographic)
Stromal Keratitis ( Disciform, interstitial, necrotizing)
.
Decreased corneal sensation is highly suggestive of
viral keratitis especially of herpetic origin
Diagnosis
- Clinical / Viral Culture/Antigen &DNA Detection

The hallmark of
herpetic epithelial
keratitis is the
superficial dendritic
or geographic
ulcer(22%) (best
demonstrated with
fluorescein)

Treatment
Anti viral
Routes --- Topical/Systemic
Drugs ---Acyclovir/Trifloridine /Vidarabine/Valacyclovir
Antiviral agents are toxic to the corneal epithelium, and
prolonged treatment may delay epithelial healing.
With topical antiviral therapy, dendritic ulcers clear over
the course of a week without leaving a corneal scar.

Corticosteroids
Are used for stromal keratitis but are contraindicated in
epithelial keratitis with ulceration
The use of topical glucocorticoids in patients with dendritic
lesions has been thought to promote the development of
geographic ulcers.
Geographic ulcers respond more slowly to treatment and are
more likely than dendrites to lead to scarring.
Surgical treatment -- Penetrating keratoplasty
Indication visually significant corneal opacity or Corneal
perforation

Herpes Zoster Ophthalmicus

Occurs from reactivation of VZV infection
Is self limited in children but severe in elderly or immunocompromized.
CLINICAL PRESENTATION
Blepharo conjunctivitis
Epithelial keratitis
Stromal keratitis
Diagnosis---- Clinical
Treatment ----with systemic antiviral
Drugs --- Famciacyclovir/ Valacyclovir/ Acyclovir
Treatment of post herpetic neuralgia
* Capsasin cream / Amitriptyline / Carbamazepine

Fungal keratitis
Less common
Risk Factors

Trauma with plant or vegetable material

Contact lens wear
Prolonged topical corticosteroid use
Corneal surgery
Chronic keratitis( E.g HSK, HZVK)
Clinical Presentation
Few inflammatory signs on the cornea
*Gray white infiltrates with irregular feathery or filamentous margin
* Occasionally multifocal or satellite infiltrates

 Etiologies
-Candidia ,Aspergillus, Fusarium
Diagnosis
-Clinical plus Laboratory(KOH)
Treatment
Mainly topical natamycin/ Amphotericin B/Miconazole
Adjunctive oral ketoconazole or fluconazole
Surgery
-Penetrating keratoplasty for progressive disease despite
antifungal therapy.

DISEASES OF THE SCLERA

Immune mediated or Infectious (rare)
SCLERITIS
Is frequently associated with underlying systemic
immunologic diseases e.g. SLE, Rumatoid arthritis or
infectious disease like syphilis, TB, VZV, leprosy
More common in women of age fourth to sixth
decade.
Half of the scleritis cases are bilateral

CLINICAL PRESENATSION
OnsetGradual
Pain
Headache, watering of the eye, ocular redness, and photophobia
ScleraTender, edematous and Violate colored Vessels are adherent
to the sclera and can not be moved with cotton tipped applicator

Classification based on

Location Anterior/Posterior
Area involved Nodular/Diffuse
SeverityNecrotizing/ Non-necrotizing
Posterior scleritis is defined as involvement of the sclera by
inflammation posterior to the insertion of the medial and lateral
rectus muscles.

Diagnosis
Clinical and Laboratory evaluation for systemic diseases
Treatment

Is mainly with systemic steroid but for milder cases-Topical steroid/

Po NSAID
For severe cases IV Steroid or Immunosuppressive drugs

Episcleritis
Mild and self limited
Painless and non tender
Not associated with systemic diseases
Bright red colored vessels can be moved with cotton tipped applicator

uveitis
Inflammation is the most common disease of uvea
Uveitis defined as inflammation (i.e, -itis) of the uvea

Uveitis
Classification:
1. Anterior uveitis Main site of inflammation is the anterior chamber
Iritis
Anterior cyclitis
Iridocyclitis

2. Intermediate uveitis Main site of inflammation is the vitreous

Posterior cyclitis
Hyalitis

3. Posterior uveitis Main site of inflammation are the choroid & retina
- Choroiditis
- Chorioretinitis
4 . Panuveitis (diffuse uveitis) when the whole uvea is involved

uveitis
Iridocyclitis & choroiditis are the most common
Panuveitis and intermediate uveitis are much less common
Causes of uveitis:
Infectious, traumatic, neoplastic or autoimmune.
Infective: bacteria, viral, fungi, protozoa, parasites
Non-infective: e.g., sarcoid,
By far, most types of anterior uveitis are sterile inflammatory
reactions, where as many of the posterior uveitis syndromes are
infectious in origin.

Anterior Uveitis
Can have a range of presentations, from a quiet white
eye with low-grade inflammatory reaction to a painful
red eye with moderate or severe inflammation.
Symptoms
Acute: pain, red eye, photophobia, mild decreased vision,
tearing.
Chronic: Recurrent episodes, fewer or none of the acute
symptoms.

Anterior Uveitis
Signs
Injection of the perilimbal blood vessels(circumcorneal
injection)
Keratic precipitates (collections of inflammatory cells on the
corneal endothelium)
Cells and flares in anterior chamber(A/C)
Hypopyon (layers of white cells in the A/C)
Pupillary miosis, iris nodules
Synechiae, both anterior and posterior.
Low IOP, but occasionally elevated.
Occasionally cataract.

Anterior Uveitis
Work-up
Obtain a history, attempting to define the
etiology(including systemic review)
Complete ocular examination including IOP check and
a dilated fundus exam.
Initial laboratory work-up (CBC, ESR, VDRL, Chest xray)

Complications of uveitis

Secondary glaucoma
A fall in IOP( hypotony) phthisis bulbi
Cataract
Cystoid macular edema
Retinal detachment
Loss of vision

Anterior Uveitis
Treatment:
The basic treatment for all types of uveitis is corticosteroid
(topical/systemic)
Cycloplegics( pupil dilating drugs e.g atropine 1% drop)
for iridocylitis
Antiglaucoma drugs if increased IOP
If infective cause identified, treat accordingly.

POSTERIOR UVEITIS
The overlying vitreous can be involved with
inflammatory process, and cells or collections of cells
may be seen in the vitreous.
Symptoms
Patients with posterior uveitis complain of floaters,
decreased visual acuity, metamorphopsia, scotoma, or a
combination of; occasionally redness, pain, and
photophobia.

POSTERIOR UVEITIS
Signs
White blood cells and opacities in the vitreous(vitritis),
retinal or choroidal infiltrates, edema, vascular sheathing.
Other signs
Disc swelling, retinal hemorrhages or exudates, or signs of
anterior segment inflammation(e.g aqueous cells and flare,
posterior synechiae) may be present.
Glaucoma, cataract, or retinal detachment may develop.

POSTERIOR UVEITIS
Etiology
Can be infectious ( including viruses, bacteria, fungi,
protozoa,or helminthes) or noninfectious
causes(immunologic origin or unknown cause)
Infectious causes: Toxoplasmosis,ARN,PORN,,
Cytomegalovirus(CMV) in AIDS patients, sarcoidosis,
syphilis

Work-up
1. Complete medical history and review of systems including
risk factors for AIDS, recent eye trauma or surgery, use of
steroids, etc.
2. Complete ocular examination, including IOP measurement and
careful ophthalmoscopic examination.
3. Laboratory tests. E.g. antitoxo titer, VDRL.

Treatment
- Depends on the cause of posterior uveitis.

Surgery
-Retinal detachment /Vitreous hemorrhage or
opacity

Toxoplasmosis
The most common cause of infectious retinochoroiditis in both
adults and children
Caused by the parasite Toxoplasma gondii
Cats are the definitive hosts of T gondii
Exists in 3 major forms:
Oocyst, or soil form
Tachyzoite, or infectious form
Tissue cyst or latent form /bradyzoites
Congenital/ acquired

Symptoms
Unilateral blurred or hazy vision
Floaters
Symptoms of mild to moderate granulomatous anterior uveitis

Sign
Acutely elevated lOP at presentation.
Classically, focal, white retinitis with overlying moderate vitreous
inflammation (headlight in the fog), often adjacent to a pigmented
chorioretinal scar

The lesions occur more commonly in the posterior pole but may
occasionally be seen immediately adjacent to or directly involving
the optic nerve

 Focal retinitis in the absence of chorioretinal scarring should

raise the suspicion of acquired disease
Retinochoroiditis developing in immunocompromised and older
patients is;
-Large, multiple, bilateral lesions, with or without associated
chorioretinal scars

Complication
-Cataract, CME, serous retinal detachment, and CNV

Diagnosis

Made clinically, on the basis of the appearance of the

characteristic lesion plus
Serologic evaluation using ELISA tests to detect specific anti
-T gondii antibodies.
IgG antibodies
Appear within the first 2 weeks after infection; typically
remain detectable for life
Its presence supports but its absence rules out the Dx
Cross the placenta

IgM antibodies
Rise early during the acute phase of the infection, typically
remain detectable for less than 1 year
Do not cross the placenta
The presence of IgM in newborns confirms congenital
infection and is indicative of acquired disease when present in
adults

