OPHTHALMOLOGY LEC

Anatomy of the Eye 01

  09272345449  
4th PERIODICAL Dr. Genevieve B. Pantig-De Jesus
Monday, Novemeber 4, 2013
TP38
Isa
Viv 09179810385

OUTLINE:
I. Orbit
II. Eyeball
A. Conjunctiva
B. Sclera and episclera
C. Cornea
D. Uveal tract – iris, ciliary body, choroid
E. Lens
F. Retina
III. Extraocular muscles
IV. Ocular adnexae
A. Eyebrows
B. Eyelids
C. Orbital septum Fig 2. Sinuses as viewed in the medial wall
D. Lid retractors
E. Lacrimal complex The lamina papyracea (part of the ethmoid bone) is a very
V. Optic nerve thin bone which can easily rupture with blunt injury and it can
VI. Self-test even be eaten away with just an infection. Therefore, spread of
infection to the ethmoid sinus (air cells) is very common and
ORBIT dangerous.
• The orbit is a bony cavity which is part of the skull Orbital Apex
• It is a pear shaped (pyramidal or conical) structure with the
• The orbital apex is the entry site of all nerves and blood
optic nerve as its stem
vessels to the eye and almost all the extraocular muscles
o There is a 45˚ angle between lateral and medial
• One of the most important structures in the orbital apex is
wall
the Annulus of Zinn
o Therefore, both orbits are directed outwards
(exotropia), but since the medial muscles are
working together the orbits are straight
§ Medial muscles does not only mean
medial rectus muscle, secondary action
of lateral rectus and inferior rectus also
contribute to adduction (will be
discussed further later)
• 30mL in volume for adults
• Contains the globe, EOMs, fat, nerves and blood vessels
o The globe (eye) occupies 20% of the space,
Fig 3. Orbital apex at the right most portion
while the muscles and fat account for the rest
locating the annulus of Zinn
• Limited anteriorly by the orbital septum, which serves as
a barrier between the eyelid and the orbit Annulus of Zinn
• Also known as the annular tendon/common tendinous ring
The Orbital Walls
• A fibrous tissue surrounding the optic nerve
Consist of 7 bones: • It is the tendinous insertion of FIVE of the six extraocular
1. Frontal bone – roof and medial wall muscle EXCEPT the inferior oblique
2. Zygomatic bone – floor and lateral floor o The origin of the inferior oblique comes from the
3. Maxillary bone – floor and medial wall medial floor of the orbit
4. Sphenoid bone – roof, medial, and lateral wall
§ Greater wing – lateral wall
§ Lesser wing – roof
5. Ethmoid bone– medial wall
6. Lacrimal bone – medial wall
§ You will know if you are looking at the
right or left orbit by identifying this bone
7. Palatine bone – floor

Fig 4. Annulus of Zinn

• There are openings through or in between bones in the

orbit through which several structures pass (only three
were emphasized in class)
o Superior orbital fissure (SOF)
§ The Annulus of Zinn divides the superior
orbital fissure into extraconal and
intraconal
Fig 1. Walls of the left orbit
o Optic canal
o Inferior orbital fissure (IOF)

OPHTHA Anatomy of the Eye Page 1 of 10

 
Table 1. Structures which pass by the following fissures/canal The semilunar fold is a thickened fold of bulbar conjunctiva at
SOF SOF Optic canal IOF the inner canthus and corresponds to the nictitating
(extraconal) (intraconal) membrane of lower animals.
nd
Lacrimal nerve Superior and Optic nerve 2
inferior division branch of Functions of the Conjunctiva
Frontal nerve of CN III & IV Ophthalmic trigeminal • Protective barrier to noxious agents
artery nerve • Allows eyelids to move smoothly over the globe
Trochlear nerve Nasociliary (CN V2) • Allows eyeball to move, since the bulbar conjunctiva is just
nerve loosely adherent to the globe
Superior • Folds enlarge the secretory surface containing these
ophthalmic vein glands
*inferior ophthalmic vein from superior orbital fissure, either o Glands of Krause
extraconal or intraconal § Very small accessory lacrimal glands similar
in structure and secretions to the lacrimal
Blood Supply of the Orbit gland – aqueous secretion
A. Arterial Supply § More are located on the upper lid
• The major arterial supply is the Ophthalmic Artery which o Glands of Wolfring
is a branch of the internal carotid artery § Also accessory lacrimal glands, but fewer in
number and a lot bigger – aqueous secretion
1. Central retinal artery o Goblet cells
• Supplies the retina § Secrete mucin
2. Lacrimal artery
• Lacrimal gland and upper eyelid The lacrimal glands, glands of Krause and glands of Wolfring
3. Muscular branches to the muscles contribute to aqueous tears, while the goblet cells contribute to
4. Long posterior ciliary arteries the mucin layer of tears.
• Since they are long, supplies the anterior portion
of the eye
• Ciliary body and iris
5. Short posterior ciliary arteries
• Supplies the posterior portion of the eye
• Choroid and part of the optic nerve
6. Medial palpebral ateries
• Both upper and lower eyelids

B. Venous Drainage
• Blood drains to the superior and inferior ophthalmic veins
which communicates with the CAVERNOUS SINUS
• Blood from the skin of the periorbital region drain to the
angular vein àsupraorbital and supratrochlear vein
àbranches of the superior ophthalmic vein àcavernous
sinus
C linical Pearl: Cavernous Sinus Thrombosis
The direct communication between the ophthalmica veins and
the cavernous sinus may potentially cause a posterior and
intracranial spread of infection of an orbital abscess or
cellulitis. “be careful in pricking a pimple, especially in this
danger zone, and don’t undermine a stye”
EYEBALL
A. Conjunctiva
• The conjunctiva is a thin transparent mucous membrane
covering the globe anteriorly. It consists of 2 parts:
1. Palpebral conjunctiva – lines the posterior surface
of the eyelid
2. Bulbar conjunctiva – the conjunctiva that is reflected
onto the eyeball
• loosely attached to the orbital septum at the
fornices (junction between the palpebral
bulbar conjunctiva) and is folded many times
• thus, contact lenses will not go all the way to
the back because of the conjunctival fornix
Fig 6. Accessory glands
B. Sclera and episclera
• The sclera is the fibrous outer layer of the eye consisting
mainly of collagen
• It is dense and white and continuous with the cornea
anteriorly and the optic nerve dural sheath posteriorly
• Measurements
o at the macula – 1 mm (thickest)
o at the equator and elsewhere – 0.6 mm
o at the insertion of the recti muscles – 0.3 mm
§ any trauma such as injury to the recti
muscles can rupture sclera at this point
because it is thinnest here
• The outer layer of the anterior sclera is covered with a thin
layer of fine elastic tissue, the episclera (meaning on top
of the sclera), which contains blood vessels that nourish
the sclera
C. Cornea
• The cornea is a transparent tissue inserted to the sclera
at the limbus (corner of the sclera and cornea)
• lacks melanocytes, blood vessels and lymphatics
• Completely avascular
o The oxygen supply comes from – the tear film
§ Therefore contact lens wearers should
put lubricants so that tear film may be
distributed and thus avoid deprivation of
oxygen to the cornea
o Metabolic needs – aqueous humor, limbal
vessels and tears
o Sensory innervations – from ophthalmic division
of trigeminal nerve

C linical Pearl: Herpes Simplex Corneal Ulcer

The Herpex simplex virus (HSV) commonly affects the

trigeminal ganglion which is the main source of sensory nerve
supply to the cornea. The cornea exhibits hypoesthesia at the
ulcer site. This is one characteristic of an HSV corneal ulcer
that helps differentiate it from other types of corneal ulcer.
Fig 5. Conjunctiva

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• Measurements of the cornea
o 11.7 mm in its horizontal plane
o 10.6 mm in the vertical plane
o 0.5 mm thick
§ but peripherally thickens to 0.67 mm
§ this is important because individuals
with thicker cornea are good candidates
for LASIK. It should be at least 0.5 mm
at the very center
o radius of curvature = 7.5 mm
§ anything steeper or flatter causes
astigmatism and errors of refraction
5 layers of the cornea:
1. Corneal Epithelium (A)
2. Bowman’s membrane (B) Fig 8. Pupillary light reflex
3. Corneal Stroma (C)
• 90% of corneal thickness Being afraid, excited, in love = sympathetic activity = dilated
4. Descemet’s membrane (D) pupils
5. Endothelium (E)
• Single layer of hexagonal cells 2. Ciliary body
The ciliary body consists of 2 zones:
• Responsible for maintaining deturgescence
• Pars plicata
(state of relative dehydration) of the cornea
and failure of function leads to corneal o The ciliary process arise from this zone =
edema responsible for production of aqueous humor
o Also has the zonular fibers which suspends
• Cell loss occurs with age and injury
the lens
• Pars plana

Pathway of the Aqueous Humor

*recall that the anterior and posterior chamber is filled with
aqueous humor and this is produced by the ciliary body

• From the posterior chamber – aqueous pass through the

pupil – anterior chamber – then drains into the
trabecular meshwork – Schlemm canal – veins
• Some passes directly from ciliary body through sclera
Fig 7. Cross section of cornea (UVEOSCLERAL PATHWAY)
o Preferred pharmacologic treatment for glaucoma
Functions of the Cornea makes use of this pathway and is very effective in
• The cornea is the main refractive component of the eye reducing intraocular pressure
• 67% of the total focusing (the rest is provided by the lens)
• The three dimensional organization of small collagen fibrils
of uniform diameter and regular interfibril spacing
accounts for corneal transparency
• Corneal transparency is also dependent on the
maintenance of corneal hydration – precise water content
of 78% is needed to remain transparent.

*Transparency of the cornea due to: AVASCULARITY,

UNIFORMITY, and DETURGESCENCE

D. Uveal tract
• The uveal tract is composed of the iris, the ciliary body
and choroid. It is the middle vascular layer of the eye and
contributes to the blood supply of the retina
Fig 9. Pathway of Aqueous Humor
1. Iris
• The iris is a flat surface with a central opening, the pupil Physiology of Aqueous Humor
• Divides the anterior part of the eye containing the aqueous • The pressure created by aqueous humor enable the
humor into globe to retain its normal semiglobular shape
o Anterior chamber – anterior to the iris o During trauma, aqueous humor is used up so the
o Posterior chamber – posterior to the iris cornea will flatten a bit
• Diameter = 21 mm • The aqueous humor contains many of the nutrients
• Color of the iris is determined by the number of needed by the iris, cornea and lens
melanocytes in the anterior iris stroma and the amount of • Density slightly greater than H2O
pigment within them. Variations in the amount of pigment • Compared to plasma, it has lower protein and higher
are responsible for the different colors of the iris ascorbic acid concentration
o Brown eyes = more melanocytes than blue and • Intraocular pressure is maintained with 10-21 mmHg
green eyes by balance between the production and drainage
The Pupil o In uveitis and inflammation, will not produce
• The pupil ranges in diameter from 1-8 mm much aqueous = softer eye
• The iris regulates the amount of light that enters the o If there is a problem with drainage, such as
eye by modifying the size of the pupil blockage at the Schlemm’s canal and trabecular
meshwork = harder eye, higher pressure
Response Iris muscle Pupil size
Bright Parasympathetic Sphincter Miosis The Anterior Chamber Angle
light (CN III) papillae (small pupil) This is the angle of the anterior chamber formed by the
• Schwalbe’s line: termination of the corneal
Dark Dilator Mydriasis
Sympathetic endothelium
light papillae (large pupil)

OPHTHA Anatomy of the Eye Page 3 of 10

 
 • Trabecular meshwork: perforated sheets of collagen
and elastic tissue
• Scleral spur: inward extension of the sclera to which
the ciliary body and the iris are attached
• The lens is normally completely transparent due the
highly organized arrangement of the crystallins
Functions of the Lens and Zonules
• The primary optical function of the lens is
accommodation. This is achieved because the lens
is anchored to the ciliary body by zonules composed
of elastic microfibrils
• Accommodation – the ability of the eye to focus on
both close and near objects by changing the shape of
the lens through contraction of the ciliary muscle

Accommodative Reflex
1. For distant vision
• Absence of parasympathetic stimulation
• Ciliary muscles relax
Fig 10. Anterior chamber angle
• Zonular fibers under tension
• Lens is stretched thin
C linical Pearl: Acute angle glaucoma 2. For near vision
• Parasympathetic stimulation
A Gonioscope is needed to evaluate the anterior chamber • Ciliary muscles contract
angle because it is hidden within the sclera. This examination • Zonular fibers relax
is done to determine if there is narrow-angle glaucoma • Lens become more spherical (thicker)
• There is varying degrees of narrowing:
• If the ciliary body band (bacon-looking) is seen,
the angle is still very open, but if only the
Schwalbe’s line is seen, then there is very narrow
or acute angle glaucoma
• Note that glaucoma does not only occur when
there is narrow or closed angle anterior chamber,
open angle glaucoma can also occur such as in
cases where there is blockage of drainage or
problems in the outflow tract of the aqueous
humor causing increased intraocular pressure

3. Choroid
• The posterior portion of the uveal tract located
between the retina and the sclera
• Very vascular and brownish red in color
• Nourishes the outer portion of the retina

Fig 12. Accommodative reflex

As mentioned, as we age, the lens thicken and harden due to deposits

of lens fibers. Accommodative reflex is impaired such that even if the
ciliary muscles contract, the lens still does not become spherical for
near vision. This occurs slowly, so that by age 40, we start to need
reading glasses at a lower grade, but later the grade becomes higher.

F. Retina
Fig 11. Uveal tract and other structures of the eyeball • Lines the inner wall of the posterior 2/3 of the eye
• It is the sensory neural layer of the eyeball
• Extends anteriorly as the ora serrata
E. Lens • The outer surface of the retina is apposed to the retinal
• There is no blood supply and innervations pigment epithelrium (RPE)
o Thus it is easy to remove a cataract from the
C linical Pearl: Retinal Detachment
lens because it is not bloody and painful but
a little bit of anesthesia is needed because
the ciliary body is innervated
In some forms of inflammation, such as uveitis, fluid may leak
• Held in place by zonules connected to the pars
out of the retinal vessels and accumulate in the subretinal
plicata of the ciliary body
space separating the retina and RPE, causing exudative
• The lens, together with the cornea are the main
retinal detachment
refractive components of the eye
o In cataract, the lens become opaque, then
light can no longer pass through the lens
• Anterior to the lens is the aqueous humor, posterior to
it is the vitreous
• Consists of 65% water and 35% protein and minerals
• Metabolically active
o Throughout the day, lens fibers will
continually be produced, therefore as we age,
lens will become thicker and harder =
presbyopia
• The adult lens measures ~10 mm in diameter and
~45 mm in width
o But again, this can become thicker as we Fig 13. Retinal Detachment
age
OPHTHA Anatomy of the Eye Page 4 of 10
 
Layers of the retina
1. Internal limiting membrane
2. Nerve fiber layer
3. Ganglion layer
4. Inner plexiform layer
5. Inner nuclear layer
6. Outer plexiform layer
7. Outer nuclear layer
8. External limiting layer
9. Photoreceptor layer – contains the rods and cones
• Rods are more numerous and more sensitive
than cones. However, only cones are sensitive to
color. Fig 16. Movements of the Eye
• The cones are much more concentrated in the
fovea centralis (also known as foveola) *recall: extraocular muscles originate from the Annulus of Zinn
10. Retinal pigment epithelium (RPE) except for the inferior oblique muscle

There are 7 extraocular muscles – 6 move the eyeball and 1

elevates eyelid:

Extraocular Primary Secondary

Innervation
muscle Action Action
Elevation Adduction,
Superior rectus CN 3
intorsion
Depression Adduction,
Inferior rectus CN 3
extorsion
Lateral rectus Adduction -- CN 6
Medial rectus Abduction -- CN 3
Abduction,
Superior oblique intorsion CN 4
depression
Abduction,
Inferior oblique Extorsion CN 3
elevation
Levetor
Elevates
palpebrae CN 3
the eyelid
Fig 14. Layers of the retina superioris
*recall: LR6SO4AO3
• The retina is 0.1 mm thick at the ora serrata and 0.56 mm CN 3 – oculomotor nerve; CN 4 – trochlear nerve; CN 6 – abducens
thick at the posterior pole nerve
• In the center of the posterior retina is the macula
C linical Pearl: Abducens nerve palsy
Macula
• It is clinically seen as a 3 mm area of yellowish The abducnes nerve is responsible for contracting the lateral
pigmentation due to xanthophylls pigments rectus muscle to abduct the eye. The inability of an eye to turn
• In the center of the macula is the fovea outward results in a convergent strabismus or esotropia.
• The foveola is the most center portion of the fovea, in
which the photoreceptors are all cones, and the
thinnest part of the retina

Blood supply
• The blood supply to the extraocular muscles comes
from the branches of the ophthalmic artery.

OCULAR ADNEXAE
Fig 15. Retina

• The retina receives its blood supply from A. Eyebrows

o Choriocapillaries – supply outer 1/3 of retina • The eyebrows are folds of thickened skin covered with
o Central retinal artery – inner 2/3 of retina hair
• The fovea is supplied entirely by choriocapillaries and • Glabella is the hairless prominence in between the
is susceptible to irreparable damage when the macula is eyebrows
detached • Their main function is hypothesized to prevent sweat,
water, and other debris from falling down into the eye
socket
C linical Pearls: Retinal Hemorrhage
B. Eyelids
Retinal hemorrhage is a disorder of the eye in which bleeding • The upper and lower lids (palpebrae) are folds of skin that
occurs into retina. It can be caused by hypertension, retinal can close to protect the anterior portion of the eye
vein occlusion, or diabetes mellitus (which causes small fragile • Blinking helps spread the tear film, keeping cornea and
blood vessels to form and become easily damaged). conjunctiva wet
• The free lid margin is 25-30 mm long and 2 mm wide.
EXTRAOCULAR MUSCLES • Divided into:
1. Anterior margin
Movements of the eye along three different axes: § Eyelashes
• Transverse axis – elevation & depression § Glands of Zeis
• Vertical axis – abduction & adduction • modified SEBACEOUS glands
• A-P axis – lateral (extorsion) & medial (intorsion) rotation
OPHTHA Anatomy of the Eye Page 5 of 10
 
 • open onto hair follicles at the D. Lid retractors
base of eyelashes The lid retractors are responsible for opening the eyelids
1. Upper lid
§ Glands of Moll a. Levator palpebrae superioris
• Modified SWEAT glands b. Muller’s muscle (superior tarsal muscle)
• Open in a row near the base of 2. Lower lid
eyelashes a. Inferior rectus muscle
2. Posterior margin b. Inferior tarsal muscle
§ In close contact with the globe
§ Along its margins are the small orifices E. Lacrimal complex
of the meibomian glands (modified A. Lacrimal gland
SEBACEOUS glands) B. Accessory lacrimal glands of Krause and Wolfring
C. Canaliculi
D. Lacrimal sac
E. Nasolacrimal duct
• Drains out to the nasal cavity

Tears drain through the superior and inferior puncta à superior

and inferior canaliculi à common canaliculi à lacrimal sac à
nasolacrimal duct à nasal meatus

Fig 17. Sebaceous and sweat glands of the eyelid

3. Lacrimal punctum – passage of tears for

drainage

Fig 20. Lacrimal drainage system

Blood supply = lacrimal artery

Venous drainage = ophthalmic vein
Lymphatics = preauricular lymph node
Nerve supply
Fig 18. Lacrimal punctum 1. Sensory: Lacrimal nerve, branch of V1
2. Secretory: great superficial petrosal nerve
Layers of the eyelids 3. Sympathetic nerves
1. Skin
2. Orbicularis oculi muscle OPTIC NERVE
• Function to close the eyelids
*recall that the optic nerve, together with the ophthalmic artery,
• Innervated by the facial nerve (CN 7) enters the optic canal at the Annulus of Zinn
3. Areolar tissue
4. Tarsal plates • Optic Nerve (CN 2) – transmits visual information from
• Dense fibrous tissue layer, main support of the the retina to the brain
eyelids
• The optic disc represents the point where the ganglion
5. Palpebral conjunctiva cells exit the retina to form the optic nerve. This is also
the area where the physiologic blind spot can be
C linical Pearl: Eyelid swelling located
• There are about 1.2 million axons arising from the
ganglion cells that form the trunk of the optic nerve
The thin, loose skin and the absence of subcutaneous fat
makes the eyelid vulnerable to swelling, such as in
Fibers of the optic nerve consist of
accumulation of fluid in allergy or infection and blood in trauma
1. Visual fibers – 80%
• Synapse in the lateral geniculate body of the
thalamus and terminate in the visual cortex of the
occipital lobe
2. Pupillary fibers – 20%
• Bypass the geniculate body en route to pretectal
area

Fig 19. Stye due to infection of glands of Zeis or glands of Moll. • The ganglion cells of the retina and their axons are part
Usually caused by Staphylococcus aureus of the CNS and as such, do not regenerate if severed.
• The optic nerve sheath is continuous with the meninges
C. Orbital septum
• The orbital septum is the fascia behind the portion of the
orbicularis muscle between the orbital rim and tarsus
• Serves as a barrier between the lid and the orbit

C linical Pearl: Preseptal and Orbital Cellulitis

An infection which causes inflammation of the eyelids and

periorbital structures is termed preseptal cellulitis if the orbital
contents are not involved. Restriction of ocular motility,
abnormal papillary reaction and decreased visual acuity
suggest involvement of the cranial nerves and would mean that
the cellulitis is already orbital and would necessitate
aggressive and immediate management. Fig 21. Cross-section of the optic nerve
OPHTHA Anatomy of the Eye Page 6 of 10
 
Damage to the optic nerve typically causes permanent and 9. Axons comprising the optic nerve come from which cells in
potentially severe loss of vision, as well as an abnormal the retina?
pupillary reflex. A. Amacrine cells
B. Bipolar cells
The type of visual field loss will depend on which portions of C. Ganglion cells
the optic nerve were damaged. In general: D. Photoreceptor cells
• Damage to the optic nerve anterior to the optic
chiasm causes loss of vision in the eye on the same 10. Which muscle is an abductor?
side as the damage (homonymous hemianopsia) A. Medial rectus
• Damage in the optic chiasm causes loss of vision B. Lateral rectus
laterally in both visual fields (bitemporal C. Superior rectus
hemianopsia) D. Inferior rectus
o May occur in large pituitary adenoma
• Damage to the optic tract posterior to the chiasm END OF TRANS.
causes loss of vision in the visual field on the Answers to the self-test
contralateral side 1A 2C 3A 4D 5C 6C 7C 8E 9C 10B

Reference:
SELF-TEST
Self-Instructional Materials in Ophthalmology by Valbuena and
This self-test was made by the authors of the book reference Castillo, MDs UPPGH
for this lecture. Chapter 1
1. An anti-glaucoma drug which decreases aqueous
production acts on the epithelial cells of the
SUMMARY
A. Pars plicata
B. Choroid
C. Iris THE ORBIT
D. Pars plana • Pear-shaped, bony structure
• Deviated outwards with a 45˚ angle
2. The rectus muscle tendon that inserts on the sclera • Total Volume = 30mL
nearest the corneal limbus belongs to the o Globe (eye) = 20%
A. Superior rectus o Fat, muscle, blood v., nerves = 80%
B. Inferior rectus • Limited anteriorly by the orbital septum
C. Medial rectus
D. Lateral rectus The Orbital Walls
• 7 bones
3. Paralysis of this cranial nerve will result in inability to close • nasal bone is not part of the orbital wall
the eyelid
A. III Roof Medial Lateral Floor
B. IV Frontal bone √ √
C. V Zygomatic bone √ √
D. VII Maxillary bone √ √
Sphenoid bone* √ √ √
4. The following structures are part of the medial orbital wall, Ethmoid bone √
EXCEPT Lacrimal bone √
A. Ethmoid bone Palatine bone √
B. Lacrimal bone *greater wing of sphenoid = lateral wall; lesser wing = roof
C. Maxillary bone
D. Sphenoid bone Clinical: The lamina papyracea easily ruptures with blunt
injury and infection; allowing spread of infection to the ethmoid
5. Layer of the retina that receives its oxygen supply from the sinus (air cells).
choriocapillaries is the
A. Ganglion cell layer The Orbital Apex
B. Nerve fiber layer
• Entry site of all nerves and blood vessels to the eye and
C. Photoreceptors
almost all the extraocular muscles
D. Inner nuclear layer
• Annulus of Zinn (annular tendon/common tendinous
ring)
6. Which of the following statements regarding the cornea is
o A fibrous tissue surrounding the optic nerve
FLASE?
o Origin of 5/6 EOMs EXCEPT the inferior
A. The corneal endothelium is important in maintaining
oblique (origin at the medial floor)
corneal dehydration
• Openings through which several structures pass
B. The water content of the cornea is less than that of
the sclera o Superior orbital fissure (SOF)
§ The Annulus of Zinn divides the SOF
C. Normal central corneal thickness is 1 mm
into extraconal and intraconal
D. Corneal diameter is greater horizontally than vertically
o Optic canal
o Inferior orbital fissure (IOF)
7. Which is not a layer of the eyelid?
A. Skin
B. Conjunctiva SOF SOF Optic canal IOF
C. Tenon’s capsule (extraconal) (intraconal)
nd
D. Orbicularis muscle Lacrimal nerve Superior and Optic nerve 2
E. Tarsus inferior division branch of
Frontal nerve of CN III & IV Ophthalmic trigeminal
8. In order to ensure good vision, the following structures artery nerve
must maintain their clarity, EXCEPT Trochlear nerve Nasociliary (CN V2)
A. Conea nerve
B. Aqueous Superior
C. Lens ophthalmic vein
D. Vitreous *inferior ophthalmic vein from superior orbital fissure, either
E. Choroid extraconal or intraconal

OPHTHA Anatomy of the Eye Page 7 of 10

 
Blood Supply of the Orbit
Arterial Supply
• major arterial supply: Ophthalmic Artery (from ICA)
• Central retinal artery: retina
• Lacrimal artery: lacrimal gland and upper eyelid
• Muscular branches to the muscles
• Long posterior ciliary arteries: anterior eye (Ciliary body
and iris)
• Short posterior ciliary arteries: posterior eye (Choroid
and part of the optic nerve)
• Medial palpebral ateries: upper and lower eyelids
Venous Drainage
• All veins eventually drains to the Cavernous Sinus
• Periorbital skin drainage: angular vein
o angular vein àsupraorbital and supratrochlear
vein à branches of the superior ophthalmic vein
àcavernous sinus
• Superior and inferior ophthalmic veins -> cavernous sinus
Clinical: Cavernous Sinuses Thrombosis - intracranial spread
of infection of an orbital abscess or cellulitis.
o Bowman’s membrane
o Corneal Stroma = 90% of corneal thickness
o Descemet’s membrane
o Endothelium = maintains deturgescence (state
of relative dehydration) of the cornea
§ 78% water
§ failure = corneal edema
• Function: main refractive component (67%)
Uveal Tract
• Composed of the iris, the ciliary body and choroid
• Middle vascular layer – supply the retina
1. Iris
• Flat surface with a central opening
• Divides the anterior part of the eye containing the aqueous
humor into anterior and posterior chambers
• Color of the iris is determined by the number of
melanocytes and the amount of pigment within them.
• Pupil – central opening of he iris
o 1-8mm in diameter
o The pupil size is modified to regulate amount of
light entering the eye

THE EYEBALL
Response Iris muscle Pupil size
Bright Parasympathetic Sphincter Miosis
light (CN III) papillae (small pupil)
Dark Dilator Mydriasis
Sympathetic
light papillae (large pupil)

2. Ciliary body
• Consists of Pars plicata and Pars plana
• Pars plicata
o responsible for production of aqueous humor
o has zonular fibers w/c suspends the lens
• Aqueous Humor Pathway
o posterior chamber -> pupil -> anterior
chamber -> drains into trabecular meshwork
Conjunctiva -> schlemm canal -> veins
• A thin transparent mucous membrane covering the globe o Some Aq humor passes directly from ciliary
anteriorly. It consists of 2 parts: body through sclera (uveoscleral pathway)
3. Palpebral conjunctiva – posterior the lid • Physiology of Aqueous Humor
4. Bulbar conjunctiva – folded over eyeball o Contains many of the nutrients needed by the
• Semilunar fold – thickened at bulbar iris, cornea and lens
conjunctiva at the inner canthus o Maintains globe at a semiglobular shape
§ Intraocular pressure is maintained with
• Fornix connects palpebral to bulbar conjunctiva
10-21 mmHg by balance between the
• Functions of the Conjunctiva
production and drainage
o Protection
• The Anterior Chamber Angle – formed by
o Smooth eyelid movement
o Schwalbe’s line
o Allow eyeball movement
o Trabecular meshwork
o Tear Secretion (fr. multiple folds of bulbar c.)
o Scleral spur
§ Glands of Krause: small glands on
upper lid secreting aqsecretion
Clinical: Acute Angle Glaucoma - use gonioscope to evaluate
§ Glands of Wolfring: fewer, bigger
anterior chamber angle; if only Schwalbe’s line is visible =
than Krause
acute angle glaucoma
§ Goblet Cells: secrete mucin
3. Choroid
Sclera and Episclera
• Posterior portion of the uveal tract located between
• Sclera: dense, white, fibrous outer layer of the eye
the retina and the sclera
consisting mainly of collagen
• Very vascular and brownish red in color
o thickest at the macula (1mm)
o thinnest at recti m. insertion (0.3mm) • Nourishes the outer portion of the retina
• Episclera: thin, fine elastic tissue at the outer layer of the
anterior sclera Lens
o contains blood v. that nourish the sclera • Also a main refractive component of the eye
Cornea • No blood supply and innervations and completely
• Transparent tissue due to: avascularity, uniformity and transparent due the highly organized arrangement of
deturgenscence the crystallins
• Oxygen supply - from the tear film • Metabolically active
• Metabolic needs - from aq humor, limbal v. and tears o continually produces lens fibers and become
thicker and harder
• Sensory innervations – from ophthalmic division of
trigeminal nerve (CNV1) • Anterior to the lens is the aqueous humor, posterior to
it is the vitreous humor
o Clinical: HSV affects CN V -> corneal
hypoesthesia and ulcer • Held in place by zonular fibers
o
• 0.5 mm thick at center (min req’t for LASIK) • 1 Function of the Lens and Zonules: accommodation
• radius of curvature = 7.5 mm
• 5 layers of the cornea:
o Anterior Corneal Epithelium
OPHTHA Anatomy of the Eye Page 8 of 10
 
 Distant Vision Near Vision • Posterior margin
Parasympathetic Absent Present 1. Meibomian glands – modified sebaceous gland
Ciliary muscles Relax Contract • Lacrimal punctum – passage of tears for drainage
Zonular fibers Tense Relax • Layers of the eyelids
Lens Thin Thick 1. Skin
2. Orbicularis oculi muscle
Clinical: cataract – lens become opaque. Since no blood § Function: close lids
supply, removal is non-painful § Innervation: CN7
3. Areolar tissue
Clinical: lens thickens with age; more difficult to reshape, 4. Tarsal plates – main support of the eyelids
resulting to impaired accommodation 5. Palpebral conjunctiva

Retina Clinical: eyelids have no subcutaneous fat so vulnerable to

infection (ie. stye) and swelling
• Lines the inner wall of the posterior 2/3 of the eye
• It is the sensory neural layer of the eyeball
3. Orbital septum
• Apposed to the retinal pigment epithelium (RPE)
• Fascia behind the portion of the orbicularis muscle
• Photoreceptor layer – contains rods and cones between the orbital rim and tarsus
o Rods are more numerous and more
• Serves as a barrier between the lid and the orbit
sensitive than cones. However, only cones
are sensitive to color.
Clinical: preseptal cellulitis – infection of eyelids and periorbital
o The cones are much more concentrated in
structures; orbital cellulitis – involves orbital contents (ie.
the fovea centralis (also known as foveola)
cranial nerves)
• In the center of the posterior retina is the macula
o Seen clinically as a 3 mm area of yellowish
4. Lid retractors
pigmentation due to xanthophylls pigments
• Responsible for opening the eyes
o In the center of the macula is the fovea
• Upper lid
o The foveola photoreceptor layer contains all
o Levator palpebrae superioris
cones, and is the thinnest part of the retina
o Muller’s muscle (superior tarsal muscle)
• The retina receives its blood supply from
• Lower lid
o Choriocapillaries – supply outer 1/3 of retina
o Inferior rectus muscle
o Central retinal artery – inner 2/3 of retina
o Inferior tarsal muscle
• The fovea is supplied entirely by choriocapillaries
and is susceptible to irreparable damage when the
5. Lacrimal complex
macula is detached
• Parts:
o Lacrimal gland
EXTRAOCULAR MUSCLES
o Accessory lacrimal glands of Krause and
• Movements of the eye along three different axes:
Wolfring
o Transverse axis – elevation & depression
o Canaliculi
o Vertical axis – abduction & adduction
o Lacrimal sac
o A-P axis – lateral (extorsion) & medial
o Nasolacrimal duct – drains the nasal cavity
(intorsion) rotation
• Tears drain through the superior and inferior puncta
• There are 7 extraocular muscles – 6 move the eyeball
à superior and inferior canaliculi à common
and 1 elevates eyelid:
canaliculi à lacrimal sac à nasolacrimal duct à
• Blood supply: from the branches of the ophthalmic a.
nasal meatus
• Blood supply = lacrimal artery
Extraocular Primary Secondary Venous drainage = ophthalmic vein
Innervation •
muscle Action Action
• Lymphatics = preauricular lymph node
Elevation Adduction,
Superior rectus CN 3 • Nerve supply
intorsion
o Sensory: Lacrimal nerve, branch of V1
Depression Adduction, o Secretory: great superficial petrosal nerve
Inferior rectus CN 3
extorsion o Sympathetic nerves
Lateral rectus Adduction -- CN 6
Medial rectus Abduction -- CN 3 OPTIC NERVE (CN2)
Abduction, • Enters the optic canal at the Annulus of Zinn
Superior oblique intorsion CN 4
depression • Transmits visual info from the retina to the brain
Abduction, • The optic disc represents the point where the
Inferior oblique Extorsion CN 3
elevation ganglion cells exit the retina to form the optic nerve.
Levetor o Also the area of the physiologic blind spot
Elevates
palpebrae CN 3 • There are about 1.2 million axons arising from the
the eyelid
superioris ganglion cells that form the trunk of the optic nerve
o Visual fibers – 80%
OCULAR ADNEXAE o Pupillary fibers – 20%
• The ganglion cells of the retina and their axons are
1. Eyebrows part of the CNS and do not regenerate if severed.
• Folds of thickened skin covered with hair • The optic nerve sheath is continuous with the
• Function: prevent sweat, water, and other debris from meninges
falling down into the eye socket • Damage to the optic nerve typically causes
• Glabella is the hairless prominence in between the permanent and potentially severe loss of vision, as
eyebrows well as an abnormal pupillary reflex.
• The type of visual field loss will depend on which
2. Eyelids portions of the optic nerve were damaged. In general:
• Folds of skin that can close to protect the anterior portion • Anterior to the optic chiasm = homonymous
of the eye hemianopsia
• Blinking helps spread the tear film, keeping cornea and • In the optic chiasm = bitemporal hemianopsia
conjunctiva wet • Posterior to the chiasm = contralateral side
• Anterior margin
1. Eyelashes
2. Glands of Zeis – modified sebaceous gland
3. Glands of Moll – modified sweat gland

OPHTHA Anatomy of the Eye Page 9 of 10

 
   OPHTHALMOLOGY LEC
The Five-Step Eye Examination 02
 
4th PERIODICAL Video (Dr. Ruben Lim Bon Siong)
Monday, November 11, 2013
TP18
Maria Cornea Rigunay 09178101387
Ermalyn Dinopter

THE FIVE-STEP EYE EXAMINATION

1. Visual acuity determination
a. Distance and near visual acuity
2. Gross ocular inspection
a. Position and alignment of the globe
b. Gross examination of the eyelids and
external eye
3. Extra ocular muscle actions
4. Intraocular pressure measurement via tonometry
5. Retinal exam or fundoscopy

Basic Eye Examination Tools:  

• Distance reading chart, like the Snellen chart
• Pocket near vision chart Figure  5.  If  the  patient  is  able  to  read  only  the  second  line,  then  her  
distance  acuity  is  6/30  (20/100).  
• Occluder
• Pinhole
• If vision is not 6/6, one should check further using a
• Penlight or transilluminator
pinhole.
• Ruler
o If the vision improves by looking through the
• Schiotz tonometer pinhole, then most probably the reason for the
• Direct ophthalmoscope blurred vision is refractive or poor focusing.
• Topical mydriatic/ topical anesthetic o If the vision does not improve, suspect a non-
refractive pathology.
• If the patient has available correction, such as glasses,
ask him/her to wear it.