Treatment

Cytomegalovirus
Double-stranded DNA virus in the Herpesviridae family.
CMV retinitis is the most common ophthalmic manifestation
of both congenital CMV infection and in the context of HIVAIDS
3 distinct variants have been described:
1. A classic or fulminant retinitis with large areas of retinal
hemorrhage against a background of whitened, edematous, or
necrotic retina, typically appearing in the posterior pole, from
the disc to the vascular arcades
2. A granular or indolent form found more often in the retinal
periphery, characterized by little or no retinal edema,
hemorrhage, or vascular sheathing, with active
3. A perivascular form

Treatment
HAART therapy
Intravenous ganciclovir (5 mg/kg twice daily)
Or
Foscarnet (90 mg/kg twice daily) for 2 weeks followed by
low-dose daily maintenance therapy
Or
Oral valganciclovir (900 mg twice daily) for 3 weeks followed
by maintenance therapy (900 mg/day).
Intravitreal injection of ganciclovir or foscarnet, and
ganciclovir implant

Acute retinal necrosis

Affects healthy adults, children and immunocompromised
patients
Caused by HSV and HZV
Acute, fulminant disease may/not follow cutaneous or systemic
herpetic infection/
Usually present with acute unilateral loss of vision,
photophobia,floaters, and pain

 Pan uveitis is observed, beginning with

significant anterior segment inflammation with
corneal edema, KPs, posterior synechiae, and
elevated lOP, together with heavy vitreous
cellular infiltration.
Within 2 weeks, the classic triad of occlusive
retinal arteriolitis, vitritis, and a multifocal
yellow-white peripheral retinitis has evolved

Treatment
Timely diagnosis and prompt antiviral therapy are essential
given the rapidity of disease progression, the frequency of
retinal detachment, and the guarded visual prognosis.
Intravenous acyclovir 10 mg/kg/ day in 3 divided doses over
10-14 days followed by
Oral acyclovir at 400/800 mg orally 5 times daily
Or
Valacyclovir (1 g orally 3 times daily)
Or
Famciclovir 500 mg orally 3 times daily should be
continued for 3 months

 After 24-48 hours of antiviral therapy, systemic corticosteroids

prednisone 1 mg/kg/day) are introduced to treat active
inflammation.

Progressive outer retinal necrosis (PORN)

Morphologic variant of acute necrotizing herpetic retinitis

Occurs most often in patients with advanced AIDS.
The most common cause of PORN is VZV; HSV has also
been isolated.
Begins as patchy areas of outer retinal whitening that
coalesce rapidly;
In contrast to ARN, the posterior pole may be involved
early in the course of the disease, vitreous
inflammatory cells are typically absent, and the retinal
vasculature is minimally involved

Treatment
Resistant to intravenous acyclovir alone
Treated with combination of systemic and intraocular therapy
with foscarnet and ganciclovir

CATARACT
A cataract is a clouding/opacity of the crystalline lens
Signs and symptoms
-Reduced vision
-Myopic shift
-Glare
-Reduced contrast sensitivity
-Monocular diplopia
The lens is best examined through a dilated pupil

Causes
-Aging
- Ultraviolet light exposure
- Diabetes
-Trauma
- Genetic (congenital cataract)
- Drugs(corticosteroids, phenothiazins, miotcs, amiodaron,
statins)

Classification
1.Congenital/presenile/senile
2.Capsular/subcapsular/cortical/epinuclear/
nuclear
3.Immature/mature/hypermature/morgangian

Congenital cataract..if it occur at birth

Presenile cataract..if it occurs below the age of55 years.
Senile cataract.. If it occurs above the age of 55 years.
Immature cataract..if it is dense enough, and doesnt involve all
layers especially the anterior cortex
Mature cataract.. it is dense, blocks the view of the posterior
segment structures, involves all layers including the anterior cortex
Hypermature cataract..if contents of the lens leaks through an intact
capsule and the capsule shrinks
Morganian..if the cortex liquefies and nucleus floats with in the
capsular bag.

Epidemiology
-Age-related cataract is the leading

cause of blindness

world wide
-Responsible for 48% of world blindness, which represents about
18 million people, according to the World Health Organization
(WHO).
Complications
-Dislocation or subluxation of a lens
- Uvietis
-Glaucoma

Treatment
INDICATION FOR SURGERY
-Significant visual reduction
-Diminished peripheral vision
-Disturbing glare
-Symptomatic anisometropia
-Lens induced glaucoma
-Lens induced uvietis
-Lens dislocation
-Dens cataract that obscures the view of the fundus and impairs in
the diagnosis and management of other ocular diseases like
glaucoma, dm retinopathy

Surgical
Extracapsular cataract extraction (ECCE)
Intracapsular cataract extraction (ICCE).
Small incision cataract surgery(SICS)
Phacoemulcification(PHACO)
Plus
IOL Or Aphakic glasses

** Pseudophakia..presence of an implanted artificial intraocular

lens following cataract extraction.
** Aphakia..is a complete absence of a lens.

Glaucoma
Definition
The term glaucoma refers to a group of diseases that have in
common a characteristic optic neuropathy associated with
visual function loss
IOP is one of the primary risk factors, its presence or absence
does not have a role in the definition of the disease.
Normal IOP in the general population is 10-21 mmHg.

 3 factors determine the IOP:

1. The rate of aqueous humor production by the ciliary body
2. Resistance to aqueous outflow across the trabecular
meshwork-Schlemms canal system
3. The level of episcleral venous pressure.
In most cases elevated IOP is caused by increased
resistance to aqueous humor outflow

Normal Aqueous flow

Types of glaucoma

Open-angle
Angle-closure
Congenital
Childhood
Secondary

 The primary glaucomas are not associated with known ocular

or systemic disorders that cause increased resistance to
aqueous outflow.
Usually affect both eyes and may be inherited.
Secondary glaucomas are associated with ocular or systemic
disorders responsible for decreased aqueous outflow.
Often unilateral, and familial occurrence is less common.

PREVALENCE
1-2% of the white population over age 50
Half of these people are unaware they have the
disease

POAG
Magnitude of the problem
POAG represents a significant public health problem
WHO esitmates
people with high IOP(> 21 mm Hg) at 104.5 million.
Incidence(new cases) of POAG: 2.4 million people per year.

Blindness prevalence for all types of glaucoma: 8 mln ( 4 mln from

POAG)
Glaucoma is responsible for 15% of blindness ( 3rd leading cause of
blindness)

Ethiopia
4th leading cause of blindness( 5.2% of blindess) following cataract,
trachoma, refractive error.

GLAUCOMA: GROUPS AT RISK

Elderly
Blacks
Individuals with:
Elevated IOP
Immediate relatives with glaucoma
High myopia?
Cardiovascular disease?
Diabetes?

POAG RISK FACTORS

BLACK RACE
Blindness = 3-4 times more common
Age > 70 = 10% prevalence (2% for whites > 70)
POAG occurs at earlier age
POAG more advanced when discovered

Symptoms
Patients seldom recognize early symptoms
/signs of primary open angle glaucoma!!
Early diagnosis and treatment is important to
prevent vision loss

IOP
Average IOP reading is 16 mmHg (10-21
mmHg is the range of normal)
> 21 mmHg = glaucoma suspect
20% of those affected with glaucoma have
IOPs in the normal range (Normal Tension
Glaucoma)

GLAUCOMA: OPTIC NERVE HEAD

CHANGES

Increased size of the cup

Thinning of disc rim
Progressive loss of neural rim tissue
Disc hemorrhages

Effect of glaucoma on visual field

TREATMENT
Goal
Halt further visual loss
Halt further optic nerve damage

Medications

BETA-ADRENERGIC BLOCKING
AGENTS:
SIDE EFFECTS

Exacerbation of asthma
Slow heart rate
Decreased blood pressure
Decreased libido
Altered mentation

Newer:
Brimonidine

EPINEPHRINE DRUGS:
SIDE EFFECTS

Allergic conjunctivitis
Elevated blood pressure
Headache
Palpitation

MIOTIC DRUGS:
SIDE EFFECTS

Dimming of vision (miosis)

Browache (ciliary muscle spasm)
Myopic shift (ciliary muscle contraction)
Tearing
Sweating

Newer:
Dorzolamide
Brinzolamide

CARBONIC ANHYDRASE INHIBITORS:

SIDE EFFECTS

Increased urination
Decreased appetite
Nausea
Depression
Malaise

Transient peripheral
neuropathy
Increase in kidney
stones
Aplastic anemia
Potassium depletion

NEW MEDICATIONS
Latanoprost (Xalatan), a prostoglandin
analogue. Increases uveoscleral outflow.
SEs include iris color change, eye lash
lengthening
Travaprost (Travatan)
Bimataprost (Lumigan)

COMBINATION DROPS
Timpilo - Timolol and Pilocarpine. Decreases
production and increases outflow
Cosopt - Timolol and Trusopt. Decreases
production of aqueous
Xalacom Xalatan and Timolol
Combigan Alphagan and Timolo
More convenient for the patient, improved
compliance, less cost

Surgery
Trabeculoplasty
Glaucoma tube implants

The most effective screening strategy is periodic, comprehensive

eye examinations, especially for patients in high risk groups

Primary care providers are essential in the

diagnosis and management of glaucoma

SECONDARY GLAUCOMAS:
SOME CAUSES

Trauma
Uveitis
Chronic steroid use
Diabetic retinopathy
Ocular vascular occlusion

ACUTE ANGLE CLOSURE GLAUCOMA

Is an emergency!!!

Primary Angle-Closure Glaucoma

Risk factors
Race
The prevalence of primary angle-closure glaucoma(PACG)
varies among different racial and ethnic groups.
Among whites in US and Europe :0.1%.
Inuit populations(Eskimos) from Arctic regions: 20-40 x
whites
Asian population groups have a prevalence rate of PACG
between that of whites and Inuits.
Acute angle-closure glaucoma is relatively uncommon
among blacks

Primary Angle-Closure Glaucoma

Gender
Acute angle-closure glaucoma has been reported
more often in women than in men. Shallow A/C
than men

Age
The anterior chamber decreases in depth and
volume with age.
Acute angle-closure glaucoma is most common
between the ages of 55 and 65 years

Primary Angle-Closure Glaucoma

Refraction
The anterior chamber depth and volume are smaller in
hyperopic eyes
Although PACG may occur in eyes with any type of
refractive error, it is thus typically associated with
hyperopia.
Inheritance
Relatives of subjects with angle-closure glaucoma are at
greater risk of developing angle closure than is the general
population

Acute Angle-Closure Glaucoma

SYMPTOMS
Severe ocular pain, redness
Blurred vision
Halos around lights
Headache
Nausea and vomiting

Acute angle closure glaucoma

Initial treatment
Pilocarpine 2% gtt q 15 min x 2
Acetazolamide 500mg po or IV
Oral glycerine or isosorbide, 1cc/kg body
weight
IV mannitol 20% 300-500cc

Surgery
Laser/surgical iridectomy

CHILDHOOD GLAUCOMA
Primary congenital/infantile glaucoma
Glaucoma associated with congenital anomalies
Secondary glaucoma. E.g Seconadary to
retinoblastoma.

Asymptomatic in early stages

Can result in total optic nerve atrophy and
blindness

Clinical features
Symptoms (Triad)
Tearing
Photophobia (Painful over sensitivity to light)
Blepharospasm (Involuntary protective closing of the
eyelids)
Signs
High IOP
Ciliary injection
Large cornea that could be cloudy
Enlarged globe
Optic nerve cupping
Diagnosis
Examination under anesthesia

Clinical features of Congenital glaucoma

Parents may notice enlargement of the eye and may
initially consider the large eyes an attractive feature
rather than a warning sign of glaucoma
If an infant or a young child shows any of these
symptoms, parents or caregivers should seek medical
care as soon as possible from an ophthalmologist
because they might be signs of glaucoma.

Management of congenital glaucoma

Medical treatment to lower IOP is a temporary measure till the
child is ready for surgery
Surgery to open the drainage of aqueous humor or by pass
surgeries are definitive treatment for glaucoma
After glaucoma surgery, long-term follow up is essential, to
make sure the intraocular pressure is controlled and vision is
developing as normally as possible

Vitreous floaters
Small inclusions in the vitreous may be visible as mobile
shadows resembling bubbles, strings of pearls, or bundles of
filaments. (Muscae volitantes (Latin for flying gnats))
Vitreous floaters are common, frequently visualized in the
normal eye, tend to increase with increases in myopia or age
and often are a source of concern to the patient.

 Once developed, a vitreous floater may persist for life, but the
sudden onset of numerous floaters may be the initial sign of a
retinal detachment.
The vitreous floater associated with retinal detachment may
represent blood particles in the vitreous.
The non-hemorrhagic vitreous opacities may be due to
condensed vitreous, white blood cells, tumor cells or pigment
cells.

Retinal detachment
The normal retina lies in close contact with underlying retinal
pigment epithelium(RPE). However, the two layers are not
joined together.
Retinal detachment is the separation of sensory retina from the
RPE
Predisposing factors for RD:
Presence of hole or tears in the retina
Vitreous degeneration
Myopia
Ocular surgery
Trauma

Retinal detachment
Types of retinal detachment:
Rhegmatogenous RD
Tractional RD
Exudative RD

Retinal detachment

Rhegmatogenous - Caused by a

retinal break

Exudative

Tractional retinal detachment

Retinal detachment
Symptoms
Floaters
Flashing lights
Visual Field defect
Sign: Elevation of the retina.
Treatment:
Needs surgery, refer to vitreoretinal specialist.

Age-related macular degeneration(AMD)

DEFINITION
Leading cause of central visual loss in patients
over 50 years
Characterized by:

Hard /Soft drusen

Hyper or hypopigmentation of RPE
RPE and associated neurosensory retina detachment
Retinal, subretinal hemorrhage
Geographic atrophy of RPE
Fibrous scarring

Drusen
Histopathology

Hard

Soft

Small well-definedLarger, ill-defined spots

spots
May enlarge and coalesce
Usually innocuous
Increased risk of AMD

Age-related macular degeneration(AMD)

Symptoms
Gradual loss of central vision
Signs
Drusens, almost always in the macular area of both
eyes
Retinal pigment epithelial atrophy
Choroidal neovascular membrane, macular scar
Treatment: -Laser,Anti-VEGF
- Refer to ophthalmologist.

Drusen and AMD - progression

Atrophic AMD

Exudative AMD

DIABETIC RETINOPATHY

Ocular complications of DM

Vision

Hyperglycaemia
Cataract

DR

Background

Ischemic
Maculopathy

Exudative
Cystoid

Pre-proliferative
Proliferative

Glaucoma ( primary & neovascular )

Cranial nerve palsies ( diplopia )
Retinovascular disease
Retinal vein and artery occlusion
Ischaemic optic neuropathy

Diabetic Retinopathy
EPIDEMIOLOGY
Leading cause of blindness in the west
Both in Type I and Type II DM
Duration of DM a significant risk factor
After 20 years of DM 100% of patients with Type I DM and 60% of
those with Type II DM will have some degree of DR

Other risk factors:

Chronic hyperglycemia
Hypertension
Pregnancy

- Hyperlipidemia
- Renal disease
- Autonomic dysfunction

Diabetic Retinopathy
PATHOGENESIS:
Exact mechanism of DR not known
Prolonged hyperglycemia
biochemical/physiologic
changes
vascular endothelial damage
Thickened BM of retinal capillaries
Loss of pericytes
Endothelial damage:
Capillary obstruction retinal ischemia, cotton wool
spots, NV
Capillary leakage hard exudates, hemorrhages

Pathogenesis of diabetic retinopathy

Consequences of retinal ischaemia

Consequences of chronic leakage

Location of lesions in background

diabetic retinopathy

Pathogenesis
Microangiopathy
Capillary
Occlusion

Microvascular
occlusion
Retinal ischaemia

VEGF, Angiotensins
IGF-1, GH, FGF

Microvascular
leakage
Breakdown of the
blood-retinal barrier
VEGF

Cotton wool spots

Capillary closure

Retinal haemorrhage

Arteriovenous
shunts

Retinal exudates/
oedema

Diabetic Retinopathy
Clinical Features:
Earliest sign microanuerysms sacular dilations of retinal
capillaries (weakened capillary wall)
Hemorrhages from damaged, leaking retinal vessels
Dot/blot hemorrhages round, intraretinal
Flame shaped hemorrhages feathery border, in NFL

Hemorrhages from abnormal new vessels

Preretinal boat shaped
Vitreous hemorrhage

Diabetic Retinopathy
Microaneurysms

Dot and blot hemorrhages

Diabetic Retinopathy
Flame shaped hemorrhages

Preretinal hemorrhage

Diabetic Retinopathy
Clinical Features:
Retinal Exudates:
Hard Exudates
Yellowish intraretinal deposits
Remnants of serum/lipid exudate from damaged capillaries
Cause loss of vision if they involve the macula macular edema

Soft Exudates

Whitish opacities in the nerve fiber layer

The result of NFL infarcts from ischemia(blocked capillaries)
Not a real exudate
Other more proper name cotton wool spots

Diabetic Retinopathy
Clinical Features:
hard exudates, macular edema

cotton wool spots

Diabetic Retinopathy
Clinical Features:
Venous caliber abnormalities Signs of severe retinal hypoxia
Venous congestion and dilatation
Venous beading
Venous loops

Intraretinal Microvascular Abnormality (IRMA)

Intraretinal proliferation of endothelial cells forming shunts in areas of
non-perfusion

Diabetic Retinopathy
Clinical Features:
Venous beading

IRMA

Diabetic Retinopathy
Clinical Features:
Retinal Neovascularization
Widespread ischemia of retina
Release of vascular endothelial growth factors
Retinal neovascularization
Retinal new vessels are fragile bleed easily
They bridge the space between vitreous face and retina bleed
easily when the vitreous detaches from the retina

 NV are accompanied by fibrous tissue proliferation

Traction on the retina
Tractional retinal detachment
Neovascularization of the iris Cause closure of the
aqueous outflow channel neovascular glaucoma

Diabetic Retinopathy
Clinical Features:
Retinal Neovascularization

Diabetic Retinopathy
Clinical Features:
NV with fibrovascular proliferation

NV- with tractional retinal detachment

Diabetic Retinopathy
Clinical Features:
NV with pre-retinal hemorrhage

NV - with vitreous hemorrhage

Diabetic Retinopathy
Classification of DR:
Non-proliferative DR (background):
Mild
At least one microaneurysm

Moderate
CWS, hemorrhages, venous beading, IRMA

Severe (one of the 4-2-1 rule)

More extensive MA/ hemorrhages, venous beading & IRMA

Very severe (2 of the 4-2-1 rule)