• Sometimes, the vision of the patient is so bad, that even

the biggest figure cannot be seen at 6 meters. If this
occurs, slowly bring the patient closer until he just sees
 
Figure  1.  Occluders the biggest letter or number of the chart.
Figure  2.  Pinhole
• Record this appropriately by adjusting the numerator.

3
60
 
For  example,  if  the  patient  can  only  see  the  big  letter  E  at  3  meters,  
then  record  this  as  the  numerator.  
The  denominator  still  stands  for  the  distance  at  which  a  normal  
person  can  see  that  line.  
   
Figure  3.  Schiotz  tonometer
• For the pinhole test, bring the patient back to 6 meters. If
the patient cannot see the biggest line, then bring the
STEP 1: VISUAL ACUITY DETERMINATION
patient closer to the chart with the pinhole on, until he
• The patient should be placed at an appropriate distance can just read the first line.
away from the Snellen chart • If the patient cannot see the biggest letter or number at
o 20 feet/6 meters one meter away, despite the use of pinhole, spectacle, or
• The chart should be recognizable and well-illuminated. any form of correction, then one should test for finger
o The biggest figure (usually the letter E), is usually at counting.
6/60 or 20/200. • Record the farthest distance that the patient can count
• One eye is tested at a time. The other eye is totally fingers correctly.
occluded while testing.
• As much as possible, test first without any corrective VA  =  CF  @  1  foot  
lenses on.
• Ask the patient to read aloud the smallest recognizable  
figures. Figure  6.  Figure  6.  Sample  documentation.  "Counting  fingers  at  1  
6 foot".  VA  -­‐  visual  acuity.

6 • If the patient cannot see your fingers at 6 inches away,

  then check for hand movement by simply moving your
The  numerator  stands  for  the  TEST  DISTANCE  (6  meters).   hand across the eye of the patient.
The  denominator  stands  for  the  distance  at  which  a  normal  
person  can  see  that  line.   VA  =  (+)  HM  
 
Figure  7.  Record  this  as  (+)  HM  -­‐  hand  movement

• It will also be helpful if you check for light projection.

  • This is done by shining the light from four different
Figure  4.  In  this  example,  if  the  patient  is  able  to  read  the  bottom   directions and asking the patient to identify where the light
line,  the  distance  acuity  of  the  tested  eye  is  6/6  or  20/20.   is coming from.
• Note down on the chart the directions where light is
perceived.

OPHTHA The Five-Step Eye Examination Page 1 of 4

 
• If the patient cannot tell where the light is coming from § Grasp the upper lid lashes with one hand, while
after trying all directions, ask the patient if he can applying a fulcrum on the upper edge of the lids
perceive light. with your upper hand.
o If yes, record as “light perception” (LP) § A blunt instrument, such as a cotton tip applicator,
o If none at all, record as “no light perception” (NLP) can be used.

Considerations for Visual Acuity Testing of Pediatric

Patients
• One should observe the alignment of the eyes, and if
there are rotatory, angular, or jerky eye movements. If
present, one should suspect poor vision on that eye.
• Normally, infants should be able to fixate and follow
light or bright-colored moving objects.  
o This is recorded as “can follow and fixate.” Figure  8.  Examination  of  the  upper  palpebral  conjunctiva.  Cotton  
• For older children, one can employ a hand game for tip  applicator  was  used  as  a  fulcrum.
finger counting technique.
o The hand game requires the child to imitate the • With the aid of a penlight, examine the cornea next.
hand position of the examiner, such as an open • This dome-shaped portion of the eye should be clear,
palm or a clenched fist. shiny, and transparent.
o This should be done until the maximum distance of • In the elderly it is normal to see a white ring located
6m or 20ft is reached. peripherally → arcus senilis
o This is recorded as “can do hand game at
maximum distance possible.”
• Proceed to check the pupils. These are normally round, at
the center, and of the same size.
• For patients 40 years old and above, you should check for
• Check the pupillary reaction to light next. Normally, the
near or reading vision.
pupil should constrict 1-2 mm from baseline when
o This is done by making the patient read a near-vision
stimulated by light.
chart at a distance of 14 inches under a well-lighted
• Swing your penlight from one eye to the other, normally,
condition.
both should constrict. When you see paradoxical
• One eye is tested at a time.
dilatation, this is not normal. Suspect a pathology in that
• If the patient has reading glasses, let him/her wear them. eye that dilates paradoxically.
• Note down the location at the side of the line of numbers
or letters corresponding to the smallest line the patient can
STEP 3: EXTRAOCULAR MUSCLE ACTIONS
read easily.
• Position yourself in front of the patient. Instruct the patient
STEP 2: GROSS OCULAR INSPECTION to look at your raised index finger and to follow the
movement of your finger without moving his/her head.
• It is important to be systematic so that you do not miss out • Version – the eyes should move synchronously and
anything important. symmetrically in the same direction.
• Always get a total view before focusing on the eye itself. • Move your finger to the configuration of the capital letter H.
• Start by looking at the position of both eyes in relation to • Normally, the eye should be able to follow smoothly up to
other structures of the face. the edges of the palpebral fissure.
o Normally, both sides should be symmetrical. The eyes
should be the same level, and should not be
protruded or sunken.
• The opening of the lids, called the palpebral fissures
should be the same height and width.
• To check for alignment, ask the patient to look at your
penlight situated at 3 feet away. If the eyes are aligned,
the corneal light reflex should fall at the center of both
pupils. If this is not so, then there might be misalignment,  
Figure  9.  Why  we  test  the  EOMs  with  the  capital  letter  H.
or squint. This is not normal.
• Proceed by checking the eyelids, both upper and lower.
STEP 4: INTRAOCULAR PRESSURE (IOP) MEASUREMENT
o Normally, the skin of the lids is smooth and thin with
no masses or discoloration. • There are basically 3 ways to determine the IOP
o In the elderly, it is normal for the skin of the lids to be 1. Digital palpation (finger palpation tonometry)
wrinkled and droopy. o A simple way of roughly gauging the eye
o The lid margins should be continuous with no pressure.
irregularities and should be well-opposed to the o Ask the patient to look downwards without
eyeball. closing the eye.
o The lashes should all be directed outward. o Then with your two index fingers on the upper lid,
• Examine the conjunctiva next. alternately, gently press down on the globe.
o There are basically three parts. o Normally, the globe should be soft and easily
§ The bulbar conjunctiva lines the globe. indentable.
§ The palpebral conjunctiva lines the lids. 2. Indentation tonometry
§ The forniceal conjunctiva, which is the part that o A more objective method to measure the IOP is
joins the bulbar and palpebral. by using the Schiotz indentation tonometer
o Pull the lower lid down and ask the patient to look up. § This instrument is relatively inexpensive and
§ The palpebral conjunctiva is normally pinkish, all you need is a topical ocular anesthetic.
moist and, smooth. § Place the patient in a supine position.
o Ask the patient to look down while you pull the upper § After instilling topical anesthetic, hold the lids
lid up. open with one hand, making sure you are
§ This will expose the upper bulbar conjunctiva, not pressing on the eye ball.
which is normally clear and transparent, with few § Place the footplate of the instrument at the
visible blood vessels. center of the cornea. Let the plunger indent
§ Examine also the underlying sclera, which should the cornea by sliding down the carriage.
be white and opaque. § The value indicated on the scale at the top of
o In order to examine the upper palpebral conjunctiva, it the instrument is recorded and converted to
is necessary to flip the upper lids. millimeters mercury (mmHg).
§ Ask the patient to look down.

OPHTHA The Five-Step Eye Examination Page 2 of 4

 
 Figure  10.  Schiotz  tonometry  

3. Applanation tonometry  
Figure  122.  Retinal  hemorrhages.
o The most accurate among the three. However,
this method needs expensive equipment, like the
• The last part of the retina you should examine is the
Goldmann applanation tonometer, and a slit lamp
macula.
biomicroscope.
o This is the most important and most sensitive part of
the retina, responsible for fine and color vision.
o The macula is located just lateral to the optic disc.
o Usually, especially in young patients, a tiny white
reflex may be elicited, emanating from the center of
the macula. This is called the foveal reflex.
o As in the rest of the retina, this area should be devoid
of bleeding, white or yellow lesions.

 
Figure  10.  Goldmann  applanation  tonometry. END OF TRANS.

Reference: UPCM-PGH video

STEP 5: RETINAL EXAMINATION OR FUNDOSCOPY
• One needs a direct ophthalmoscope to be able to visualize
the retina.
• Before starting this exam, turn down the lights of the
examination area.
• Ask the patient to look at a distant fixating point. Both of
you should be in a comfortable position. Position yourself
about 2 feet away from the patient.
• Use your right eye to examine the right eye of the patient
and vice versa.
• Shine the light of your ophthalmoscope into the eye. Look
for a bright reflection, called the Red Orange Reflex
(ROR).
o This is the light that is reflected back to you from the
inside of the eye.
o This reflex is not seen if the media is opaque, which
may be due to corneal, lens, or vitreous opacities.
• Follow the ROR by bringing your eye closer to the patient
until you’re just inches away.
o Try to look for structures in the retina, like blood
vessels.

 
Figure  111.  Diagram  of  stuff  than  can  be  seen  on  the  retina.

§ Look for the optic disc by following the vessels.

You are in the correct direction if the caliber of
the vessels get larger.
o Once you see the optic disc, assess if the borders
are distinct.
o Check for the cup-disc ratio.
§ This is the ratio of the central depression of the
disc to its total diameter.
§ Normally, the ratio is less than 0.4
o Examine the blood vessels.
§ The arteries are brighter and narrower.
§ Veins are darker and wider.
§ There should be no hemorrhages or bleeding on
the retina. These appear as red blotches. You
should not see any white or yellow lesions as well.

OPHTHA The Five-Step Eye Examination Page 3 of 4

 
 SUMMARY
Five-step eye exam:
1. Visual acuity determination
2. Gross ocular inspection
3. Extra ocular muscle actions
4. Intraocular pressure measurement via tonometry
5. Retinal exam or fundoscopy
1. VISUAL ACUITY DETERMINATION
• Snellen chart: 20 feet/6 meters
o Read aloud the smallest recognizable figures.
o The numerator stands for the TEST DISTANCE
(6 meters).
o The denominator stands for the distance at which
a normal person can see that line.
• If vision is not 6/6, one should check further using a
pinhole.
o Improves → refractive problem or poor focusing.
o Does not improve → non-refractive pathology.
• If the patient has available correction, test pt with it.
• If biggest figure cannot be seen at 6 meters, slowly bring
the patient closer until he just sees the biggest letter or
number of the chart.
• Record this appropriately by adjusting the numerator.
• Bring the patient closer to the chart with the pinhole on.
• If the patient cannot see the biggest at one meter away,
despite correction, test for finger counting.
o Record the farthest distance that the patient can
count fingers correctly. VA = CF @ 1 foot
• If the patient cannot see your fingers at 6 inches away,
then check for hand movement. VA = (+) HM
• Check for light projection. Shine the light from four
different directions and askthe patient to identify where the
light is coming from.
o Note down on the chart the directions where
light is perceived.
• If the patient cannot tell where the light is coming from
after trying all directions, ask if he can perceive light. LP
or NLP.
• 40 years old and above check for near or reading vision.
o This is done by making the patient read a near-vision
chart at a distance of 14 inches
Pediatric Patients
• Alignment of the eyes
• Rotatory, angular, or jerky eye movements → poor
vision
• Infants: Fixate and follow light or bright-colored moving
objects. “Can follow and fixate.”
• Older children: hand game for finger counting
technique. Imitate the hand position of the examiner.
“Can do hand game at maximum distance
possible.”
2. GROSS OCULAR INSPECTION
• Total view
• Position of both eyes in relation to other
o Normal: symmetrical. Same level, not be protruded or
sunken.
• Palpebral fissures same height and width.
• Alignment, look at your penlight 3 feet away. Corneal
light reflex should fall at the center of both pupils.
• Eyelids
o Normal: Skin of the lids is smooth and thin with no
masses or discoloration.
o In the elderly, wrinkled and droopy.
o Margins continuous with no irregularities, well-
opposed to the eyeball.
o Lashes outward.
• Conjunctiva
o The bulbar conjunctiva lines the globe.
o The palpebral conjunctiva lines the lids.
o The forniceal conjunctiva, joins the bulbar and
palpebral.
o Pull the lower lid down and ask the patient to look up.
§ The palpebral conjunctiva is normally pinkish,
moist and, smooth.
o Ask the patient to look down while you pull the upper
lid up.
OPHTHA The Five-Step Eye Examination
§ Upper bulbar conjunctiva, normally clear and
transparent, with few visible blood vessels.
§ Sclera, white and opaque.
o Upper palpebral conjunctiva, flip the upper lids.
• Cornea
o Normal: clear, shiny, and transparent.
o In the elderly: arcus senilis
• Pupils, normally round, at the center, and of the same
size
o Pupillary reaction to light next.
o Normally, the pupil should constrict 1-2 mm from
baseline when stimulated by light.
• Swing your penlight from one eye to the other, normally,
both should constrict. Paradoxical dilatation is not
normal.
3. EXTRAOCULAR MUSCLE ACTIONS
• Instruct the patient to look at your raised index finger and
to follow the movement of your finger without moving
his/her head.
• Normal: Able to follow smoothly up to the edges of the
palpebral fissure.
4. INTRAOCULAR PRESSURE (IOP) MEASUREMENT
• 3 ways
1. Digital palpation (finger palpation tonometry)
o Two index fingers on the upper lid,
alternately, gently press down on the globe.
o Normal: globe soft and easily indentable.
2. Indentation tonometry
o Schiotz indentation tonometer
§ Place the footplate of the instrument at the
center of the cornea. Let the plunger indent
the cornea by sliding down the carriage.
§ The value indicated on the scale at the top of
the instrument is recorded and converted to
millimeters mercury (mmHg).
3. Applanation tonometry
o The most accurate. Expensive. Goldmann
applanation tonometer.
5. RETINAL EXAMINATION OR FUNDOSCOPY
• Turn down the lights
• Patient to look at a distant fixating point.
• Look for a bright reflection, called the Red Orange Reflex
(ROR).
o NOT seen if the media is opaque.
• Follow the ROR by bringing your eye closer to the patient
o Try to look for structures in the retina
§ Look for the optic disc by following the vessels.
o Optic disc, distinct borders.
o Cup-disc ratio.
§ Ratio of the central depression of the disc to its
total diameter.
§ Normal: less than 0.4
o Blood vessels.
§ Arteries are brighter and narrower.
§ Veins are darker and wider.
§ There should be no red (hemorrhages or
bleeding), white or yellow lesions.
• Macula.
o Most important and most sensitive part of the retina
o Fine and color vision.
o Lateral to the optic disc.
o Tiny white reflex may be elicited, emanating from the
center of the macula → foveal reflex
o Should be devoid of bleeding, white or yellow lesions.
End of summary. J
Page 4 of 4
 OPHTHALMOLOGY LEC
The Eye as an Optical Instrument 02
Dr. Jay Marianito S. Vicencio feat. Dr. Mark Agas  Macula Cornea Retinay 09178101387
4th PERIODICAL Thursday, November 14, 2013
TP18
Ermmatrope Dinopters
OUTLINE:
I. Optics
II. Geometric Optics
A. Basic Principles
B. The Eye is an Optical Instrument
1. Ocular Light Transmitting Media
a. Refraction Figure 1. From a source, light always moves in a divergent
b. Errors of Refraction manner. However, once this light has travelled a distance of 6 m
c. Refractive Surgery or 20 ft (distance of infinity), light rays begin to move in a parallel
i. Corneal Refractive Surgery direction.
 PRK
 LASIK
ii. Lens-based Refractive Surgery
 Phakic IOL
 Pseudophakic IOL
 Refractive lens exchange
Dear 2016,
 These are audio bullets Figure 2. Light rays passing through a prism are bent towards the
Housed in these fancy dotted boxes are short review stuff to enhance base.
your reading pleasure. 
xo, m+m

OPTICS
 Defined as the “science of vision”
 Four types:
o Physical optics
 Physical properties of light
o Geometric optics Figure 3. Two prisms with their bases placed together, bend light
 Focusing of light/images onto the retina to converge at a point. This is the principle of convex lenses. The
 Basically “the eye as an optical instrument” magnifying glass is an example.
reflects on geometric optics, hence this lecture
focuses on this mainly.
o Physiologic optics
 Processes occurring in the retina producing
visual energy or stimuli
 When an image is focused on to the retina, the
retina, as a neurosensory organ, will produce
visual energy and then transmit it. This would go
on to the next phase, which is neuro-
ophthalmologic optics
o Psychologic or neuro-ophthalmologic optics
 Conduction of visual energy/stimulus to the Figure 4.Two prisms with their apices (apex) placed together,
occipital visual center bend light rays to diverge. This is the principle of concave
 Vision is integrated in the occipital visual center. lenses, used by most people for correction of myopia (more on
The eyeball does NOT integrate vision. this later).
 For our intended purposes, we will be discussing the first two for
this lecture.  In myopic patients, you want to make the distance a little
clearer; concave lenses are used to diverge the focus.

GEOMETRIC OPTICS
VERGENCE
 The process occurring between physical optics and
 A measure of either diverging or converging light rays
physiologic optics
 Expressed in diopters
 Starts from the moment light strikes the eye, until it hits the
retina
Light diverging Vergence is Concave lenses
 Its principal basis is the transmission and bending of the from a point negative (-)
direction of travel of light rays  REFRACTION
Light converging Vergence is Convex lenses
to a point positive (+)

BASIC PRINCIPLES
THE EYE IS AN OPTICAL INSTRUMENT
 Light, from a point source, moves in a divergent  Composed of
manner
 From a source, such as a candle or flashlight, light
Ocular light
spreads Neurosensory Visual
transmitting Optic nerve
retina cortex
 Distance of infinity is 6 meters or 20 feet media
 This is also the distance we use when we check
the visual acuity
 Light could be reflected (by mirrors), absorbed (by
opaque objects), or refracted (bent)
 Light passes through a prism and is bent towards the
base

OPHTHA The Eye as an Optical Instrument Page 1 of 7

 OCULAR LIGHT TRANSMITTING MEDIA
 Composed of the transparent structures of the eye
 Outwards going in:

Vitreous
Aqueous gel
Cornea Lens • In the
humor
vitreous
cavity

 The aqueous humor is the space

between the cornea and the lens
 The vitreous gel becomes more
liquid as people get older Figure 6. The eye is basically like a simple zoom lens camera
system. The retina is the film, the cornea and the lens are the
 These structures are transparent, which allow them to zoom lens.
transmit light
o Permit the eventual transit of light rays on the retinal
surface
 Red-Orange Reflex (ROR) is seen when the ocular media
is clear.
 If there is no ROR, something is wrong in any part of
the ocular light transmitting media  that defective
part may NOT be as transparent as it should be.
 ROR has basically the same principle as the “red eye” or
red reflex you see when you take a picture of a person in a
darkened room.
 In the dark, the pupils dilate, allowing the camera
flash (light) to be the stimulus to elicit this reflex.
 This is proof that the ocular light transmitting media is Figure 7. REFRACTION. What we want is to focus the light on to
transparent and effectively transmitting light rays. the retina.

Mini anatomy review: The first part is the cornea, which is
dome-shaped. Next is space filled with the aqueous
humor, located between the iris and the lens. The natural
crystalline lens is suspended by ciliary zonules. The
vitreous cavity, filled with the vitreous gel, and then
posterior to that is the retina. The retina is a semi-
transparent membrane. Behind that is a plexus of blood
vessels called the choroid. It is the choroid that emits this
red-orange hue of ROR.
Figure 5. Right eye: seeing a red-orange reflex with a clear and
transparent ocular light transmitting media. L eye is abnormal.
REFRACTION
 The transmission and bending of the direction of travel of
light rays until it is focused on to the retina.
 Two main structures responsible for refraction: the cornea
and the lens
•Accounts for 2/3 of the total refraction
Cornea
•STATIC/FIXED type of refraction
•Responsible for the remaining 1/3
•DYNAMIC type of refraction
Lens
•May change its shape via ciliary muscle
contraction and zonular tension
ACCOMMODATION
 Ability of the lens to re-focus divergent rays of light on the
retina
 Dynamic type of refraction
 As the ciliary muscles contract, zonules relax
o Results in an increase in the AP diameter of the lens
 Lens “bulges”/becomes more globular in
shape/its surface becomes more convex 
increased refractive power (can converge light
rays better)
o Refocus on objects closer to the eye (such as in
reading books)
 Accompanied by constriction of the pupil (miosis) and
convergence of both eyes
 With increasing age and progressive sclerosis of the lens
(stiffening of the lens fibers), accommodation weakens
and diminishes
 Even when the ciliary muscles contract and the
zonules relax, the lens barely changes its shape
 Significant/most noticed in emmetropes in their 40s
 Emmetropes are those who do NOT have significant
errors of refraction
 This phenomenon leads to an error of refraction called
PRESBYOPIA
 Progressive loss or weakening of accommodation,
such that the near-vision tasks suffer.
 Patients may experience associated headaches
and sleepiness
 Since accommodation is weakening, treatment is applied
to help the convergence compensate for this. Presbyopia
therefore is treated with additional plus (+) or convex
lenses, called reading glasses
ERRORS OF REFRACTION: Remember!
1) PRESBYOPIA
2) MYOPIA or “near-sightedness”
 Most common
 Problem: Objects at a distance are NOT very
clear/sharp.
 The patient may either have:
o A long eyeball (front-to-back); or
o Steeply-curved corneas

OPHTHA The Eye as an Optical Instrument Page 2 of 7

  More convex lens, refracts and converges
light rays BETTER
 Focus of light is anterior to the retina
 Goal: Move the focus backwards toward the retina
 How to achieve this: Diverge the light rays
 Myopia correction: Biconcave or minus (-) lenses

Figure 10. With astigmatism, one can read but the image is not as
sharp. This affects distance and near-vision.

Figure 8. Myopia and correction with a biconcave (minus) lens.

3) HYPEROPIA or “far-sightedness”
 Problem: Reading up-close (Distance is NOT a
problem)
 Patient has either a short eyeball or flatly-curved
corneas
 More concave lens, refracts and converges
light rays POORER
 Focus of light is posterior to the retina
 Goal: Move the focus forward, toward the retina
 How to achieve this: Converge the light rays
 Hyperopia correction: Biconvex or convergent or plus
(+) lenses

Figure 11. Top: Astigmatism. Different axes are focused before

and after the retina. Bottom: Corrected with cylindrical or toric
lenses.

REFRACTIVE SURGERY
Can be done on either of the two refracting parts of the eye:
A. Corneal Refractive Surgery
B. Lens-based Refractive Surgery

CORNEAL REFRACTIVE SURGERY

 More popular than Lens Refractive Surgery
Figure 9.Hyperopia and correction with a biconvex (plus) lens
 An excimer laser is used
o Instrument that produces a concentrated beam of
ultraviolet (UV) light delivered in pulses
4) ASTIGMATISM
o Each pulse removes or ablates a small amount of
 Presence of a disparity in corneal curvature
corneal tissue
between the different axes
 Cornea is not a perfect dome but rather an oblong
Let’s review the layers of the cornea:
structure
 Results to image distortion, regardless of
distance from the observer
 Takes greater effort to read
 Corrected with cylindrical or toric lenses
 These are neither lenses convex or concave

 The cornea is rich with pain nerve endings.

 Corneal epithelium is one of the fastest healing
epithelia of the body.
 Stroma contains uniformly-arranged collagen
fibrils.

OPHTHA The Eye as an Optical Instrument Page 3 of 7

 Corneal refractive surgery can be done by Preparation
A. Surface ablation  Photorefractive keratectomy • Retraction is applied to separate the lids
(PRK) • Suction microkeratome
 In the late 90’s, this was the most common type • Suction pressure is applied to the eye to stabilize it.
of corneal refractive surgery • Fixation of target is done with a targeting laser.
• Lubrication with balanced salt solution
 Procedure:
Removal of corneal epithelium
•By blunt spatula or chemical like
absolute alcohol for 1 minute

Creation of an anterior corneal flap

• By an automated microkeratome (a vibrating blade)
• The flap is around 120-140 microns thick
Laser ablation • Flap is not removed completely, attached with a hinge.
•Higher grade, more ablated tissues

Epithelium heals over the area Lifting the flap exposes the corneal stroma,
•From periphery towards the center which is then subjected to laser ablation

Flap is placed back in position

• Debris are washed away prior
• Corneal flap sticks to the cornea to heal

Figure 12. Photorefractive keratectomy (PRK)

B. Stromal ablation after creation of a corneal flap 

Laser in situ keratomileusis (LASIK)
 Currently the more popular procedure (as
compared to PRK)
 After the procedure,
 There are limitations to activities, because
you don’t want that flap to move. Figure 13. LASIK eye surgery, in not-as-gory-as-the-video
 No swimming for about a month diagrams. :)
 No contact sports
 A protective glass is also worn.
 Basically a “two-stage” procedure done under  Another way to do the LASIK is via a bladeless procedure.
topical anesthesia: In lieu of a blade (the automated microkeratome) another
 A flap is made to expose the stroma first. laser is used.
 Stromal ablation by the excimer laser.  So there are two lasers in total for the bladeless LASIK:
 Procedure:  The excimer laser for ablation.
 The femtosecond laser, which is like a very precise
surgical scalpel. It cuts a thinner amount of tissue,
and is therefore safer.

OPHTHA The Eye as an Optical Instrument Page 4 of 7

Comparing PRK and LASIK… B. Pseudophakic intra-ocular lens
PRK LASIK o Removal of the crystalline lens with the replacement
Main Removes the surface Ablates the stroma. of an intra-ocular lens with a certain power to effect
Difference epithelium. Ablates Exposed cornea is the refractive change (pseudophakic)
the Bowman’s layer only that o The artificial lens does NOT accommodate.
and the anterior circumferential line in
portion of the the periphery of the
stroma. cut. C. Refractive Lens Exchange
Since we remove the o Natural crystalline lens is removed.
epithelium, it takes a o Peripheral and posterior capsule are retained.
while to grow back o The anterior capsule is opened so that cortical and
and cover the area nuclear material can be removed and an IOL lens
that was treated. (pseudophakic lens) is inserted after.
o The new IOL provides static refraction and does not
Post- Pain (mahapdi) when Foreign body perform as well as the natural crystalline lens.
procedure blinking, for up to 5 sensation for 6-8 o Again, this artificial lens does NOT accommodate.
sensation days hours after. After o Procedure:
which the epithelium
has healed already,
and pts feel much
better.
Visual Slower; Blurred vision Faster; The next day,
healing for 5 days to 2 weeks. patients see better
Once the epithelium (some 20/20) already.
starts to move to the
center, the surface is
NOT uniform.
Haze - Increased chance of Less chance
Cornea not developing haze,
very since we traverse
transparent
Bowman’s layer and
our country is on the
equatorial belt
(increased UV light
exposure).
 Corneal refractive surgery is limited when correcting
higher errors of refraction. Ablation of too much tissue
Figure 14. Refractive Lens Exchange.
thins the cornea significantly, which weakens it
(remember higher grade, more tissue ablated in
myopic procedures).
 A test is done to determine one’s eligibility to undergo Pupil is dilated
corneal refractive surgery.
 Grades of minus 700 or below are usually
successfully treated.
 Those with higher grades or with concomitant
astigmatism are tested thoroughly first.
Incision is done on the cornea

LENS-BASED REFRACTIVE SURGERY

 When corneal refractive surgery is not amenable, lens-
based refractive surgery is done. Peel off the central anterior
 Capable of correcting higher errors of refraction portion of the lens capsule
 More invasive procedures •This exposes the cortex and the
capsule
Let’s first review the parts of the lens:
An aspirating device that utilizes
ultrasound energy is used.
•Same as in cataract surgery.

Lens with a specific grade is

A. Insertion of a phakic intra-ocular (IOL) lens
o Greek word “phakos” meaning lens
 A new lens is inserted but the native lens is NOT
removed
o Placed in the anterior or posterior chamber in front of
the natural crystalline lens
The iris delineates the anterior chamber from
the posterior chamber. The natural crystalline
lens is at the posterior chamber.
o Accommodation is preserved.
 This is an advantage of NOT touching the native
lens.
implanted inside, that will
reflect the refractive outcome
needed.
LECTURE SUMMARY
The eye is an advanced optical instrument
 An integral part of which is the ocular light transmitting
media
 The cornea and the lens are responsible for focusing
divergent light rays on to the retina for perception of a
clear image
 Errors of refraction occur when there is an inability to
focus on the retina
 Prescription spectacles, contact lenses and refractive
surgery aid in correcting error of refraction

END OF TRANS. 
OPHTHA The Eye as an Optical Instrument Page 5 of 7
 SUMMARY Correction Diverge the light rays!!
 OPTICS - “science of vision” Biconcave or minus (-) lenses
Physical optics Physical properties of light HYPEROPIA
Geometric optics Focusing of light/images onto the Problem Near vision
retina Pathophysiology Short eyeball or flatly-curved corneas
Physiologic optics Processes occurring in the retina Focus of light Posterior to the retina
producing visual energy Correction Converge the light rays!!
Psychologic or neuro- Conduction to the occipital visual Biconvex or convergent or plus (+)
ophthalmologic optics center lenses
ASTIGMATISM
Problem Image distortion, regardless of
GEOMETRIC OPTICS
distance
 Starts when light strikes the eye, until it hits the retina Pathophysiology Disparity in corneal curvature between
 Its principal basis is the transmission and bending of the the different axes. Oblong cornea.
direction of travel of light rays  REFRACTION Focus of light Irregular
Correction Cylindrical or toric lenses
Basic principles:
 Light moves in a divergent manner REFRACTIVE SURGERY
 Distance of infinity: 6 meters or 20 feet
CORNEAL REFRACTIVE SURGERY
o Once distance of infinity is reached, move in a
parallel direction.  More popular
 Light could be reflected, absorbed or refracted  Excimer laser is used
 Light passes through a prism and is bent towards the o Pulses ablates corneal tissue
base A. Surface ablation  Photorefractive keratectomy (PRK)
Removal of
VERGENCE Epithelium heals
corneal Laser ablation
over the area
 A measure of either diverging or converging light rays epithelium

Prisms Bend light to Principle of Vergence

Bases Converge at Convex Vergence is B. Stromal ablation  Laser in situ keratomileusis (LASIK)
together a point lenses positive (+)
Apices Diverge Concave Vergence is
together lenses negative (-) Preparation

Ocular light
Neurosensory Visual
transmitting
media
retina
Optic nerve
cortex Creation of an anterior corneal flap
• Automated microkeratome, or femtosecond
laser for bladeless LASIK
OCULAR LIGHT TRANSMITTING MEDIA • Flap is not removed completely, attached
 transparent structures of the eye with a hinge.
Aqueous Vitreous
Cornea Lens
humor gel
Lifting the flap exposes the
 Red-Orange Reflex (ROR) - proof that the ocular light corneal stroma: laser ablation
transmitting media is transparent
 Choroid – emits this red orange hue

REFRACTION Flap is placed back in position

Cornea •STATIC/FIXED type of refraction

Lens •DYNAMIC type of refraction PRK LASIK
Main Removes the surface Ablates the stroma
Difference epithelium. only.
ACCOMMODATION
 Ability of the lens to re-focus divergent rays of light on the Ablates the
retina Bowman’s layer and
 Dynamic type of refraction the anterior portion
of the stroma.
 Ciliary muscles contract, zonules relax = increase in
Post- Pain for up to 5 days Foreign body
the AP diameter of the lens
procedure sensation for 6-8
o Lens “bulges”  increased refractive power sensation
(converge light rays better) hours after
Visual Slower; Blurred vision Faster
o Refocus on objects closer to the eye (such as in
healing for 5 days to 2 weeks.
reading books)
Haze - Increased chance of Less chance
 Accompanied by constriction of the pupil (miosis) and
Cornea not developing
convergence of both eyes very
transparent
ERRORS OF REFRACTION  A test is done to determine one’s eligibility to undergo
PRESBYOPIA corneal refractive surgery.
Problem Near-vision tasks  Grades of minus 700 or below are usually successfully
Pathophysiology Aging and progressive lens sclerosis treated.
→ accommodation weakens
Correction Plus or convex lenses (reading LENS-BASED REFRACTIVE SURGERY
glasses)
 When corneal refractive surgery is not amenable
MYOPIA
 Capable of correcting higher errors of refraction
Problem Distance vision
Pathophysiology Long eyeball/steeply-curved corneas 1. Insertion of a phakic intra-ocular (IOL) lens
Focus of light Anterior to the retina

OPHTHA The Eye as an Optical Instrument Page 6 of 7

 o Placed in the anterior or posterior chamber in front of
the natural crystalline lens
o Accommodation is preserved.

2. Pseudophakic intra-ocular lens

o Removal of the crystalline lens with the replacement
of an intra-ocular lens with a certain power to effect
the refractive change (pseudophakic)
o The artificial lens does NOT accommodate.

3. Refractive Lens Exchange

o The new IOL provides static refraction and does not
perform as well as the natural crystalline lens.
o Artificial lens does NOT accommodate.

Pupil is dilated

Incision is done on the cornea

Peel off the central anterior portion of

the lens capsule
•This exposes the cortex and the
capsule

An aspirating device which uses

ultrasound energy is applied

Lens with a specific grade is

implanted inside.