Proliferative DR:
New vessels on the disc (NVD) or elsewhere (NVE)
Preretinal hemorrhage, Vitreous hemorrhage, Tractional RD

Diabetic macular edema

Clinically, macular edema is retinal thickening within 2 disc
diameters of the center of the macula (not fluorescein leakage
without thickening).
Retinal thickening or hard exudates with adjacent retinal
thickening that threatens or involves the center of the macula is
considered to be clinically significant.
CSME as defined by the ETDRS includes any one of these lesions:
1. Retinal thickening at or within 500 m of the center of the macula or
2. Hard exudates at or within 500 m of the center of the macula, if there
is thickening of the adjacent retina or
3. An area or areas of retinal thickening at least 1 disc area in size, at least
part of which is within 1 disc diameter of the center of the macula

Clinically significant macular oedema

Retinal oedema
within 500 m
of centre of fovea

Retinal oedema one disc area or larger any

part of which is within one disc diameter
(1500 m) of centre of fovea

Hard exudates
within 500 m
of centre of
fovea with adjacent
oedema which may
be outside 500 m
limit

Diabetic Retinopathy
Treatment of DR:
Proliferative DR laser treatment
Pan-retinal photocoagulation (PRP)
Anti-VEGF
Diabetic Macular edema laser treatment
Focal laser treatment
Anti-VEGF
Vitreous hemorrhage and tractional retinal detachment
vitrectomy

Diabetic Retinopathy
Treatment of DR:
PRP for PDR

Diabetic Retinopathy
Treatment of DR:
Laser treatment for macular edema pretreatment and
postreatment

Diabetic Retinopathy
Treatment of DR:
Vitrectomy for TRD pretreatment and post treatment

Diabetic Retinopathy
Follow-up guideline
Type of DM

1st examination

Minimum
follow-up

Type I

5 years after dx

yearly

Type II

At time of dx

yearly

Pregnancy

At 1st trimester &

more as needed

3-6 months postpartum

Hypertensive retinopathy
The effects of arterial hypertension can be directly
visualized in the fundus of the eye.
Retina is the only place in the body where retinal
vessels could be viewed directly.
These changes may involve the retinal arterioles, the
choroid, and the optic nerve

Hypertensive retinopathy
Symptoms:
Mild to moderate degree of hypertension often
result in asymptomatic fundus changes.
Severe or malignant hypertension produce fundus
changes resulting in blurred or distorted vision.

Hypertensive retinopathy
Signs:
3 stages
1. Mild hypertensive retinopathy
Thickened walls of retinal arteriole (silver or copper wiring)
Arteriovenous nicking

2. Moderate
Same changes in vessel wall as mild form
Cotton wool spots, hard exudates,
Flame-shaped hemorrhages

3. Severe
All changes of moderate hypertension and swelling of optic disc
(papilledema)

Silver wiring

AV nicking

Flame-shaped hemorrhage, hard exudates

Swollen disc,
hemorrhage

Hypertensive retinopathy
Treatment
The primary treatment is systemic arterial blood
pressure control.
Refer the patient to Internist.

COLOR BLINDNESS

The neuroretinal cells concerned with the processing of vision

are known as the rods and the cones, the latter being
concerned with color vision.
There are three types of cones: red cones, blue cones, and
green cones.
Each type of cone has a different range of light sensitivity.
Human color vision is normally trichromatic in the sense that a
suitable mixture of red, green and blue lights can match any
color that we can see.

Visible light is small part of

electromagnetic spectrum.

IR

UV
700

600

500

400
437

 Retinal ConesNormal Color Vision

Blue
cones
cones
absent in
central
fovea

Red cones
Green cones
Blue cones
Brightness =
R+G
Color = R G
Color = B
(R+G)
Red cones
outnumber
green cones
2/1
438
Red + Green

 Retinal ConesNormal Color Vision

Red, green and blue

cone sensitivity vs.
wavelength curves

439

COLOR BLINDNESS
Color blindness is the inability to distinguish certain colors. It occurs when
one or more of the cone types are absent, or present but defective and
unable to send correct signals to the brain.
Dichromats base their color vision with two cones(one of the cones absent)

Protanopia: absence of red photopigment.

Deuteranopia: absence of green photopigment
Tritanopia: absence of blue photopigment.

Anomalous trichromats
Protanomalia
Deuteranomalia
Tritanomalia

 What happens in
hereditary color
deficiency?
Red or green cone peak sensitivity
is shifted.

Red or green cones absent.

441

437 nm

533 nm
564 nm

NORMAL CONE SENSITIVITY CURVES

(TRICHROMAT)
442

5% of
Males
437 nm

564 nm

Deuteranomaly
(green shifted toward red)
443

1% of
Males

437 nm

564 nm

Deutan Dichromat
(no green cones; only red and blue)
444

1% of Males (there is no
green curve)
437 nm

564 nm

Deutan Dichromat
(no green cones; only red and blue)
445

1% of
Males

437 nm

533 nm

Protanomalous
(red shifted toward green)
446

1% of
Males
437 nm

533 nm

Protan Dichromat
(no red cones; only green and blue)
447

1% of Males (there is no red

curve)
533 nm
437 nm

Protan Dichromat
(no red cones; only green and blue)
448

COLOR BLINDNESS
Defective color vision can be either congenital or acquired.
Congenital color deficiencies are caused by inherited photopigment
abnormalities.
Impaired color vision, in the case of red-green color blindness, is
genetically determined by X-linked recessive inheritance. 8-10% of
males and 1/200 females (0.5%) are born with red or green color
deficiency.
prevalence of the red-green color deficiencies is much higher in men
than in women and that deuternormal trichromatism is the most
common color deficiency encountered.

Hereditary tritan defects are rare (0.008%).

COLOR BLINDNESS

Color vision is tested using Ishihara pseudoisochromatic plate.

Impaired color vision has implications concerning the performance of

household, educational and occupational activities.

Currently, no treatment exists for congenital color vision defects. However,

studies showed that diagnosis of these defects early in life may help
children adjust better to tasks at school and may help adults understand
their limitations at work.

Retinoblastoma
It is a rare but very malignant tumor of the retina which occurs
in infants and young children
It is the commonest malignant intraocular tumor of childhood.
It usually occurs in the first 4 years of life especially in the
first year.
The tumor grows b/n retina and choroid & also in to vitreous,
forming a white mass in the posterior part of the eye.
It may spread to cornea and sclera
optic nerve to brain
Lymph nodes, bones and liver

Retinoblastoma
It is essential to make the diagnosis in the early stages
before tumor has spread beyond the eye,because in early
stages the childs life can be saved.
Once the tumor has spread beyond the eye the child will
probably die.
Clinical presentations:
White mass inside the eye (leukocoria)
Squint
Painful inflammed eye
Proptosis
Fungating mass

Presentations of retinoblastoma

Leukocoria - 60%
Strabismus - 20%
Secondary glaucoma

Anterior segment invasion

Orbital invasion
Orbital inflammation

Retinoblastoma
Treatment options:
Surgery
Radiotherapy
Chemotherapy
Early referral to ophthalmologist!

Neuro-ophthalmologic Disorders

Pupillary abnormalities
Visual field defects
Optic neuritis
Papilloedema
Optic nerve atrophy
Disorders of cranial nerves
Nystagmus

PUPILLARY ABNORMALITIES

Pupil
Pupillary size is determined by a number of
factors including
Age
Level of alertness
Level of retinal illumination
Accommodative effort

Factors affecting pupil size

Topical medications
Mydriatics/ miotics

Trauma
Traumatic (injury or surgical) mydriasis (pupillary
sphincter tear), posterior synechae

Ocular diseases
Uveitis, angle closure glaucoma

Systemic medication
Narcotics cause miosis

 Traum
atic
mydria
sis

 Anatomy of pupillary pathway

Afferent limb
Efferent limb
Parasympathetic pathway
Sympathetic pathway

Near response

LIGHT REFLEX PATHWAY

The pupillary light reflex gives information about the integrity

of both the afferent and efferent neuronal outflow to each pupil.

3-neuron arc
1. The afferent neurons from retinal ganglion cells to the
pretectal area;
2. An intercalated neuron from the pretectal complex to the
parasympathetic motor pool (EdingerWestphal nucleus)
of the oculomotor nuclear complex and
3. The efferent parasympathetic outflow with the oculomotor
nerve to the ciliary ganglion; and from there to the
pupillary sphincter.

OCULOSYMPATHETIC PATHWAYS

NEAR REFLEX AND ACCOMMODATION

ABNORMAL PUPILS
Diseases of the visual and nervous system can
cause the pupils to become poorly reactive to
light or near stimuli.
These disorders can be classified into the
following major categories.
1. Afferent Pupillary Defects
2. Efferent Pupillary Defects.

Afferent Pupillary Defects

These are seen in disorders that interfere with the input of light
to the pupillomotor system:
by blocking light from stimulating the retina;
by damaging any of the retinal layers; or
by damaging the optic nerve, chiasm, optic tract, or
midbrain pretectal area.

Afferent Pupillary Defects

Common diseases producing RAPD:

Central or branch retinal artery or vein occlusion

Retinal detachment
Anterior ischemic optic neuropathy
Optic neuritis
Compressive optic neuropathy
Chiasmal compression
Optic tract lesion
Midbrain tectal damage

 RAPD
Combination of subnormal direct pupillary light response
and a normal indirect (consensual) response when the
opposite eye is illuminated
Relative afferent pupillary defects do not cause anisocoria
(pupillary inequality) in humans, because any changes in
light input are distributed equally to both pupils.

Efferent Pupillary Defects

These are seen in disorders that interfere with the constriction

or dilatation of the pupil.
The location of damage affecting the pupillary response to
light, dark, or near may be in
the midbrain
along the course of the peripheral nerves supplying the iris dilator or
sphincter muscle, or
directly in the iris tissue itself.

Most diseases causing efferent pupillary defects are unilateral

or asymmetric and therefore cause unequal pupils (anisocoria)

Anisocoria
Difference in pupillary size (may be physiological
or pathological)
Physiological anisocoria
Usually less than 1mm difference
2% of general population
A normal, asymmetric contribution of the sympathetic
and parasympathetic nervous systems to each pupil

 Greater anisocoria in the light reflects damage to the

parasympathetic pathway
Anisocoria that is worse in the dark reflects damage
to the sympathetic pathway.

Etiology of anisocoria:
The abnormal pupil is constricted
Unilateral use of miotic drugs e.g pilocarpine
Iritis
Horners syndrome
Argyll Robertson pupil
Long-standing Adies pupil

The abnormal pupil is dilated

Iris sphincter muscle damage from trauma
Adies tonic pupil
Third-nerve palsy
Unilateral use of dilating eye drop e.g atropine
Physiologic anisocoria

HORNERS SYNDROME( oculosympathetic defect)

Symptoms: Droopy eyelid, pupil size disparity; often
asymptomatic
Signs:
Ptosis due to paresis of Muller's muscle
Miosis ( anisocoria greater in dim illumination)
Anhydrosis(loss of sweating ability)- due to denervation of sweat fibers
Pseudoenophthalmos( b/c of ptosis & lower lid elevation)
Ocular hypotony
Conjunctival congestion(transient dilated conjunctival & facial
vessels) denervation vasoconstrictor fibers
Iris heterochromia (if congenital)
Paradoxical contralateral eyelid retraction

Rt Horners syndrome

HORNERS SYNDROME( oculosympathetic defect)

Etiology
1. First order neuron disorder: Stroke, tumor
2. Second order neuron disorder: Tumor(e.g. lung
carcinoma)=>pancoasts tumor
3. Third-order neuron disorder: headache
syndrome(e.g. cluster migraine), internal carotid
dissection, herpes zoster virus, otitis media
Congenital Horners syndrome: Trauma ( e.g.
during delivery)

HORNERS SYNDROME( oculosympathetic defect)

Work-up
Diagnosis confirmed with a cocaine test(10%)
If the sympathetic discharge is impaired, less norepinephrine is
released , resulting in less mydriasis compared with the normal eye.

HORNERS SYNDROME( oculosympathetic defect)

Hydroxyamphetamine 1% is used to distinguish a 3 rd order neuron

disorder from 1st or 2nd order neuron disorder.
Failure of the Horners pupil to dilate to an equivalent degree as the
fellow eye indicates a 3rd order neuron lesion.

ADIES TONIC PUPIL

Damage to the ciliary ganglion or the short ciliary nerves may
cause a tonic pupil
Symptoms:
Difference in the size of the pupils, blurred vision; may be
asymptomatic

ADIES TONIC PUPIL

Signs:
An irregularly dilated pupil exhibiting minimal or no reaction to
light, slow constriction to convergence and slow redilatation.
It is typically unilateral and is found most often in young women
The pupil demonstrates supersensitivity to weak cholinergic
agents(e.g. pilocarpine 0.125%)
It may develop acutely and may become bilateral
The pupil dilates normally to mydriatic agents.
Deep tendon reflexes (knee and ankle) are often absent( Adies
syndrome)
The involved pupil may become smaller than the normal pupil over
time.

ADIES TONIC PUPIL

Etiology
Idiopathic, orbital trauma or infection, herpes zoster
infection, diabetes, autonomic neuropathies, others

Work-up
Observe the suspected pupil with slit lamp. The Adies
pupil will contract slowly and irregularly.
Test for supersensitive pupil: instill a drop of
pilocarpine 0.125% in each eye. Check after 15 min.
The tonic pupil constricts significantly more than the
contralateral pupil in Adies syndrome.

ARGYLL ROBERTSON PUPIL

Symptom: usually asymptomatic

Signs:
Small, irregular pupil that reacts poorly or not at all to
light but constricts normally during convergence.
The pupil does not dilate well.
Initially it may be unilateral, but it becomes bilateral,

Etiology
Tertiary syphilis (neuro - syphilis )

ARGYLL ROBERTSON PUPIL

Work-up
Test the pupillary reaction to light and convergence
Slit-lamp exam: look for interstitial keratitis
Dilated fundus exam: search for chorioretinitis, papilitis,
and uveitis
Lab tests: FTA-ABS or MHA-TP, RPR or VDRL
Lumbar puncture

Treatment
Decision is based on whether active disease is present and
pt has been treated appropriately in the past.

Visual field defects

 The normal visual field

is defined as Island of
vision surrounded by a
sea of blindness

The normal extent of field of vision

50superiorly
60nasally.
70inferiorly .
90 temporally

Common causes of VF defect

Central field loss occurs with:

Optic neuropathy
Macular degeneration
Macular hole
Cone dystrophies
A number of rare conditions like Bests disease, Stargardt's

.
central

disease and achromatopsia

Normal

ceco-central

Peripheral field loss occurs with:

Retinitis pigmentosa
Chorioretinitis
Glaucoma
Retinal detachment
Leber's optic atrophy

Ring scotoma

Advanced glaucoma

Assessing for visual field defects

Screening tests
Confrontational visual field testing
Amsler grid (assesses the central 10 the visual
field ) .
Quantitative measurements using perimetry.

Terms
Visual field defect - a portion of visual field missing.
Scotoma - visual field defect surrounded by normal visual
field.
Relative scotoma - an area where objects of low luminance
cannot be seen but larger or brighter ones can.
Absolute scotoma - nothing can be seen at all within that area.

 Hemianopia - binocular visual defect in each eye's hemifield.

Bitemporal hemianopia - the two

halves lost are on the outside of
each eye's peripheral vision,
effectively creating a central
visual tunnel.
Homonymous hemianopia- the
two halves lost are on the
corresponding area of visual field
in both eyes, i.e. either the left or
the right half of the visual field.

 Altitudinal hemianopia refers to the dividing line

between loss and sight being
horizontal rather than
vertical, with visual loss
either above or below the
line.
Quadrantanopia - is an
incomplete hemianopia
referring to a quarter of the
schematic 'pie' of visual field
loss.

Sectoral defect - is also an

incomplete hemianopia

Lesions before the chiasm

These will produce a field deficit in the ipsilateral eye.

Field defects from damage to the optic nerve tend to be
central, asymmetrical and unilateral.
Lesions just before the chiasm can also produce a small defect
in the upper temporal field of the other eye

Lesions at the chiasm

These classically produce a bitemporal hemianopia.

If they spread up from below, for example, pituitary tumours,
the defect is worse in the upper field.
If the tumour spreads down from above , e.g.
craniopharyngioma, the lesion is worse in the lower quadrants.

Lesions after the chiasm

These produce homonymous field defects.

A lesion in the right optic tract produces left visual field
defect.
Lesions in the main optic radiation cause complete
homonymous hemianopia without macular sparing.
Lesions in the temporal radiation cause congruous upper
quadrantic homonymous hemianopia commonly with macular
sparing.

 Lesions in the parietal radiation (rare) cause inferior

quadrantic homonymous hemianopia without macular sparing.
Lesions in the anterior visual cortex (common) produce a
contralateral homonymous hemianopia with macular sparing .
Lesions in the macular cortex produce congruous
homonymous macular defect
Lesions of the intermediate visual cortex produce a
homonymous arc scotoma, with sparing of both macula and
periphery.

Occipital lobe lesions

If both occipital lobes are injured then the patient is in a state

of cortical blindness.
Some patients deny their blindness and attempt to behave as if
they have vision. This state of denial of cortical blindness is
called Anton's syndrome.

Localising the lesion

Monocular visual field defects indicate lesions
anterior to the optic chiasm
Bitemporal defects are the hallmark of chiasmal
lesions
Binocular homonymous hemianopia result from
lesions in the contralateral postchiasmal region
Binocular quadrantanopias reflect optic tract lesions

OPTIC NEURITIS
Optic neuritis is the term used for inflammation of the optic
nerve.
Symptoms
Optic neuritis may be symptomatic or asymptomatic.
Symptomatic cases present with a triad of symptoms: loss of vision,
ipsilateral eye pain, and dyschromatopsia.
Loss of vision deteriorating over hrs(rarely) to days(most commonly).
Usually unilateral, but may be bilateral
Age typically 18-45 yrs
Orbital pain, especially with eye movement
Acquired loss of color vision
Reduced perception of light intensity
Occasionally Uhthoffs sign(visual deficit with exercise or increase in
body temperature)
May have neurologic symptoms or an antecedent viral syndrome(e.g.
upper respiratory, GI)

OPTIC NEURITIS
Signs
RAPD in unilateral or asymmetric cases
Decreased color vision
Central, cecocentral, arcuate or altitudinal VF defects
Swollen disc with or without peripapillary flame-shaped
hemorrhages(papillitis-most commonly seen in children &
young adults) or a normal disc( retrobulbar optic neuritis-more
commonly in adults)
Posterior vitreous cells may be seen

Visual field defects

Central scotoma

Altitudinal

Centrocaecal
scotoma

Nerve fibre bundle

OPTIC NEURITIS
Etiology

Idiopathic
Multiple sclerosis
Childhood infections (e.g measles, mumps, chicken pox)
Other viral infections(e.g. herpes zoster)
Contigious inflammation of meninges, orbit,or sinuses
Granulomatous inflammations (e.g. TB, syphilis,
sarcoidosis)
Intraocular inflammation
Drugs (INH, Ethambutol.)