End of Summary. 

Why people need glasses:

However…


OPHTHA The Eye as an Optical Instrument Page 7 of 7
 OPHTHALMOLOGY LEC
Ocular Pharmacology and Therapeutics 04
Jay MS Vicencio, MD Josh
4th PERIODICAL Monday, November 25, 2013
TP34
Mae

OUTLINE: 4. Avoid having dispenser tip touch any ocular tissue

I. Routes of Administration o Make sure there is a distance (≈1 inch)
II. Guidelines for Topical Ocular Therapeutics between the tissue and the dispenser to
III. Topical Ocular Diagnostic Drugs avoid contamination of the solution.
IV. Topical Ocular Therapeutic Drugs 5. For maximum ocular absorption and minimum
systemic side effects:
Italic text: audio a. Eye closure for about 2 minutes
ROUTES OF ADMINISTRATION b. Punctal occlusion (see below)

LOCAL ADDITIONAL NOTES

 Topical
o Most common
o Targets: conjunctiva and cornea.
o Some medications can penetrate the cornea and may
also target the anterior chamber.
 Subconjunctival
o Next most common
o Target: Anterior chamber (absorbed by conjunctival
vessels)
 Intra-cameral
o Enter the corneal tissue and directly inject the
medication
o Targets: tissue around the anterior chamber, iris,
lens, cilliary body, and other structures found in this
chamber.
 Intra-vitreal
o Access the vitreous humor though the Pars plana
o Use a needle to pass thru the sclera
o Target: more direct acting medications for the retina
(remember retina begins where ciliary body ends)
 Retrobulbar
o Behind the globe
o Entails sticking a needle through the conjunctival
fornix and delivering the meds behind the eyeball
o Target: usually for anesthetics to paralyze EOM or
provide anesthesia.
SYSTEMIC
 Oral
 Intravenous
 Intramuscular or Subcutaneous (rarely used in Optha)
GUIDELINES FOR USE OF TOPICAL OCULAR
THERAPEUTICS
Note: This part was emphasized to be very important by the
lecturer. Please learn the proper techniques of application. =)
OBJECTIVES:
 To learn proper technique of applying drugs to conjunctival
sac
 To know the ocular effects and complications of common
topical ocular drugs
 To know systemic side effects of ophthalmic medication
STEPS IN INSTILLATION OF TOPICAL MEDICATION
1. Proper sanitation and disinfection of the hands
o Wash or use a hand sanitizer. This will also
prevent contamination of the bottle tip in case of
contact.
2. Look up with the chin up
o (To avoid hitting the lids or the eyelashes)
o For geriatric patients, ask them to lie down
3. Expose palpebral conjunctiva by gently pulling
downward on the lower lid and instill in conjunctival
fornix
o Increases the exposure of the target area in the
lower conjunctiva (least stinging sensation)
o Avoid dropping medications directly on the
cornea, may cause stinging.
o Do not open both lids, this may trigger blinking
reflex.
OPHTHA Topic Title
 For multiple medications: apply 5 minutes apart
o Not giving a gap between medications may wash away
the first medication. Allow adequate time for absorption.
 Just put one drop unless otherwise indicated
o One drop has more than enough active ingredient to
affect action. Putting a second drop is just a waste.
 For suspensions: shake the bottle before use.
PUNCTAL OCCLUSION
 Apply pressure on the nasal part of the lower and upper lids
where the lacrimal punctum of drainage is located.
 Avoid repetitive blinking to “spread the medication”. Blinking
creates a vacuum that sucks in fluid and debris. Blinking
only facilitates drainage.
TOPICAL OCULAR DIAGNOSTIC DRUGS
FLUORESCEIN DYE
o Orange yellow dye
o Fluoresces to a brilliant green under cobalt blue light
o Used to detect epithelial defects (i.e. Corneal abrasions)
o Aid in applanation tonometry (Helps us see well the
measurements of the tonometer)
o Other dyes: Lissamine green and Rose Bengal
o Vital dyes
o Clings to devitalized cells and aids in diagnosis
o Conditions such as bell’s palsy and lag ophthalmos expose
the cornea and cause the corneal epithelium to dry up.
When we blink, devitalized tissue sloughs off and the
bowman layer is exposed, causing pain. This dye can be
helpful in the diagnosis of exposure kerathopathy.
TOPICAL ANESTHETICS
 Proparacaine HCl 0.5%, Tetracaine 0.5%
 Onset of action: within 10-15 seconds “almost instantaneous”
 Duration of action: 10 to 15 minutes
 Common uses:
o Corneal manipulation (i.e. Removal of foreign body)
o Tonometry
o Examination of damaged cornea and conjunctiva
 Usual side effects: local or systemic allergy (rare)
 They are NEVER prescribed for repeated use:
o Toxic to corneal epithelium by inhibiting mitosis and
cellular migration (cause ulceration!)
 Other notes:
o The patient will feel numb, “parang makapal”.
o Tell the patient not to rub their eyes because this will
cause abrasions.
o Urgency to blink lessens (normal is every 6 seconds),
so ask the patient to blink voluntarily for the next 10-
15 minutes until the numbness wears off.
o Never used for maintenance. Bacterial
superinfection may occur with ulceration.
Page 1 of 3
DILATING MEDICATIONS
 Drugs used to dilate the pupil (mydriasis)
 Common uses:
o to facilitate ophthalmoscopy
o to widen accessibility of lens prior to cataract surgery
o to break posterior synechiae
o to relieve pain caused by ciliary spasm
 During cataract surgery, the pupil aperture has to be as
wide as possible to access the lens
 When you have inflammation in the iris, posterior
synechiae (adhesions between iris and lens) may result.
This prevents dilation of the pupils. Putting dilating
medications can dilate the pupils and break the adhesions.
 Painful ciliary spasm can occur during inflammatory
conditions of the eyes. Dilating medications can also
paralyze ciliary muscles (cycloplegia). Cycloplegic mydriatic
eye drops can help relieve ciliary spasm.
A. Cholinergic Blocking Drugs (Parasympatholytic)
 Cause pupil dilation by paralyzing the iris sphincter muscle
 Also paralyzes other ciliary body muscles, paralyzes
accommodation (cycloplegics)
 Tell the patient to anticipate sudden brightness and inability
to read temporarily
 Examples:
o Tropicamide – short half-life. Weak cycloplegic and
mydriatic.
o Cyclopentolate
o Atropine – long half-life. Powerful cycloplegic.
B. Adrenergic-Stimulating Drugs (Sympathomimetic)
 Stimulating the pupillary dilator muscle
 Has no effect on accommodation (pure mydriatic)
 If absorbed systemically, goes to nasal cavity, may cause
vasoconstriction (increases BP)
 Examples:
o Phenylephrine
o Epinephrine (not used often due to systemic effects)
TOPICAL OCULAR THERAPEUTIC DRUGS
DECONGESTANTS
 Most popular topical ocular drugs
 Weak adrenergic-stimulating agents
 Action: temporary relief of conjunctival hyperemia through
vasoconstriction
 Effect: relieves redness due to minor eye irritation
 Examples:
o Naphazoline hydrochloride (Naphcon-A)
o Tetrahydrozaline hydrochloride (Eye-Mo, Visine)
 Most common complication: rebound redness (vasodilation)
due to overuse
ANTI-ALLERGY AGENTS
A. Antihistamines
 Antazoline and Pheniramine - often used in combination with
Naphazoline as over the counter remedies
 Fast onset of action.
B. Mast-cell stabilizers
 Olopatidine, Ketotifen and Lodoxamide
 Prevent release of inflammatory mediators
 Administered chronically for prevention of allergic symptoms
 Delayed onset of action (1-2 weeks). For habitual symptoms.
C. Non-steroidal anti-inflammatory agents – for mild
conditions
D. Corticosteroids – for more severe conditions
 Additional notes on anti-allergy agents:
o Nasal steroids can relieve eye allergies, but
topical drugs are preferrable
o Allergic sneezes occur in rapid succession
OPHTHA Topic Title
ANTI-INFLAMMATORY AGENTS
A. Corticosteroids
 Prednisolone, Dexamethasone, Fluoromethalone
 Used in a variety of ocular conditions
 May also be used for allergies, suppression of inflammatory
rections, and in post-operative conditions.
 Serious Complications:
o Keratitis - may aggravate viral and fungal corneal
infections
o Increased intra-ocular pressure (secondary glaucoma)
o Cataract formation
B. Nonsteroidal anti-inflammatory agents
 Ex. Diclofenac, Ketorolac, Nepafenac
 Given to reduce chances of serious complications
associated with prolonged steroid use
 Not potent enough to control significant intra-ocular
inflammation. Used if we want to avoid complications of
steroid use. If the patient already has initial cataract, give
NSAIDS instead of steroids.
 Common uses: itchiness, macular edema, prevention of
miosis in cataract surgery
ANTIBIOTICS
 Used for bacterial infections of the conjunctiva and cornea
 Prophylaxis for infections
 Choice of agent is based on the suspected infecting
organism
 Preparations: drops or ointments
 Drops are eliminated faster from the eyes, and will
therefore have a shorter duration of action. Ointments stay
in the eyes longer but can cause temporary blurring of
vision. You will need to apply drops more often than
ointments. Ointments are therefore recommended for
children for better compliance.
 Common examples: fluoroquinolones, sulfas,
aminoglycosides
ANTI-GLAUCOMA AGENTS
 Consider glaucoma when there is increase IOP, optic nerve
looks damaged, and there is diminution of field of vision.
 In glaucoma, there is a problem in the outflow and there is
continuous production of aqueous humor. The pressure
increases and can damage the optic nerve head. Visual
fields eventually become constricted, starting from the
periphery to the central field.
 Normal pressure is 10-20 mmHg
A. Beta Adrenergic Blockers
 Decreases aqueous production by the ciliary body
 Ex. Timolol, betaxolol
 Systemic side effects: (don’t give to px with heart disease)
o Bronchospasm
o Bradycardia
o Hypotension
B. Cholinergic Agents
 Increases aqueous outflow through the trabecular
meshwork
 Ex. Pilocarpine
 Local side effects:
o Diminished vision - due to pupillary constriction
o Headache - from ciliary spasm
C. Prostaglandin Analog
 Increases aqueous outflow through the uveoscleral
pathway
 Ex. Latanoprost, travaprost, bimatoprost
 Local side effects:
o Darkened iris color
o Lengthening and thickening of the eyelashes
D. Carbonic Anhydrase Inhibitors
 Decreases aqueous production
 Oral agents: acetazolamide, dichlorphenamide
o For short term use only
o On a chronic basis: can cause paresthesias, potassium
depletion - weakness, formation of renal calculi
 Topical agent: dorzolamide, brinzolamide
Page 2 of 3
E. Alpha-2 Adrenergic Agonists STEPS IN INSTILLATION OF TOPICAL MEDICATION
 Dual mechanism 1. Proper sanitation and disinfection of the hands
 Decrease aqueous production 2. Look up with the chin up
 Increases aqueous outflow through the uveoscleral 3. Expose palpebral conjunctiva by gently pulling downward
pathway on the lower lid and instill in conjunctival fornix
 Ex. Brimonidine, apraclonidine 4. Avoid having dispenser tip touch any ocular tissue (Make
sure there is a distance ≈1 inch)
5. For maximum ocular absorption and minimum systemic
side effects:
a. Eye closure for about 2 minutes
b. Punctal occlusion

 For multiple medications: apply 5 minutes apart

 Just put one drop unless otherwise indicated
 For suspensions: shake the bottle before use.

END OF TRANS.

Reference:
Lecture, Powerpoint

“God is our refuge and strength,

an ever-present help in trouble.
Therefore we will not fear, though the earth give way
and the mountains fall into the heart of the sea,
though its waters roar and foam
and the mountains quake with their surging.”
Psalm 46:1-3

Happy Studying!

Drugs Summary

Class Examples Notes

Fluorescein dye Epithelial defects
Topical Proparacaine Not for prolonged
Anesthetics Tetracaine use
Cholinergic Tropicamide Parasympatholytic
blocking drugs Cyclopentolate cycloplegic and
Atropine mydriatic
Adrenergic- Phenylephrine Symphathomimetic
stimulating drugs Epinephrine mydriatic
Decongestants Nephazoline Most popular
Tetrahydrozaline topical ocular drug
Antihistamines Antazoline Fast onset of
Pheniramine action
Mast-Cell Olopatidine Delayed onset of
Stabilizer Ketotifen action
Lodoxamide
Corticosteroids Prednisolone May cause
Dexamethasone cataract
Fluoromethalone
NSAID Diclofenac Less complications
Ketorolac than steroids
Nepafenac
Beta Adrenergic Timolol Decrease aqueous
Blockers Betaxolol production
Cholinergic Agent Pilocarphine Increase aqueous
outflow
Prostaglandin Latanoprost Increase aqueous
Analog Travaprost outflow
Bimatoprost
Carbonic Acetazolamide Decrease aqueous
Anhydrase Dichlorphenamide production
Inhibitors Dorzolamide
Brinzolamide
Alpha-2 Brimonidine Decrease aqueous
Adrenergic Apraclonidine production
Agonists Increase aqueous
outflow
OPHTHA Topic Title Page 3 of 3
 OPHTHALMOLOGY LEC
Anterior Segment Problems of the Eye 01
Dr. Joseph Anthony Tumbocon Nat - 09175627475
5th PERIODICAL Monday, December 09, 2013
TP
Jake - 09276995215

OUTLINE: Nerve Supply of the Lacrimal Glands

I. Dry Eye/Dysfunctional Tear Syndrome
II. Corneal Abnormalities Trigeminal (CN V) sensory afferent fibers from
the ocular surface receive stimulus
a. Infectious Keratitis
b. Trauma
c. Dystrophies
d. Non-inflammatory Ectatic Disorders Superior salivary nucleus in the pons
III. Cataract
IV. Glaucoma

References:
Efferent fibers to the pterygopalatine ganglion
 Doc Tumbocon’s powerpoint slides
 Vaughan and Asbury’s General Ophthalmology 17e
 Valbuena, Self-Instructions in Ophthalmology
Lacrimal gland, nasopharynx and orbital vessels
Dry Eye/Dysfunctional Tear Syndrome
Tear Film
 Blink reflex:
 Made up of lipid, aqueous and mucus layer o Afferent: CN V
 A moist and smooth ocular surface is needed for clear o Efferent: CN VII
vision

st
1 line of defense against microbes Tearing
 Maintains health of the ocular surface  Classified into two entities
 Ensures comfort during blinking or eye movement o Lacrimation –excess production of tears
 Has three functional layers o Epiphora –overflow of tears due to blockage
o Superficial lipid layer (0.1 μm) of the lacrimal drainage system
 Produced by Meibomian and Zeis  The pH of tears average 7.4
glands  Amount of tears in our eye is dictated by 3 factors:
 Retards evaporation and forms a o Production
watertight seal when the lids are o Evaporation
closed o Drainage
o Middle aqueous layer (7 μm)
 Produced by the lacrimal glands Lacrimal Drainage System
and glands of Krause and Wolfring  The lacrimal drainage system begins at the punctum
 Contains salts and proteins leading to the canaliculus to the lacrimal sac down to
o Deep mucus/glycoprotein layer (0.2 μm) the nasolacrimal duct
 Produced by Goblet cells
 Epithelial cell surface are
composed of lipoproteins and thus
repels the aqueous layer
 The mucin layer anchors the
aqueous layer by adsorbing to the
epithelial cell surface while
providing a hydrophilic surface for
the aqueous layer to spread over

 The nasolacrimal duct opens at the inferior meatus

under the inferior turbinate
 See illustration above
o 1 = valve of Rosenmuller
 Drains the inferior and superior
canaliculi
o 5 = valve of Hasner
 Drains the nasolacrimal duct

Dysfunctional Tear Syndrome (DTS)