Classification of optic neuritis

Retrobulbar neuritis
(normal disc)

Papillitis (hyperaemia and

Neuroretinitis (papillitis
oedema)
and macular star)

Cat-scratch fever
Demyelination most Viral infections and immunization
in children (bilateral)
common
Lyme disease
Sinus-related (ethmoiditis)
Demyelination (uncommon)

Lyme disease

Syphilis

Syphilis

Work-up
1. History: determine pts age and rapidity of visual loss.
Previous episode? Pain with eye movement?
2. Complete ophthalmic and neurologic exam, including
pupillary assessment, color vision, evaluation for
vitreous cells, dilated retinal exam with optic nerve
assessment.
3. Check blood pressure
4. VF test
5. For atypical cases: CBC,ESR, RPR, MRI of brain and
orbit

OPTIC NEURITIS
Treatment
If pt seen acutely:
1. If vision 20/40 or better: Observation is
indicated
2. If vision is 20/50 or worse: steroid

Papilledema
Definition
Optic disc swelling produced by increased intracranial pressure

Papilledema
Symptoms:
Episodes of transient, often bilateral, visual loss (lasting
seconds) often precipitated by changes in posture
Headache; double vision; nausea; vomiting
Rarely, a decrease in visual acuity ( a mild decrease in VA
may occur in acute setting if associated with a macular
disturbance)
VF defects and severe loss of central VA can occur with
chronic papilledema

Clinical signs of optic disc edema;

Mechanical signs:
Elevation of the optic disc
Blurring of the optic disc margins
Filling in of the physiologic cup
Edema of the peripapillary nerve fiber layer
Retinal or choroidal folds
Vascular signs:
Hyperemia of the optic disc
Venous congestion (venous dilatation and tortuosity)
Peripapillary hemorrhages
Exudates in the disc or peripapillary area
Nerve fiber layer infarcts

 Normal pupillary response and color vision

An enlarged physiologic blind spot
As chronic papilledema progresses to optic atrophy, hges
& cotton wool spots resolve, peripapillary gliosis and
narrowing of peripapillary retinal vessels occur. Loss of
color vision, central VA , and peripheral VF also occur.

Early papilloedema

VA - normal
Mild disc hyperaemia
Indistinct disc margins - initially nasal
Mild venous engorgement
Normal optic cup
Spontaneous venous pulsation - absent (also absent in 20% of n

Established papilloedema (acute)

VA - usually normal
Severe disc elevation and hyperaemia
Very indistinct disc margins
Obscuration of small vessels on disc
Marked venous engorgement
Reduced or absent optic cup
Haemorrhages + cotton-wool spots
Macular star

Longstanding papilloedema (chronic)

VA - variable
Marked disc elevation but less hyperaemia
Disc margins - indistinct
Variable venous engorgement
Absent optic cup

ophic papilloedema (secondary optic atro

VA - severely decreased
Mild disc elevation
Indistinct disc margins
Disc pallor with few crossing vessels
Absent optic cup

Causes of Raised Intracranial Pressure

1. Space-occupying lesions
2. Blockage of ventricular system
3. Obstruction of CSF absorption
4. Benign intracranial hypertension
(pseudotumour cerebri)
5. Diffuse cerebral oedema
6. Hypersecretion of CSF

 Work-up
1. Hx & physical exam, including BP measurement
2. Ocular exam including:
Pupillary exam
Color vision test
Posterior vitreous evaluation for cells
Dilated fundus exam
3. Emergecy CT and/or MRI
4. Lp
Treatment
-Underlying cause of elevated ICP

Optic atrophy

Optic atrophy represents the permanent loss of retinal ganglion

cell axons in conjunction with retinal ganglion cell death.
Optic atrophy should not be considered a diagnosis; it is a
pathologic end-point that is clinically discernible but does not
imply cause.
Can be a consequence of any injury of the retinal ganglion cell or
its axon at the level of the nerve fiber layer; the optic nerve head;
the orbital, intracanalicular, or intracranial optic nerve; the optic
chiasm; the optic tract; or the lateral geniculate nucleus chronic
disc swelling

 Glaucoma is the most common cause of optic atrophy

Fundus changes:
Optic disc atrophy may vary widely in appearance from
slight temporal (disc) pallor to a chalk-white optic nerve
head
In its severe form, is characterized funduscopically by a
pale optic disc with clearly delineated /blured borders

Disorders of cranial nerves

3 , 4 & 6 nerve palsy

rd

th

th

Anatomy
The final common pathway for ocular motor control
consists of the three pairs of ocular motor nerves and the
muscles that they innervate.
The nerves originate in paired nuclei within the midbrain
and pons, and their axons course as fascicles through the
brain stem parenchyma, run freely for variable distances
within the subarachnoid space, pass through the
cavernous sinus, and enter the orbit to supply the
extraocular muscles.

 CN IIIMotor innervation for SR, MR, IR, IO, and levator

palpebrae superioris muscles
Parasympathetic input to the pupillary constrictor and
ciliary muscles
Superior division: SR, levator palpebrae
Inferior division: MR, IR, IO, Pupil

CN IVSO
CN VI LR

3 nerve palsy
rd

Symptoms:
Double vision that disappears when one eye is closed; droopy
eyelid, with or without pain

Signs:
A. External ophthalmoplegia
Complete palsy: limitation of ocular movement in all fields of
gaze except temporally
Incomplete palsy: partial limitation of ocular movement.
Superior division palsy: Ptosis & inability to look up
Inferior division palsy: Inability to look nasally or inferiorly ;
pupil is involved.

3 nerve palsy
rd

Signs:
B. Internal ophthalmoplegia
Pupil-involving: A fixed, dilated or minimally reactive
pupil
Pupil-sparing: pupil not dilated and normally reactive to
light
Relative pupil-sparing: pupil partially dilated & sluggishly
reactive to light

3rd nerve palsy

Etiology
A.Pupil-involving
Aneurysm (particularly posterior comminicating artery),
tumor..

B. Pupil-sparing
Microvascular disease (DM, HTN)

C. Relative pupil-sparing: Microvascular diseases

3rd nerve palsy

Treatment
Treat underlying abnormality
If double vision, patch the involved eye
Patching not performed in children younger
than 9-11 year( risk of amblopia)

 Workup
Pupil-involving 3rd nerve palsy: immediate hospitalization
& work-up(CT and MRI)
Pupil-sparing 3rd nerve palsy: if new, observe for 5-7 days
for delayed pupil involvement, then recheck every 6 weeks.
Regain function within 3 months.
If palsy does not reverse by this time or if an additional neurologic
abnormality develops, do MRI.

4th nerve palsy

Symptoms
Binocular vertical diplopia, difficulty of reading, sensation
that objects appear tilted; may be asymptomatic
Signs
Deficient inferior movement of an eye when attempting to
look and in.
The involved eye is higher (hypertropic) when patient looks
straight ahead.
The hyperopia increases when looking in the direction of
uninvolved eye or tilting the head toward the ipsilateral
shoulder
The pt often maintains a head tilt toward the contralateral
shoulder to eliminate double vision

4th nerve palsy

Etiology
More common: trauma, vascular infarct(DM,
HTN), congenital, idiopathic, or demyelinating
diseases
Rare: Tumor, hydrocephalus, giant cell arteritis,
aneurysm

Treatment
Treat the underlying disorder
Patch one eye if symptomatic diplopia
Surgery
Bothersome double vision in primary or reading position,
for cosmetic purposes, or for head tilt.

6th nerve palsy

Symptoms
Binocular horizontal diplopia, worse for distance than near, most
pronounced in the direction of paretic lateral rectus musle
Signs
One eye does not turn outward(temporally)
Etiology
ADULTS

More common: vasculopathic( diabetes, HTN, atherosclerosis),

traumatic, idiopathic
Less common: Increase intracranial pressure, cavernous sinus mass,
multiple sclerosis, sarcoidosis/vasculitis
CHILDREN

Benign postviral
Gradenigos syndrome (petrositis causing 6th and often 7th nerve
involvement, with or without 8th and 5th n. involvement on the same
side)
Pontine glioma
Trauma

6th nerve palsy

Treatment
Any underlying problem revealed by the work-up;
otherwise, pts are managed by observation
Patching the paretic eye

Nystagmus
Definition
Nystagmus is the rhythmic to-and-fro oscillation of the eyes

Symptoms
Asymptomatic unless acquired after 8 years of age, at which point the
environment may be noted to oscillate horizontally, veritcally, or
torsionally, or vision may seem blurred or unstable

Signs
Repetitive oscillations of the eye horizontally, vertically, or torsionally.
Jerk nystagmus: The eye slowly drifts in one direction(slow phase) &
then abruptly returns to its original position(fast phase), only to drift and
repeat the cycle.
Pendular nystagmus: Drift occurs in 2 phases of equal speed, giving a
smooth back-and-forth movement of the eye.

Nystagmus may be congenital or acquired

Nystagmus
A.Congenital
1.
2.
3.

Infantile nystagmus
Latent nystagmus
Nystagmus Blockage syndrome

1. Infantile nystagmus

Onset at age 2-3 months , with wide swinging eye movements

At age 4-6 months, small pendular eye movements are added,
&at age 6-12 months, jerk nystagmus and a null point(a position
of gaze where nystagmus is minimized) develop.
Compensatory head nodding develops at any point up to age 20
yrs.
Infantile nystagmus is usually horizontal and typically dampens
with convergence
Etiology

Idiopathic
Albinism
Aniridia
Lebers congenitial amaurosis
Others : bilateral optic nerve hypoplasia, bilateral congenital
cataracts, rod monochromatism, optic nerve or macular disease

Treatment
Maximize vision by refraction
Treat amblyopia
If small face turn: prescribe prism in glasses with base in direction of
face turn
If large face turn: consider muscle surgery

2. Latent Nystagmus

Latent nystagmus: occurs only when one eye is viewing. Fast

phase of nystagmus beats toward viewing eye.
Manifest latent nystagmus: occurs in children with strabismus or
decreased vision in one eye. Nonfixating or poorly seeing eye
acts as an occluded eye.
Treatment:
Maximize vision by refraction
Treat amblyopia if indicated
Consider muscle surgery if symptomatic strabismus exists.

3. Nystagmus Blockage Syndrome

Any nystagmus that decreases when fixating eye is in adduction and
demonstrates an esotropia to dampen the nystagmus.
Treatment:
For large face turn, consider muscle surgery

B. Acquired nystagmus
Etiology :
Visual loss(e.g dense cataract, trauma, cone
dystrophy)
Toxic/metabolic
CNS disorders (e.g hemorrhage, tumor,
stroke)

Treatment
The underlying etiology must be treated.

Clinical manifestations of HIV-AIDS

Patients may have recurrent opportunistic infections or of
unusual tumors in/around the eye
HIV has been demonstrated in tears, conjunctival epithelial
cells, corneal epithelial cells, aqueous, retinal,vascular
endothelium, and retina.

Ophthalmic manifestations
1. Microvasculopathy
2. Tumor e.g. Kaposis sarcoma, Squamous cell
carcinoma,lymphoma
3. Neuro-ophthalmopathy e.g. cranial nerve palsy, optic atrophy
4. Opportunistic infection e.g. herpes zoster ophthalmicus, herpes
simplex infection, toxoplasmosis ,CMV, fungal infections
Over 70% of AIDS cases have some form of ophthalmic
manifestation.

HIV retinopathy
It is a non-infectious micro-vascular disorder characterized by
cotton wool spots, microaneurysm, retinal hemorrhages, and
area of capillary non-perfusion.
These micro vascular changes are the most common retinal
manifestations of HIV disease and are clinically apparent in
about 70% of persons with advanced HIV disease.

Refractive error
Emmeteropia is a refractive state of an eye which forms a
sharp retinal image of an object.
Gives a clear image of an object
A normal refractive state
Ammeteropia is a refractive state of an eye which exists
when objects are not focused sharply on the retina
Gives a blurred image of an object
Abnormal refractive state

 Causes
Short or long axial length
Weak or strong ocular power
Types
1. Myopia (short sight)
- Excessive positive power
- Long axial length
- Parallel images from the object meet in front of the
retina forming a blurred image
- Corrected by a negative lens ( concave lens)

2. Hyperopia (long Sight)

Positive power less than normal
Short axial length
Forms image behind the retina
Corrected by a positive lens (convex lens)
3. Astigmatism
Refractive error at a certain meridian (axis)
Either myopic or hyperopic astigmatism
Corrected by cylinder

4. Aphakia
Absence of a lens
Congenital or acquired (traumatic or surgical)
Corrected by IOL or eye glass
5. Presbyopia
We see near objects by accommodation
With aging accommodative power of our eyes will be lost
resulting in presbyopia
. Corrected by bifocal lens( convex lens) (bifocal glasses with
the upper segment focused for far-seeing and the lower
segment focused for near-seeing (e.g., for reading).)

6. Anisometropia
Is a condition in which the refractive power of one eye
differs from the other
Significant when the difference is larger than 2 diopter

Ocular motility disorders

The eyes move in different direction by the EOMs
We have 6 EOM
Medial rectus/ lateral rectus
Superior/ inferior rectus
Superior/ inferior oblique
Innervations

MR/IR/IO/SR CN III
LR CN VI
SO CN IV

 Each eye has a primary visual axis (that passes through the
fovea)
Objects from each eye along the primary visual axis will fall on
to a common visual axis
Objects on the common visual axis will be fused and seen as
single.
But when the two visual axiss can not meet at the same point,
we call it misalignment, or squint or strabismus
Nasal deviation (relative to the fixating eye) is described with
the prefix "eso," and temporal deviation with the prefix "exo."
As a general rule, the prefix "hyper" is applied to the eye that is
more superior in vertical deviations, regardless of which eye is
fixating. However, the prefix "hypo" is sometimes used to denote
an eye that is depressed relative to the fixing eye.

 A "latent" strabismus is present only when fixation is interrupted

and is known as a "phoria" (eg, esophoria, exophoria). In pts with
this condition, ocular alignment is maintained by fusion as long as
fixation is uninterrupted. Strabismus that is present without
interruption of the visual axis is "manifest" and described as a
"tropia.
Manifest strabismus can be intermittent, occurring only when
fusional capabilities are exceeded (eg, when the pt is tired) or
constant.
Manifest strabismus can be monocular, when deviation always
involves the same eye, or alternating, when either eye may deviate.
Deviation that is the same in all positions of gaze is described as
"comitant." Deviation that changes depending upon the position of
gaze is "incomitant" and usually is present with paralytic or
restrictive strabismus.

Strabismus types
1) Esotropia (ET) is a convergent strabismus
Esotropia types
a) Pseudo esotropia

False appearance of the esotropia when the visual axis are

actually aligned accurately
Cause e.g. flat broad nasal bridge or wide epicanthal fold

 The corneal light reflex test involves shining a light onto the pta eyes from a
distance and observing the reflection of the light on the cornea with respect to
the pupil. The location of the reflection from both eyes should appear symmetric
and generally slightly nasal to the center of the pupil. A) Normal corneal reflex.
B) Corneal light reflex in esotropia. C) Corneal light reflex in exotropia.

b) Congenital ET
Age from birth to 6 month
Large angle
Alternating
Not hyperops
Otherwise healthy
Usually positive family history
Treated surgically (BMRc , or MRc + LR)

 C) Accommodative ET
Older than 6 months (typically is from about 18 months to 4 years
of age. )
Hyperops
Excess convergence for each accommodation
Treated with positive lens (bifocal)
This is acquired esotropia in origin, reflecting a disturbance in the
accommodative convergence mechanism.
Most children with this form are moderately or severely
hyperopic. In order to see clearly, they exert an excessive
accommodative effort that results in overconvergence and an
esotropia.

 D) Basic or acquired ET
Age above 6 month
Not hyperops
Treated sugically (MRc and/ or LRs)

E)Acute ET
Secondary to ocular injury or paralysis
Usually associated with neurologic disease
Treated with prism or botulinium toxin and if it fails
surgery

 F) Sensory ET
Secondary to sensory causes like cataract
First treat the underlying cause then treat the
strabismus surgically

G) Consecutive ET
ET following surgery for XT
If small angle no treatment
For large angle ET treat surgically

2) Exotropia
Is a divergent strabismus
Patients have laterally turned eyes

Exotropia types
A) Pseudo exotropia is a false appearance of
exotropia when the visual axiss are well aligned
Cause e.g. large interpupilary distance, temporal
dragging of the macula secondary to retinal traction.
Retinopathy of prematurity is the most common
cause of pseudoexotropia

 B) Congenital XT
Age less than 6 month
large angle and constant
patients usually have neurologic abnormality
Treated surgically (LRc and or MRs)

 C) intermittent ET
The most common type of XT
Manifests at the time of fatigue, illness,
inattentiveness, trauma
Treated first with correction of any refractive
errors like myopia
- orthoptic exercise
- prism
- surgery if it progresses to constant XT

 D) Constant XT
Older children and adults
Secondary to decompensated intermittent XT
Treated surgically (LRc and or MRs)

E) Sensory XT
Secondary to sensory causes like cataract
Treated first the underlying cause then the squint

 HYPERTROPIA (HT)
Is a vertical strabismus where patients have
elevated eyes
Causes e.g. Superior oblique palsy with IOOA
Treated surgically (Superior oblique tuck and or
inferior oblique weakening)

 Hypotropia (HoT)
Is a vertical strabismus where pts have depressed
eyes
Cause e.g. orbital floor fracture with entrapment of
the inferior oblique muscle
Treated by surgical exploration of the wound
releasing the muscle and feeling the space with
inert material

Clinical evaluation of a patient with

strabismus
History
Age
constant/intermittent
Distance/near
Unilateral/alternating
Present when the patient is ill or fatigued
Reduced vision
History of trauma
Family history
Associated systemic illness