 Also known as keratoconjunctivitis sicca
 Disturbance in:
o Tear volume
o Tear composition
o Tear osmolality
o Release of inflammatory mediators
 Affect more than one component of the tear film (lipid,
aqueous, mucin) leading to ocular surface alterations
 Can cause irregularities on the corneal surface due to
microtrauma to the epithelium
 Certain medications can aggravate eye dryness
o Antihypertensives
 Propanolol
 Methyldopa
 Prazosin
OPHTHA Anterior Segment Problems of the Eye Page 1 of 12
  Clonidine
o Antidepressants
 TCA
 MAO inhibitors
o Antihistamines
 Diphenhydramine
o Antiparkinsonism
 Benztropine
o Antiarrythmics
 Disopyramine
o Others
 Marijuana
 Thiabendazole
 Occupational history/Review of systems
o Occupation
 Works on computer for prolonged
periods (call center agents, med
students, etc.)
o History of trauma
 Ocular disease
 Ocular surgery
o Identify patients with dry mouth (xerostomia)
 Sjogren’s syndrome
o Systemic/autoimmune disorders
 Dry eye symptoms
o Burning, stinging, itching
o Foreign body sensation
 Most frequent complaint
o Dryness, soreness, heaviness of eyelids,
photophobia, ocular fatigue
o Worse in the afternoon or evening or upon
waking up
o Aggravated by reading, computer work,
environmental factors
 Warning: Lacrimation may develop in dry
eye as “reflex tearing” due to irritation
 Dry eye signs
o Dull corneal luster
o Tear film instability
o Reduction in aqueous production
o Debris in tear film
o Ocular surface epitheliopathy
 The most characteristic feature on slit lamp
examination is the interrupted or absent tear
meniscus at the lower lid margin
Evaluation of Tear Production
 Schirmer’s Test
 Schirmer’s strip is placed in each lower
eyelid for 5 minutes with the strip hanging
out
 The strip with the corner cut off is
traditionally placed in the right eye
o Done without anesthesia (Schirmer’s I) or
with anesthesia (Schirmer’s II)
o Dry eye is suspected if the result is
 Schirmer’s II/Van Bijsterveld: <5
mm in 5 mins
 Less reliable
 Schirmer’s I/Jones: <10 mm in 5
mins
 Local reference states that 2mm of
tears in 5 mins is considered
abnormal
 Tear Break-up Time (TBUT)
 Estimates the mucin content of the tear film
 Mucin deficiency may not be seen in
Schirmer’s test but can cause tear instability
o Uses fluorescein dye and cobalt blue light of
slit lamp
o Normally, “dry spots” develop when a person
stops blinking for more than 15 secs
o Abnormal
 Presence of dry spots in <10 secs
 Dry spots lead to exposure of the
corneal or conjunctival epithelium
that ultimately damages the
epithelial cells
 Damaged epithelial cells are shed
from the cornea leaving areas
susceptible to staining
OPHTHA Anterior Segment Problems of the Eye
 Seen as punctate areas of staining
thus the term “punctate keratitis”
 May lead to exposure keratopathy
 Exposed cornea opacifies
due to the drying effect
 Rose Bengal/Lissamine Green dye
o Stains dead or degenerated
CONJUNCTIVAL epithelial cells
o May also stain the cornea to a lesser extent
 Seen as fine punctate stippling in
the interpalpebral fissures
o More sensitive and specific than TBUT or
Schirmer’s
 Other tests
o Tear lysozyme
 Reduced in dry eye seen in Sjogren
o Tear osmolality
 Hyperosmolal tears
o Lactoferrin
 Low in patients with lacrimal
hyposecretion
o Impression cytology
 Loss of goblet cells
o Ocular ferning test
 Absence or reduced ferning of
conjunctival scrapings
Sjogren’s Syndrome
 Presence of serum antibodies
o Antinuclear antibodies (ANA) -titer ≥1:160)
o Rheumatoid factor (RF) -titer ≥1:160)
o Sjogren’s syndrome specific antibodies
 Anti-Ro (Sjogren’s A/SS-A)
 Anti-La (Sjogren’s B/SS-B)
 Criteria for Sjogren’s aqueous tear deficiency
1. Abnormal Schirmer’s + DTS
2. Decreased salivary flow
3. Lymphocytic infiltration of salivary glands
4. Presence of serum antibodies (either ANA,
RF, anti-Ro (SS-A) or anti-La (SS-B))
o Definitive diagnosis: 4/4 of the criteria
o Possible diagnosis: 3/4
 Autoimmune disorders associated with Sjogren’s
syndrome (no need to memorize)
o Rheumatoid arthritis
o SLE
o Scleroderma
o Lymphocytic interstitial pneumonitis
o TTP
o Hypergammaglobulinemia
o Reynaud’s phenomenon
o Polymyositis/Dermatomyositis
o Polyarteritis nodosa
o Hashimoto’s thyroiditis
o Chronic hepatobiliary cirrhosis
o Waldenstrom’s macroglobulinemia
o Interstitial nephritis
 Dry Eye Severity Level (very important, see
appendix)
Page 2 of 12
Management for Dry Eye
 Lubricating eye drops and ointments
 Artificial tears are the mainstay of
treatment
 Ointments are used for prolonged lubrication
especially when sleeping
 Remove aggravating factors and treat associated
diseases, if present
 Topical anti-inflammatory
o Steroids
o Cyclosporine
 Conserve endogenously produced tears
o Environmental modification
 Avoid air drafts
 Room humidifier
o Eye goggles (moderate to severe cases)
o Punctal occlusion (moderate to severe
cases)
o Tarsorrhaphy (severe cases)
 A surgical procedure by which the
upper and lower lid margins are
united
Corneal Abnormalities
Cornea
 Occupies the anterior portion of the eyeball
 Highly specialized avascular tissue to refract and
transmit light (responsible for 2/3 of the refracting
power of the eye)
 Unique architecture and deturgescence accounts for
corneal transparency (78% water content)
 Layers of the cornea (ABCDE)
o A-pithelium (epithelium)
o B-owman’s layer
o C-orneal stroma
o D-escemet’s membrane
o E-ndothelium
 Common pathologies that affect the cornea
o Infectious keratitis/central microbial keratitis
o Trauma
o Dystrophies
o Non-inflammatory ectatic disorders
o Ocular surface diseases
 Misdirection of eyelashes
 Lid anatomy abnormalities
 Tear film deficiencies
 Adjacent infections (conjunctivitis,
blepharitis, canaliculitis,
dacryocystitis)
 Clinical manifestation
o Symptoms
 Eye redness, tearing and
photophobia
 Eye pain, discharge
 Blurring of vision develops if
infection affects the visual axis
o Signs
 Corneal epithelial defect with
stromal infiltrate (hazy cornea)
 Ciliary injection
 Purulent eye discharge (in bacterial
and fungal infections)
 Anterior chamber inflammation with
or without hypopyon
 Hypopyon -pus in the anterior
chamber
 Specific manifestations
 Pneumococcal corneal ulcer
 Advancing border showing active
ulceration as the trailing border
begins to heal
 Creeping effect gave rise to the
term “acute serpiginous ulcer”

Infectious Keratitis/Central Microbial Keratitis

 Invasion of microorganisms into the cornea induces
an intense inflammatory response causing corneal  Pseudomonas aeruginosa corneal ulcer
necrosis, melting and rupture  Very painful, rapidly spreading
 Possible etiologies corneal ulcer
o Bacterial (76%)  Large bluish-green hypopyon
 Locally, most common bacterial
agents
 S. pneumoniae
 Pseudomonas
 Moraxella
 Other countries
 S. aureus
 Coagulase (-) S. aureus
 S. pneumonia
 S. viridans
 Pseudomonas
 Enterobacteriaceae
o Viral (16%)
 Most common: Herpes simplex
virus (HSV)  Moraxella liquefaciens corneal ulcer
o Fungal (12%)  Usually no hypopyon or only a
 Risk factors (don’t memorize but familiarize) small one
o Exogenous  Surrounding cornea is usually clear
 Use of contact lenses (as opposed to hazy cornea in other
 Trauma (chemical, thermal, foreign infections)
body, irradiation)  Occurs in patients with alcoholism,
 Ocular surgeries (eyelid surgery, diabetes or immunosuppression
refractive surgery, keratoplasty)
 Loose sutures
 Medications
 Immunosuppression
 Factitious diseases (includes
anesthetic abuse)

OPHTHA Anterior Segment Problems of the Eye Page 3 of 12

  Fungal corneal ulcers
 Most common in agricultural
workers
 Presence of satellite lesions
(infiltrates at sites distant from the
main area of ulceration)
 Herpes simplex corneal ulcers
 Mostly caused by HSV-1
 Presence of dendritic ulcer
 Branching linear pattern
with feathery edges with
terminal bulbs
Corneal Dystrophies
 Diagnosis
o Diagnosis is generally clinical but additional
tests may be done to confirm diagnosis
o Microbiologic diagnosis
 Diagnostic staining
 Gram’s and Giemsa for
bacterial
 KOH for fungal
 Culture and sensitivity
 Blood agar plate (BAP),
chocolate agar plate
(CAP), thioglycolate broth
for bacterial
 Saboraud’s agar for fungal
 Not required in HSV
infection
 Management
o Bacterial
 Empiric treatment with broad
th
spectrum antibiotics (4 gen
fluoroquinolones) and adjusted
according to clinical response and
results of the culture and sensitivity
o Fungal
 Topic antifungal (natamycin,
voriconazole)
o Herpes simplex virus
 Topic antiviral (acyclovir,
gancyclovir)
 Preferred outcomes of management
o Resolved infection
o Resolved corneal inflammation
o Reduced eye pain
o Restored corneal integrity and minimal
scarring
o Restored visual function
 Redness and other symptoms will disappear
in recovery except for blurring of vision which
is caused by the corneal opacity
OPHTHA Anterior Segment Problems of the Eye
Traumatic Corneal Lacerations and Perforations
 Among the major causes of corneal problems in the
Philippines are mechanical and chemical injuries to
the corneal
 Caused by
o Physical
 Sharp objects (knife, scissors, nails,
glass etc)
 High velocity projectiles (iron nails
due to hammering, shattered glass,
darts, bullets etc.)
o Chemical
 Acids (denaturation and
precipitation of proteins)
 Alkalis (necrosis and melting) –
more severe
 Management
o Prevention is still the key
 Polycarbonate protective
goggles/eyeglasses for people at
risk especially in high risk
occupations
o Corneal laceration repair and suturing
 Bring about fibrosis and corneal
scarring even when repaired
o Keratoplasty may be required in some cases
 Keratoplasty
 Also known as corneal graft or
transplant
 Replace a portion of the cornea,
either involving the full thickness
(penetrating keratoplasty) or only a
superficial layer (lamellar
keratoplasty)
 Donor cornea from the same
human (autograft), another human
(homograft), or another species
(heterograft)
 Large group of hereditary corneal disorders sharing
several common features
o Bilateral and symmetrical involvement
o Absence of inflammation
o Absence of vascularization
o Positive for chromosomal abnormalities
 Caused by deposition of substances
o Dystrophies can happen anywhere in the
layers of the cornea (remember ABCDE)
 Diagnosis is based on clinical presentation and by
histopathology
 Corneal Epithelial Dystrophy types:
o Epithelial basement membrane dystrophy
 Previously knowned as Cogan’s
microcystic dystrophy
 Seen as microcysts, dots, map or
fingerprint patterns in the
epithelial basement membrane
protruding into the epithelium
 Vision usually is not significantly
affected
Page 4 of 12
 o Meesman epithelial dystrophy
 Autosomal dominant
 Progressive disorder characterized
by microcystic areas in the
epithelium
 Onset is in early childhood (first 2
years of life)
 Vision is slightly affected
o Reis-Buckler’s corneal dystrophy
 Affects primarily the Bowman's
layer
 Begins within the first decade of life
 Vision is markedly reduced
o Common symptoms for the different types
 Recurrent eye pain usually
occurring upon waking up
 Recurrent corneal erosions
o Management
 Hypertonic eye drops
 Superficial keratectomy
 Keratectomy –ablation of
the superficial cornea
 Pressure bandages
 Mechanical denudement of loose
corneal epithelium
 Corneal Stromal Dystrophy
o Types
 Granular dystrophy
 Autosomal recessive
 Abnormal accumulation of
hyaline
 Lattice dystrophy
 Autosomal recessive
 Abnormal accumulation of
amyloid
 Macular dystrophy
 Autosomal dominant
 Abnormal accumulation of
glycosaminoglycans or
mucopolysaccharides
o Symptoms
 Progressive blurring of vision
o Management
 Conservative approach
 Keratoplasty if vision is significantly
affected
 Fuch’s Endothelial Dystrophy
o Central wart-like deposits in the Descemet’s
membrane
 Characteristic thinning and pigmentation of
the endothelium and thickening of
Descemet's membrane
o Management
 Hypertonic eye drops
 Keratoplasty if vision is significantly
affected
Non-inflammatory Ectatic Disorders
 Symptoms
o Blurring of vision
o Frequent change in refractive error or
eyeglasses prescription
 Keratoconus
 Progressive thinning and bulging of the
cornea taking on a shape of a cone
 Cornea becomes abnormally and irregularly
steep resulting in very severe myopia and
astigmatism
OPHTHA Anterior Segment Problems of the Eye
o Best appreciated when examined using
specialized instruments
o Management
 Eyeglasses
 Rigid gas permeable contact lens
 Surgical
 Collagen cross-linking
 Intrastromal rings
 Keratoplasty
Cataract
Normal Lens
 Biconvex, avascular, colorless, transparent structure
 4 mm thick and 9 mm in diameter
 Located behind the iris and suspended by the zonules
of the ciliary body
 Anterior to it is the aqueous humor, posterior to it is
the vitreous humor
Cataract
 Cataract is defined as any opacification of the lens
causing deterioration of visual acuity of < 6/9 or worse
 Most common cause of REVERSIBLE blindness
 Pathogenesis of cataract is not completely
understood
 Cataractous lenses are characterized by
protein aggregates that scatter light rays and
reduce transparency
 Protein aggregates may also result to yellow
or brown discoloration of the lens
 Vesicles may be found between lens fibers
 Migration and aberrant enlargement of
epithelial cells
 Factors that contribute to cataract formation
 Oxidative damage (free radical reactions)
 Ultraviolet light damage
 Malnutrition
 Senile mature cataract is the most common form
o Related to aging that develops in varying
degrees between individuals
o Usually occurs from age 60 onwards
 Symptoms
o Gradual progressive painless blurring of
vision
 Cloudy vision
 Dull perception of colors
 Glare
 Halos around lights
 Classifications according to age of onset
o Congenital
 Present at birth or until 1 year of life
o Infantile
o Juvenile
o Pre-senile
o Senile/Developmental
 Usually starts at age 60 and above
 Classification according to stage of development
o Immature
 Early incipient stage
 Some transparent protein
o Mature
 Dense and/or visually disabling
 All of the lens proteins are opaque
o Hypermature
 Also called Morgagnian cataract
 Leakage of lens proteins out of the
capsule
 Cortical proteins have become
liquid and escapes the capsule
leaving a shrunken, wrinkled lens
Page 5 of 12
  Classification according to morphology
o Nuclear
o Cortical
o Subcapsular
 Anterior
 Posterior
Parts of the Lens
 Classification according to etiology
o Age-related cataract
 Normal condensation process in the
lens nucleus results in nuclear
sclerosis after middle age
 Earliest symptom: improved near
vision without glasses ("second
sight")
 Occurs from an increase in
the focus power of the
central lens, creating a
myopic (near-sighted) shift
in refraction
o Toxic (e.g. UV, drugs)
 Different drugs / agents affects the
enzyme system of the lens
epithelial cells causes disruption of
the active transport system and
protein synthesis
o Traumatic (non-perforating or perforating)
 Caused by direct and indirect
disruption of the capsules of the
lens
o Systemic disease (e.g. DM)
 Sugar that is entrapped inside the
lens is transformed to alcohol
resulting in the disruption lens
matrix
o Congenital Rubella
Diagnosis
 Basic tools in conducting an eye examination
o Slit lamp biomicroscopy
 Used in the assessment of
lenticular findings in the eye
 “Lenticular” –pertaining to the lens
 Presence of lenticular
opacifications
 Usually the anterior chamber is
quiet with no signs of inflammation
or flare
o Visual acuity charts
 Both for distance and near vision
 Patient with cataract present with
reduction of vision even with
correction
o Tonometer
 Used to determine the patient’s IOP
 Most patients present with normal
intraocular pressure
 When complications of cataract set
in, IOP may vary
 Glaucoma –Increase IOP
 Uveitis –Decreased IOP
(soft or hypotonic)
OPHTHA Anterior Segment Problems of the Eye
o Penlight
 For gross examination of the eye
 Cataractous eye present with
leukocoria (white pupil)
o Direct ophthalmoscope
 Used for fundus examination
 In severe cataract, fundus cannot
be appreciated (dull or absent
ROR)
 Eye ultrasound
o Normal in most cases of cataract
o Important to determine the status of the
posterior segment of the eye
o Most useful if patient’s cataract is associated
with trauma
Management
 Cataract surgery
o Intracapsular cataract extraction (ICCE)
 Consisting of removal of the entire
lens together with its capsule
 Rarely performed today because of
incidence of postoperative retinal
detachment and macular edema
o Extracapsular cataract extraction with
intraocular lens implantation (ECCE with
IOL)
 Preserves the posterior portion of
the lens capsule
 An opening is formed in the anterior
capsule and the nucleus and cortex
of the lens are removed
 The intraocular lens is then placed
in the empty "capsular bag"
supported by the intact posterior
capsule
 Nucleus is removed intact thus
requiring a relatively large incision
o Phacoemulsification with intraocular lens
implantation (Phaco or PE with IOL)
 Now the most common form of
extracapsular cataract extraction
 Utilizes a handheld ultrasonic
vibrator to disintegrate the hard
nucleus
 Nuclear material and cortex can be
aspirated through a smaller incision
 Indications for cataract surgery
o Done when the level of best corrected vision
affects activities of daily living
o Dense cataract
o Cataract causing complications
 Phacomorphic or phacolytic
glaucoma
o Congenital cataract
 Done to prevent amblyopia
Page 6 of 12
 Glaucoma  Older age
The Aqueous Humor  Chronic steroid use
 Composition  Ethnic background
o Clear liquid that fills the anterior and o South-east Asian and Inuit ethnic
posterior chambers of the eye backgrounds have a higher risk for PACG
o Slightly similar to plasma except for higher o Japanese have a higher risk for normal
concentration of ascorbate, pyruvate and tension glaucoma (NTG)
lactate  Other ocular morbidities
 Production o Proliferative diabetic retinopathy
o Produced by the ciliary body o Central retinal vein occlusion
o About 250 μL is present in each eye
o Produced at a rate of about 2.5 L/min Optic Disc Signs of Glaucoma
o Production is increased more in the day than  Generalized signs –earliest change seen in glaucoma
at night o Large optic cup
 Formation & Flow o Asymmetry of the cups
o Progressive enlargement of the cups
Produced by the stroma of the cilary processses  Focal signs
o Localized narrowing of the neuroretinal rim
(notching)
o Vertical elongation of the cup
Enters the posterior chamber o Cupping to the rim margin
o Regional pallor
o Splinter hemorrhage
o Nerve fiber layer loss
Passes through the pupil into the anterior chamber
Glaucomatous Visual Field
 Visual field changes seen in glaucoma reflect retinal
and optic nerve anatomy
Absorbed by the trabecular meshwork (through the
Schlemm's canal) in the anterior chamber angle  Scotoma –dark/blind areas of the visual field
o Location, distribution, size and shape of the
resulting visual field defect determined by
the location and extent of the anatomic
Exchange of component with the blood in the iris defect
 Visual field defects include:
o Paracentral scotomas
o Arcuate defects
 Contains the Bjerrum’s area
 Most common site of
glaucomatous visual
defect
o Nasal steps
o Temporal defects