 Physical examination
1. Visual acuity
a)
b)
c)
d)
e)

Fix and follow

Avoidance movement
Allen pictures/ lea symbols
CSM
Snellen acuity chart

2. Assessement of eye movement

a) Version in 9 diagnostic positions
b) Duction in 6 cardinal positions

3. Sensory tests for diplopia / suppression/

steriopsis
4. Measure the angle of strabismus
) Corneal light reflex test
) Cover test

5. Retinoscopy
Objective measurement of refractive error

6. Fundus evaluation
To look for sensory causes of strabismus like
retinoblastoma

AMBLYIOPIA (Lazy eye)

Is a unilateral less commonly bilateral reduction of best
corrected visual acuity that can not be attributed by the
direct effect of any structural abnormality of the eye or
the posterior visual pathway.
It is caused by
Strabismus
Anisometropia or high bilateral RE
Visual deprivation

It is primarily a defect of the central vision

It occurs in a developing brain of children

Treatment
Correcting any visual deprivation
Correcting any refractive error
Strengthenig the weak eye
- Occlusion of the dominant eye
- Optical or pharmacological degradation of the
dominant eye

Ocular Trauma

Outline
Assessment of Trauma
Types of injury
Peri-ocular
Anterior segment
Posterior segment

Chemical injury

Introduction
Although the eye is well protected by the orbit,
it may yet be subject to injuries.
Forms of injury include:
Foreign bodies
Blunt trauma
Penetrating trauma
Chemical and radiation injuries

Risk factors

Gender : 75%-80% of them are in males

Age: more in children and young age group
Occupation : construction, industry
Sports : boxing , racket sports
Motor vehicle accidents

40% of monocular blindness is related to trauma

The leading cause of monocular blindness

Effects of eye injury :

Closed globe injury or Non-penetrating trauma:
The eye globe is intact, but the seven rings of the eye
have been classically described as affected by blunt
trauma.
Penetrating trauma: The globe integrity is disrupted
by a full-thickness entry wound and may be
associated with prolapse of the internal contents of
the eye.

Effects of eye injury (cont.)

Blowout fracture of the orbit is caused by blunt
trauma, classically described for fist or ball injury,
leading to fracture of the floor or medial wall of the
orbit due to sudden increased pressure on the orbital
contents.
Perforating trauma: The globe integrity is disrupted
in two places due to an entrance and exit wound
(through and through injury). This is a quite severe
type of eye injury.

Assessment
Rule out life threatening injuries
Rule out globe threatening injuries
Examine both eyes
Image
Plan for treatment

History
Mechanism of trauma
Blunt/penetrating/mixed
Forces involved

Previous injuries
Past ocular history
Past medical history

Examination
Pt review
Are there life threatening injuries which need to be
treated first?
?Brain injury

Facial Exam
Lacerations/bruising, numbness, weakness

Ocular exam
VA, lids and lacrimal system, orbital rim/orbital bones,
ocular motility, globe, optic nerve

Lids and orbits

Assessment
History
Detailed as possible
Time and nature of injury
Missile, blunt, ? FB remaining, chemical etc

Past ocular history

Previous VA and lid function
Remember trauma is a recurrent pathology

Med Hx
?Tetanus, ? Anticoagulation

Examination

Rule out life threatening injuries

Rule out globe threatening injuries
Examine both eyes
Assess lid trauma - document +/- photos
Plan for repair

Examination - lids
Tissue loss
Layers of lid
Lid Margin
Canaliculi
Prolapsed fat/septal involvement
Levator function
Lagophthalmos
Canthal tendon/angle

Image
CT - fine cuts orbits
If ? FB
If unable to determine posterior aspect of
wound
If suspect orbital fracture/ other injuries

Lid Lacerations
Refer to ophthalmologist if there are
associated ocular injuries
Ruptured globe
Lacrimal drainage system
Levator aponeurosis
Medial canthal tendon
Tissue loss ( > 1/3 )
Involvement of lid margin

Repair
Timing
Ideally within 12-24 hours of injury
Can delay up to 1 week
Patient factors
Gross swelling
Ice packs to reduce
? steroid

Anaesthesia
GA / LA

Full Thickness Lid Lacerations

Tear lid margin

- Gray line
- Lash line
- Mucocutaneous junction

Lid Margin Repair

Laceration of lower eyelid margin

Post-operative result following a

primary repair

Lid Lacerations with tear canaliculi

Canalicular Repair

Penetrating / Ruptured Globe

Corneal or scleral lacerations
Hypotony (not always present)
Severe chemosis & hemorrhage
Intraocular contents may be outside the globe
Limitation of extraocular motility
Shallow anterior chamber
Irregular pupil

Irregular pupil

Penetrating / Ruptured Globe

Penetrating / Ruptured Globe

Ruptured globe caused by golf ball

Penetrating / Ruptured Globe : Management

Stop examination
Shield the eye (do not patch)
Give tetanus prophylaxis
NPO and systemic antibiotics
Do not apply eye ointment or eye drop
Film orbit if IOFB cant be R/O
Refer immediately to ophthalmologist

Intraocular or Intraorbital Foreign Bodies

Ocular Trauma

Traumatic cataract

Traumatic mydriasis

Traumatic lens subluxation

Traumatic lens subluxation

Orbital Fractures

Orbital #s
classification
Open or closed
Internal (orbital skeleton), rim, complex (internal +rim)

Type
Blowout - typically 10-15mm behind rim, just medial infraorbital canal
Tripod - disruption of zygoma at z-f and z-m sutures & along arch
Enophthalmos, malar flattening, inf lat cantus displacement

Pathogenesis of orbital floor blow-out fracture

Evaluation of the orbit

Eyelids
Telecanthus - tendon disruption or nasoethmoidal #, suspect nld
involvement

Globe
Displacement, proptosis

Motility - ductions and diplopia, include FDT

Pupil - APD, efferent, mydriasis
Palpate
Rim, crepitus, retropulsion

Nerves - V1 & V2

Signs of orbital floor blow-out fracture

Periocular ecchymosis
and oedema
Infraorbital nerve
anaesthesia

Enophthalmos - if severe
Ophthalmoplegia typically in up- and downgaze (double diplopia)

Imaging
CT
Axial and coronal
3mm sections
1.5 through apex if suspect TON

MRI
No good - bone, metal FB
Subdural optic n haematoma

Anterior Segment Trauma

Assessment
History
Forces involved
Blunt, FB?, Penetrating
Chemical
Acid?
Alkali?
Contact allergy?

Common Causes
Abrasion
Minor trauma - lash, finger
Recurrent Epithelial Erosion Syndrome
Plant

Foreign body
Grinding

Penetrating Injury
Hammering metal on metal
Explosion
Dirty / clean

Blunt
Fist
Ball
Bungy cord

Examination
Visual Acuity
Skin/lids
Evidence of severity of injury

Evert lids
? Subtarsal FB
Look for fine scratches on upper cornea

Conjunctiva
Laceration
Look carefully for scleral injury beneath
Sub conj hemorrhage

Examination
Cornea
Fluorescein stain - abrasion/wound
Leak
Infiltrate
FB

Anterior chamber
Cells
Hyphaema
Hypopyon

Examination.
Iris
Transillumination defects
Peaked pupil
Dilated pupil
Check for RAPD

Lens
Red reflex
Stability

IOP
+/- angle

RAPD
RAPD
Relative afferent
pupillary defect

Corneal foreign body

Grinding most common cause
Usually do not need surgery
Treatment
Removal of foreign body with needle and/or burr
Children may require GA

Corneal Abrasions

Corneal Abrasion
Common
Usually resolve quickly
Very painful initially
Treatment
Exclude other injuries
Chloramphenicol ointment
Patch 24 hours
+/- pain relief / sleeping tablets

Subconjunctival Hemorrhages

Bleeding under conj

Red eye
Discomfort
VA is not affected
Complete exam
Treatment Conservative

Hyphaema
Blunt injury
Complications:
Raised IOP
Angle recession
Corneal staining
Rebleed

Treatment
Steroid
Bed rest - debatable
Frequent monitoring wrt IOP

Traumatic Uveitis
Ranges from Mild to Severe
Usually other injuries as well
Treat as for normal uveitis but may not
require long taper

Chemical Ocular Injury

True ocular emergency
Both acid and alkali burns can be blinding
- Acid burns tend to coagulate proteins, limiting
the depth of penetration.
- Alkali burns can rapidly penetrate the cornea,
causing damage to intraocular structures.

Chemical Ocular Injury : Management

Immediate copious irrigation with a minimum of
1-2 L of saline or until pH is normalized ( 7.3-7.7 )
- Instill a topical anesthetic
- Use eyelid retractor
- Double eversion of the eyelids

Chemical Ocular Injury : Management

Immediate copious irrigation with a minimum of
1-2 L of saline or until pH is normalized ( 7.3-7.7 )
- Instill a topical anesthetic
- Use eyelid retractor
- Double eversion of the eyelids
No corneal involvement
- ATB + steroid eye drop
Ophthalmologists Referral

Chemical Ocular Injury : Classification

Grade I

Grade II

Grade III

Grade IV

Chemical Ocular Injury : Management

Preservative-free artificial tears
Topical non-preserved steroid
Topical cycloplegic
Topical antibiotics
Oral analgesics
Pressure patch or bandage CL
Antiglaucoma +