Vitreous humor outflow

Glaucoma
 A group of diseases that is characterized by loss of
retinal ganglion cells leading to characteristic optic
nerve head changes and visual field loss
 Leading cause of IRREVERSIBLE blindness Visual field of the Right eye. Clockwise from Upper left: (1) Bjerrum’s
 Majority manifest late in life (>50 y/o) area. (2) Beginnings of an arcuate scotoma. (3) Temporal wedge
defect. (4) Full arcuate scotoma.
 Most are asymptomatic until late in the disease
 Multifactorial
CLASSIFICATION OF GLAUCOMA
 Exact pathogenesis is still poorly understood
Ocular hypertension (OHT)
 The major mechanism of visual loss is retinal ganglion
 Associated with the following findings:
cell apoptosis
o Elevated IOP
o Open angle
Risk factors for Glaucoma
o (-) glaucomatous ONH damage
 Increased intraocular pressure (IOP)
 More common than PAOG
o Most significant risk factor which can be
 Presence of disc hemorrhages in OHT indicates an
modified and monitored to control the
increased risk for developing of glaucoma
disease
 Patients with OHT are considered glaucoma suspects
 Family history of glaucoma
and should undergo regular monitoring
 Systemic hypertension
 Patients with OHT have relatively thick corneas
 High refractive errors
producing an overestimation of IOP
o High myopia
o Measurement of central corneal thickness
 Higher risk for primary open angle
may thus be useful
glaucoma (POAG)
o High hyperopia
 Higher risk for primary angle
closure glaucoma (PACG)
OPHTHA Anterior Segment Problems of the Eye Page 7 of 12
Primary Open Angle Glaucoma (POAG)
 Diagnosis is based on the following findings:
o Elevated IOP
o Open angle
o (+) glaucomatous ONH damage
 Chief pathologic feature
o Degenerative process in the trabecular
meshwork
 Deposition of extracellular material
within the meshwork and beneath
the lining of the Schlemm’s canal
 Different from the normal aging
process
o Results in reduction of aqueous drainage
leading to a rise in intraocular pressure
 Many patients are asymptomatic
o The major problem in detection of primary
open-angle glaucoma is the absence of
symptoms until relatively late in the disease
 If symptomatic, may complain of blurring of vision
(frequent change in prescription glasses) or focal loss
of vision such as scotomas
 Juvenile-onset open-angle glaucoma
o Associated with mutations in the myocilin
gene on chromosome 1
Primary Angle Closure Glaucoma (PACG)
 Diagnosis is based on the following findings:
o Elevated IOP
o Closed angle
o (+) glaucomatous ONH damage
 Elevation of IOP is a consequence of iris bombè
o A condition in which there is apposition of
the iris to the lens or anterior vitreous
o Aqueous outflow is blocked leading to
increased pressure in the posterior chamber
resulting in bowing of the iris (convex iris)
 Acute primary angle closure glaucoma
o Considered a medical emergency
o Acute outflow blockage causing severe pain,
eye redness, headache, blurring of vision,
nausea, vomiting, shallow anterior chamber
o Precipitated by pupillary dilation due to
 Reduced illumination (night time)
 Medications with anticholinergic or
sympathomimetic activity
o If treatment is delayed, the iris adheres to
the trabecular meshwork (anterior
synechiae) producing irreversible occlusion
requiring surgery
 Subacute primary angle closure glaucoma
o Same etiologic factors operate in subacute
as in acute angle
o Episodes of elevated IOP are of short
duration and are recurrent
o There is accumulated damage to the anterior
chamber angle with formation of anterior
synechiae
 Chronic primary angle closure glaucoma
o Never develop episodes of acute rise in IOP
but forms anterior synechiae accompanied
by a gradual rise in IOP
OPHTHA Anterior Segment Problems of the Eye
o Present in the same way as those with
POAG
Normal Tension Glaucoma (NTG)
 Also called low-tension glaucoma
 Associated with the following findings:
o Open angle
o Normal IOP
o (+) glaucomatous ONH damage
 Associated with abnormal sensitivity to IOP due to
vascular abnormalities or diseases
 Found to be associated with an abnormality in the
optineurin gene on chromosome 10
 Disc hemorrhages are more common in NTG
o Heralds progression of field loss
Congenital Glaucoma
 Also with elevated IOP and (+) glaucomatous ONH
damage
 Earliest and most common symptom is epiphora
 Other findings:
o Photophobia
o Decreased corneal luster
o Increased corneal diameter
 >11.5 mm is considered significant
o Increased depth of the anterior chamber
(associated with general enlargement of the
anterior segment of the eye)
o Corneal epithelial and stromal edema
o Tears of Descemet's membrane
 Divided into three subtypes:
o Primary congenital glaucoma
 Developmental abnormalities are
restricted to the anterior chamber
angle
o Anterior segment developmental anomalies
 Iris and corneal development are
also abnormal
 Seen in Axenfeld-Rieger syndrome
and Peters anomaly
o Other conditions in which developmental
anomalies of the angle are associated with
other ocular or extraocular abnormalities
 Seen in aniridia, Sturge-Weber
syndrome, neurofibromatosis-1,
Lowe syndrome, and congenital
rubella
Secondary Glaucoma
 Increased intraocular pressure occurring as a
manifestation of other eye diseases
 Manifest with:
o Elevated IOP
o Open or closed angle
o (+/-) glaucomatous ONH damage
 Due to:
o Changes in the lens
o Changes in the uveal tract
o Trauma or ocular surgery
o Neovascularization of the iris
o Raised episcleral venous pressure
o Steroid use
Page 8 of 12
Clinical and Diagnostic Evaluation of the Optic Nerve Head
(ONH), Visual Field and Anterior Chamber Angle
 Optic disc
o Assessed through fundoscopy
o Round or slightly oval in shape
o Contains a central cup
o The tissue between the cup and the disc
margin is called the neuroretinal rim
o In normal patients, this rim has a uniform
width and color ranging from orange to pink
o Optic disc grading
 Compare the diameter of the cup to
the diameter of the disc (cup-to-disc
/CD ratio)
 Think of doughnuts, the cup is the
hole of the doughnut and the disc is
the doughnut itself 
 Ratio is expressed in ratio
 A horizontal cup-to-disc
ratio of up to 3/10 or 0.3 is
normal
 Cup-to-disc ratio increases with age
 Intraocular pressure (IOP)
o Measured by tonometry
o Normal IOP: 10-20 mmHg
o Traditionally considered to be solely
responsible for anatomic damage in
glaucoma
o Now have been shown that there are other
factors at play that damage the optic nerve
 Visual field
o The visual field of the eye is defined as all
the space that it can see with the eye open
and looking straight
o Blindspot –corresponds to the area of the
optic nerve head
 Located 15° temporal to fixation
 Fovea
 Where visual sensitivity is
greatest
 Visual sensitivity
decreases toward the
periphery
 The visual field of each eye is
plotted as the patient sees
The normal limits of the visual field of the Right eye
OPHTHA Anterior Segment Problems of the Eye
 Traquiar’s Island of Vision
o Graphical description of the the visual field
as a three-dimensioned “island of vision
surrounded by a sea of blindness”
o The “peak” corresponds to the area of
greatest visual sensitivity which is the fovea
o The “gorge” corresponds to the normal blind
spot approximately 15° to the temporal side
of the highest peak
Traquiar’s Island of Vision/Hill of Vision
 Visual field testing
o Also known as perimetry
o Confrontational method
 Quick demonstration of gross field
defects
 Only practical method to evaluate
patients who are unable to perform
instruments used in perimetry
testing
 Small field defects in early
glaucoma may be missed in this
technique
o Kinetic visual field testing
 Object is moved from a non-seeing
area toward a seeing area
 Location is recorded when the
patient sees the object
 Process is repeated until a
boundary of seeing and non-seeing
is determined
 The determined boundary line is
called an isopter
 The Goldmann perimeter is an
example of a manual kinetic
perimeter
o Static visual field testing
 Use of non-moving test spots
 Fixed test spots of varying intensity
of light are presented for a short
period of time
 The patient responds when light is
perceived in each test spot
 Static testing attempts to find the
light sensitivities of the eye at
selected locations in the visual field
 Describes the contour of the hill of
vision
 The Humphrey Visual Field
Analyzer and the Octopus are
examples of automated static
perimeters
 Gonioscopy
o Best method to visualize the anterior
chamber depth width
 May also be estimated using
oblique penlight illumination or by
slit lamp exam
o Angle is open (normal)
 Full extent of trabecular meshwork,
the scleral spur, and the iris
processes is visible
o Angle is closed
 Only the Schwalbe's line or a small
portion of the trabecular meshwork
is visible
 Schwalbe’s line –the termination of
Descemet's membrane located at
the junction between the cornea
and sclera which is located just
anterior to the trabecular meshwork
Page 9 of 12
  Termed shallow or narrow angle in
lesser degrees
Medical Therapy (Standard Approach)
 Suppression of aqueous production
o Carbonic anhydrase inhibitors
 Most widely used
 Dorzolamide, oral acetazolamide
o Alpha-adrenergic agonists
 Given after anterior laser treatment
 Apraclonidine, brimonidine
o Beta-adrenergic blockers
 Contraindicated in COPD, asthma,
conduction defects
 Timolol, betaxolol, levobunolol
 Facilitation of aqueous outflow
o Prostaglandin analogs
 Bimatoprost, latanoprost, travaprost
o Parasympathomimetic agents
 Pilocarpine
 Reduction of vitreous volume
o Hyperosmotic agents
 Oral glycerin (glycerol)
 Most commonly used
agent
 IV mannitol
 Miotics, mydriatics, and cycloplegics
Surgical and Laser Treatment
 Iridectomy –surgical excision of a section of the iris
to form a direct communication between the anterior
and posterior chambers
o First line for the treatment of PACG
 Iridoplasty –contracts the iris stroma by laser to burn
the peripheral iris
 Iridotomy –like iridectomy but utilizes laser
 Trabeculoplasty –laser photocoagulation of the
trabecular meshwork
 Used in the treatment of POAG
 Glaucoma drainage surgery
 Trabeculectomy –surgical procedure for
creating an additional aqueous drainage
channel in the trabecular meshwork
 Glaucoma valves
 Cyclodestructive procedures
Important points to remember
 Most types of glaucoma are asymptomatic
 Regular eye check-up with an ophthalmologist will
increase the chance of detecting glaucoma earlier
 Early detection is the key of preserving vision
 In most cases, vision loss can be prevented or
delayed with proper treatment
END OF TRANS.
OPHTHA Anterior Segment Problems of the Eye
Summary
Dry Eye Syndrome (DES)
 Aka keratoconjunctivitis sicca
 Disturbance in:
o Tear volume
o Tear composition
o Tear osmolality
o Release of inflammatory mediators
 Medications that can aggravate DES
o Propranolol
o TCA and MAOi
o Diphenhydramine
 Dry eye signs
o Dull corneal luster
o Tear film instability
o Reduction in aqueous production
o Debris in tear film
o Ocular surface epitheliopathy
 Evaluation of Tear Production
o Schirmer’s
 With anesthesia (Schirmer’s II/Van
Bijsterveld): <5 mm in 5 mins
 Without anesthesia (Schirmer’s
I/Jones): <10 mm in 5 mins
o Tear Break-up Time (TBUT)
 Abnormal: Presence of dry spots in
<10 secs
o Rose Bengal/Lissamine Green dye
 Stains dead or degenerated
conjunctival epithelial cells
Sjogren’s Syndrome
 Presence of serum antibodies
o Antinuclear antibodies (ANA) -titer ≥1:160)
o Rheumatoid factor (RF) -titer ≥1:160)
o Sjogren’s syndrome specific antibodies
 Anti-Ro (Sjogren’s A/SS-A)
 Anti-La (Sjogren’s B/SS-B)
 Criteria for Sjogren’s aqueous tear deficiency
 Abnormal Schirmer’s + DTS
 Decreased salivary flow
 Lymphocytic infiltration of salivary glands
 Presence of serum antibodies (either ANA,
RF, anti-Ro (SS-A) or anti-La (SS-B))
o Definitive diagnosis: 4/4 of the criteria
o Possible diagnosis: ¾
 Dry Eye Severity Level (very important, see
appendix)
 Management
o Artificial tears are the mainstay of treatment
o Remove aggravating factors and treat
associated diseases, if present
o Topical anti-inflammatory
 Steroids
 Cyclosporine
o Conserve endogenously produced tears
 Avoid air drafts
 Room humidifier
o Eye goggles (moderate to severe cases)
o Punctal occlusion (moderate to severe
cases)
o Tarsorrhaphy (severe cases)
Infectious Keratitis/Central Microbial Keratitis
 Etiologies
o Bacterial (76%)
 Locally, most common bacterial
agents
 S. pneumoniae
 Pseudomonas
 Moraxella
o Viral (16%)
 Most common: Herpes simplex
virus (HSV)
o Fungal (12%)
Traumatic Corneal Lacerations and Perforations
 Caused by physical or chemical insults
 Prevention: protective goggles for people at risk
 Treated with corneal laceration repair and suturing
 Severe cases require keratoplasty
Page 10 of 12
Corneal Dystrophies Glaucoma
 Corneal Epithelial Dystrophy types:  A group of diseases that is characterized by loss of
o Epithelial basement membrane dystrophy retinal ganglion cells leading to characteristic optic
 Microcysts, dots, map or fingerprint nerve head changes and visual field loss
patterns in the epithelial basement  Leading cause of IRREVERSIBLE blindness
membrane  Majority manifest late in life (>50 y/o)
o Meesman epithelial dystrophy  Most are asymptomatic until late in the disease
o Reis-Buckler’s corneal dystrophy  Multifactorial
 Affects primarily the Bowman's  Exact pathogenesis is still poorly understood
layer  The major mechanism of visual loss is retinal ganglion
o Common symptoms for the different types cell apoptosis
 Recurrent eye pain usually  Risk factors for Glaucoma
occurring upon waking up o Increased intraocular pressure (IOP)
 Recurrent corneal erosions  Most significant risk factor which
o Management can be modified and monitored to
 Hypertonic eye drops control the disease
 Superficial keratectomy o Family history of glaucoma
 Keratectomy –ablation of o Systemic hypertension
the superficial cornea o High refractive errors
 Corneal Stromal Dystrophy  High myopia
o Granular dystrophy  Higher risk for primary
 Abnormal accumulation of hyaline open angle glaucoma
o Lattice dystrophy (POAG)
 Abnormal accumulation of amyloid  High hyperopia
o Macular dystrophy
 Higher risk for primary
 Abnormal accumulation of
angle closure glaucoma
glycosaminoglycans/
(PACG)
mucopolysaccharides
o Older age
 Fuch’s Endothelial Dystrophy o Chronic steroid use
o Central wart-like deposits in the Descemet’s o Ethnic background
membrane  South-east Asian and Inuit ethnic
backgrounds have a higher risk for
Non-inflammatory Ectatic Disorders PACG
 Keratoconus  Japanese have a higher risk for
o Progressive thinning and bulging of the normal tension glaucoma (NTG)
cornea taking on a shape of a cone o Other ocular morbidities
 Proliferative diabetic retinopathy
Cataract  Central retinal vein occlusion
 Defined as any opacification of the lens causing
deterioration of visual acuity of < 6/9 or worse Classification of Glaucoma
 Most common cause of REVERSIBLE blindness
 Symptoms Anterior
o Gradual progressive painless blurring of Glaucomatous
IOP chamber
vision ONH damage
angle
 Cloudy vision OHT ↑ Open (-)
 Dull perception of colors POAG ↑ Open (+)
 Glare PACG ↑ Closed (+)
 Halos around lights NTG N Open (+)
 Diagnosis
o Slit lamp biomicroscopy Medical Therapy (Standard Approach)
 Presence of lenticular opacifications  Suppression of aqueous production
 Usually the anterior chamber is o Carbonic anhydrase inhibitors
quiet with no signs of inflammation  Most widely used
or flare  Dorzolamide, oral acetazolamide
o Visual acuity charts o Alpha-adrenergic agonists
 Patient with cataract present with  Given after anterior laser treatment
reduction of vision even with  Apraclonidine, brimonidine
correction o Beta-adrenergic blockers
o Tonometer  Contraindicated in COPD, asthma,
 Most patients present with normal conduction defects
intraocular pressures  Timolol, betaxolol, levobunolol
o Penlight
 Facilitation of aqueous outflow
 Cataractous eye present with
o Prostaglandin analogs
leukocoria (white pupil)
 Bimatoprost, latanoprost, travaprost
o Direct ophthalmoscope
o Parasympathomimetic agents
 In severe cataract, fundus cannot
 Pilocarpine
be appreciated (dull or absent
 Reduction of vitreous volume
ROR)
o Hyperosmotic agents
 Management
 Oral glycerin (glycerol)
o Cataract surgery
 Most commonly used
 Intracapsular cataract extraction
agent
(ICCE)
 IV mannitol
 Extracapsular cataract extraction
with intraocular lens implantation  Miotics, mydriatics, and cycloplegics
(ECCE with IOL)
 Phacoemulsification with
intraocular lens implantation
(Phaco or PE with IOL)

OPHTHA Anterior Segment Problems of the Eye Page 11 of 12

Surgical and Laser Treatment
 Iridectomy –surgical excision of a section of the iris to
form a direct communication between the anterior and
posterior chambers
o First line for the treatment of PACG
 Iridoplasty –contracts the iris stroma by laser to burn
the peripheral iris
 Iridotomy –like iridectomy but utilizes laser
 Trabeculoplasty –laser photocoagulation of the
trabecular meshwork
o Used in the treatment of POAG
 Glaucoma drainage surgery
o Trabeculectomy –surgical procedure for
creating an additional aqueous drainage
channel in the trabecular meshwork
o Glaucoma valves
 Cyclodestructive procedures

APPENDIX
Dry Eye Severity Level 1 2 3 4
(must have S/Sx)
Discomfort, severity and Mild, episodic; occurs Moderate, episodic or Severe, frequent or Severe, disabling and
frequency under environmental chronic; occurs under constant without stress constant
stress stress or no stress
Visual symptoms None or episodic mild Annoying and activity- Annoying, chronic and Constant and possibly
fatigue limiting episodes constant, limiting activity disabling
Conjunctival injection None to mild None to mild +/- +/++
Conjunctival staining None to mild Variable Marked central Marked
Corneal staining None to mild Variable Marked central Severe punctate
erosions
Corneal/tear signs None to mild Mild debris, ↓meniscus Filamentary keratitis, Filamentary keratitis,
mucus clumping, ↑ tear mucus clumping, ↑ tear
debris debris, ulceration
Lid/meibomian glands Meibomian gland MGD variably present Frequent Trichiasis, keratinization,
disease (MGD) variably symblepharon
present
TBUT (secs) Variable ≤10 ≤5 intermediate
Schirmer score Variable ≤10 ≤5 ≤2
(mm/5min)

OPHTHA Anterior Segment Problems of the Eye Page 12 of 12

 OPHTHALMOLOGY LEC
Posterior Segment Problems 02
Dr. Alberto Lenny 09172460268
5th PERIODICAL Monday, December 16, 2013
TP27
Chiqui 09162242226

OUTLINE: - Ciliary nerves

I. Anatomy  2 long posterior ciliary nerves, cause dilation
II. Physiology and Biochemistry of vision  10 to 20 short posterior ciliary nerves
III. Symptoms of Retinal Disease
IV. Tests that measure retinal function
 Long posterior ciliary nerves
V. Pathologies of the Retina  Short posterior ciliary nerves – carry sympathetic fibers
a. Vascular abnormalities
b. Opacities of the sensory retina The retina layers
c. Disturbances in the position of the retina
VI. Diseases of the retina
VII. Management of Retinal Disease - overview

References:
PPT, Lecturer’s discussion
***from Vaughn and Asbury‟s General Ophthalmology or SIM
^^from websites provided by Doc (links at the end of this trans) unless
otherwise indicated
Self-instructional materials in Ophthalmology: chapter on Disorders of
the Retina, Choroid, and Vitreous

RPE – retinal pigment epithelium

ANATOMY

Fig 2. Layers of retina

 The ganglion cell layer, inner nuclear layer, and outer

nuclear layer – made up of cell nuclei
 The nerve fiber layer and plexiform layer, and the outer
plexiform layer – axon and dendrites of various nerve cells
 Horizontal orientation of the fibers are responsible for flame
shaped hemorrhages – means this is usually in the nerve
fiber layer
 In deeper cellular layers, cellular elements are vertically
arranged – dot and blot hemorrhages

Macula
- Clinically:
 Region within the temporal arcades
- Histologically:
 With 2 or more layers of ganglion cells
 With xanthophylls
 With taller, more pigmented RPE cells

Fovea
Fig 1. Anatomy of the eye
- 4 to 5 mm temporal and 1.5 mm inferior to the optic disc
Pars plana  Central 500um devoid of blood vessels (on fluorescein
angiography/FAZ)
- Flattened posterior zone of the ciliary body, makes up
 Fovea is dark upon administration of contrast (normal
roughly about 3.5 mm of the ciliary body
appearance)
- provides surgical access to the vitreous and retina
Foveola
Ora serrata
- central depression of the fovea; only cones and Muller cells
- Anterior border of the neurosensory retina, corresponds to
the insertion of the medial and lateral rectus muscles
Umbo
 Nasal portion – teeth are very sharp, otherwise they
are very shallow - center of the foveola (the one that lights up when doing light
 Smooth temporally, serrated nasally reflex)
 Ora bay is wider temporally Histological section of the retina and macula
 Ora teeth are more numerous nasally

Spiral of Tillaux
- An imaginary line connecting the insertions of the recti
muscles of the eye
 Medial rectus – 5.5mm
 Inferior rectus – 6.5 mm
 Lateral rectus – 6.9mm
 Superior rectus – 7.7mm
 Spiral of TIllaux is an important marker for surgery; we
do not want to cross this line
Fig 3. Layers of the Retina in the area of Macula. ILM- internal limiting
Vortex veins and ciliary nerves membrane; XLM-external limiting membrane
- Are found in the choroid - At the macula, ganglion cell layers are piled up then
- Vortex veins 1 per quadrant disappear over the foveola
 Drain into the superior and inferior ophthalmic veins
OPHTHA Posterior Segment Problems Page 1 of 14
- Inner nuclear cell layer is visibly thickened (the middle dark
band) at the macula, but disappears at the fovea >>>
greater density of cone-connecting second-order neurons
Photoreceptors
- Specialized neuroepithelial cells from the neuroectoderm
- 2 types:
 Rods – for dim-light vision, greater in peripheral retina
 100 million cells
 Cones – for bright-light vision, for color vision and
pattern recognition
 5 million cells, maximal in the fovea
- Rod:Cone ratio = 20:1
Choroid
- derived from the mesoderm and neuroectoderm
- Blood supply to the RPE (responsible for red color on light
reflex)
- For dissipation of heat
- Responsible for pigmentation/coloration of the fundus
The vitreous
- Clear gel, 4 mL in volume, occupies 80% of the globe
- Made up of water (99%), collagen fibrils, hyaluronic acid,
hyalocytes, inorganic salts, sugar, and ascorbic acid
- Firmly attached to:
 Vitreous base, optic disc, retinal vessels, and fovea
- What is the process of Vitreous detachment?
 Synchisis or syneresis – liquefaction and collapse of
the vitreous
o ***A normal physiologic occurrence at age 45 to
50
 Posterior vitreous detachment (PVD) – an acute event
that occurs when enough collapse takes place
 Pathology depends upon the state of the vitreo-retinal
interface
- Functions of the vitreous:
 The crystal clear nature of the retina allows visual
images to reach the retina
 Keeps the sensory retina adherent to the RPE
 Contains nutrients that are important to the
maintenance of the retina
 Inhibitory effect on the transformation of lymphocytes
in response to antigens
 Inhibits angiogenesis?
 Symptom – floaters and flashes!
Fig 4. Vitreous condensation and detachment – very intense
gelatinous condensation and detachment of the vitreous after
chorioretinal detachment
Blood Supply and the Blood-retina barrier (Assigned
reading***)
The retina receives its blood supply from two sources:
1. Choriocapillaris (internal portion of the choroid vessels)
- immediately outside Bruch's membrane
- supplies the outer third of the retina, including the outer
plexiform and outer nuclear layers, the photoreceptors,
and the retinal pigment epithelium
- the fovea is supplied entirely by this vessel
2. Branches of the central retinal artery
- supplies the inner two-thirds
OPHTHA Posterior Segment Problems
The Blood–Retina Barriers - keep the retina „dry‟:
1. Inner Blood-Retina Barrier
- This is attributed to the tight endothelial cell junctions
of the retinal capillaries. The endothelium is
nonfenestrated.
- Any disturbance in the integrity of these tight
attachments leads to oozing of fluid and/or blood, as
well as lipids and proteins from the retinal vascular
tree. This manifests as retinal edema, hard exudates,
hemorrhages.
2. Outer Blood-Retina Barrier:
- Lies at the level of RPE
- The tight intercellular attachments between RPE
cells, called Zonnula Occludens keeps the RPE
layer leak proof from the highly vascular
choriocapillaris of the choroid.
- It has physiologic “pump” that keeps fluid
contained outside the retina.
Embryology (Assigned reading***)
- Origin of the retina: Neural Ectoderm
- The outer layer of the optic cup remains as a single
layer and becomes the pigment epithelium of the
retina.
- Pigmentation begins at 5 weeks
- Secretion of the inner layer of Bruch's membrane
occurs by 6 weeks. The inner layer of the optic cup
undergoes a complicated differentiation into the other
nine layers of the retina.
-
th
By 7 month, the outermost cell layer (consisting of
the nuclei of the rods and cones) is present as well as
the bipolar, amacrine, and ganglion cells and nerve
fibers.
- The macular region is thicker than the rest of the
retina until the eighth month, when macular
depression begins to develop. Macular development
is not complete in anatomic terms until 6 months after
birth.
^^PHYSIOLOGY AND BIOCHEMISTRY OF VISION
(Assigned reading)
Disclaimer: this part is wordy and boring 
^^Phototransduction
 A process by which light is converted into electrical signals
in the rod cells, cone cells and photosensitive ganglion cells
of the retina of the eye
Fig 5. Visual cycle
 The visual cycle
- The biological conversion of a photon into an electrical
signal in the retina
- Occurs via G-protein coupled receptors (GPCR) called
opsins which contain the chromophore 11-cis retinal
- 11-cis retinal is covalently linked to the opsin receptor
via Schiff base forming retinylidene protein
Page 2 of 14
  Process
When struck by a photon:
• 11-cis retinal undergoes photoisomerization to all-
trans retinal
• This changes the conformation of the opsin GPCR
• Leads to signal transduction cascades (STC)
STC causes closure of cyclic GMP-gated
cation channel
• Causing hyperpolarization of the photoreceptor cell
Following isomerization and release from the
opsin protein:
• all-trans retinal is reduced to all-trans retinol and
travels back to the RPE to be "recharged"
• First esterified by lecithin retinol acyltransferase
(LRAT)
• Then converted to 11-cis retinol by the
isomerohydrolase RPE65
- To understand the photoreceptor's behaviour to light
intensities, it is necessary to understand the roles of
different currents
- There is an ongoing outward potassium current
+
through non-gated K -selective channels. This outward
current tends to hyperpolarize the photoreceptor at
+
around -70 mV (the equilibrium potential for K ).
- There is also an inward sodium current carried by
cGMP-gated sodium channels. This so-called 'dark
current' depolarizes the cell to around -40 mV. Note
that this is significantly more depolarized than most
other neurons.
+ +
- A high density of Na -K pumps enables the
photoreceptor to maintain a steady intracellular
+ +
concentration of Na and K .

11-cis retinol is oxidized back to 11-cis

retinal before traveling back to the rod outer
segment
• Where it is again conjugated to an opsin to form
new functional visual pigment or rhodopsin

^^Photoreceptors (Rods and Cones)

 ***Are arranged such that there is an increased density of
cones in the center of the macula (fovea), decreasing to the
periphery, and a higher density of rods in the periphery
- ***In the foveola, there is a nearly 1:1 relationship
between each cone photoreceptor, its ganglion cell,
and the emerging nerve fiber
- ***In the peripheral retina, many photoreceptors
connect to the same ganglion cell
- ***The fovea is responsible for good spatial resolution Fig 6. Response of photoreceptors in the dark.
(visual acuity) and color vision, both requiring high
ambient light (photopic vision) and being best at the  In the dark:
foveola - Photoreceptor cells depolarize in response to
- ***The remaining retina is utilized primarily for motion, absence of stimuli or scotopic conditions (darkness)
contrast, and night (scotopic) vision - The relatively depolarized state of photoreceptors in
 ***Are maintained by the RPE the dark depends on the presence of ion channels in
+ 2+
- ***The RPE is responsible for phagocytosis of the the outer segment membrane that permit Na and Ca
outer segments of the photoreceptors, transport of ions to flow into the cell, thus reducing the degree of
vitamins, and reduction of light scatter, and providing a inside negativity
selective barrier between the choroid and retina o Opening or closing of these channels is regulated
- ***RPE cells have little capacity for regeneration by the levels of the nucleotide cyclic guanosine
 Contain a chromophore (11-cis retinal, the aldehyde of monophosphate (cGMP)
Vitamin A1 and light-absorbing portion) bound to cell - cGMP levels are high (in the rod outer segment) that
membrane protein, opsin keep cGMP-gated sodium channels open, allowing a
 Rods – deal with low light level and do not mediate color steady inward current, called the dark current. This
vision (***only varying shades of gray are seen) dark current keeps the cell depolarized at about -40
- ***Contains rhodopsin, a photosensitive visual pigment mV.
embedded in the double-membrane disks of the
photoreceptor outer segment Scotopic condition (dark)
- ***Made up of two components, an opsin protein
(scotopsin) combined with a chromophore
- ***Peak light absorption by rhodopsin occurs at Depolarization of the cell membrane
approximately 500 nm (the blue-green region of the
light spectrum)
 Cones – can code the color of an image through Voltage-gated calcium channels open
comparison of the outputs of the three different types of
cones
- Each cone type responds best to certain wavelengths, Increased intracellular concentration of calcium
or colors, of light because each type has a slightly
different opsin Vesicles containing neurotransmitters (glutamate)
- Three types of cones: merge with the cellmembrane
o L-cones – respond to long wavelengths (reddish
color, 575 nm)
Neurotransmitter release into the synaptic cleft
o M-cones – respond to medium wavelengths
(greenish color, 540 nm)
o S-cones – respond to short wavelengths (bluish Excitation
color, 430 nm)

- When photoreceptors are relatively depolarized, the

2+
number of open Ca channels in the synaptic terminal
is high, and the rate of transmitter release is
correspondingly great

OPHTHA Posterior Segment Problems Page 3 of 14

 In the cone pathway, glutamate:  Signal amplification
1. Hyperpolarizes on-center bipolar cells - a single light-activated rhodopsin molecule can activate
800 transducin molecules, roughly eight percent of the
Binds to molecules on the disk surface
metabotropic - Each transducin molecule activates only one PDE
Causes
Glutamate glutamate Hyper-
from receptors closure of
polarization of molecule, which is capable of catalyzing the
(mGlu6) via a non-specific breakdown of as many as six cGMP molecules
photoreceptors cation the bipolar
in the dark G-protein cell - The absorption of a single photon by a rhodopsin
channels
coupling
mechanism molecule results in the closure of approximately 200
ion channels, or about 2% of the number of channels in
each rod that are open in the dark. This number of
2. Depolarizes off-center bipolar cells
channel closures causes a net change in the
membrane potential of about 1 mV
Binds to Causes an  Light adaptation – phenomenon by which the magnitude
Depolarization of signal amplification varies with the prevailing levels of
ionotropic inward
Glutamate of the bipolar
glutamate cation
cell illumination
receptors current - At low levels of illumination, photoreceptors are the
most sensitive to light
- As levels of illumination increase, sensitivity decreases,
preventing the receptors from saturating and greatly
extending the range of light intensities over which they
operate
- Role of calcium in the light-induced modulation of
photoreceptor sensitivity:
o The cGMP-gated channels in the outer segment
+ 2+
are permeable to both Na and Ca ; thus, light-
induced closure of these channels leads to a net
2+
decrease in the internal Ca concentration
o This decrease causes changes in the
phototransduction cascade which reduce the
sensitivity of the receptor to light
 Deactivation of the phototransduction cascade

GTPase Activating Protein (GAP) interacts with the alpha

subunit of transducin

Bound GTP is hydrolyzed to GDP

Fig 7. Response of photorceptors in the light.

 In the light: Action of PDE is stopped which halts transformation of

cGMP to GMP
- In photopic conditions (light), photoreceptors
hyperpolarize to a potential of -60mV. It is this
'switching off' that activates the next cell and sends an  A decrease in calcium levels results to the following:
excitatory signal down the neural pathway.
(1) Dissociation of Guanylate cyclase
- cGMP levels drop and some of the channels close, activating protein (GCAP) from calcium ions
leading to hyperpolarization of the outer segment
membrane, and ultimately the reduction of transmitter • Free GCAP interacts with Guanylate cyclase (GC),
release at the photoreceptor synapse activating it
• GC then transforms GTP to cGMP, replenishing the cell's
Retinal moiety of cGMP levels
rhodopsin • Sodium channels that were closed during phototransduction
A light photon undergoes Retinal no longer are reopened
interacts with isomerization, fits into the opsin
rhodopsin changing from 11- binding site
cis retinal to all-
trans retinal (2) Metarhodopsin II is deactivated

Opsin undergoes (3) Recoverin (also a calcium binding protein)

Opsin activates conformational
transducin, change to
dissociates from calcium and rhodopsin
Transducin binds metarhodopsin II, kinase (RK)
causing
GTP via its alpha
dissociation of which is unstable
subunit
transducin from and splits into • Released RK phosphorylates Metarhodopsin II
GDP opsin and all- • Decreased Metarhodopsin II affinity to transducin
trans retinal

(4) Arrestin (another protein) binds

phosphorylated Metarhodopsin II
PDE breaks down
The alpha subunit- cGMP to 5'-GMP, Causes closure of
GTP complex causing lowered sodium channels • Blocks the activity of rhodopsin to activate transducin
activates cGMP and • Metarhodopsin II is completely deactivated; all-trans retinal
phospho- concentration in hyperpolarization dissociates from opsin
diesterase (PDE) the rod outer of the cell
segment

 All-trans retinal is transported to the RPE cells to be

reduced to all-trans retinol, and is transported back to the
Depolarization of
Voltage-gated
rods
on-center bipolar Decreased level of - All-trans retinal cannot be synthesized by humans and
calcium channels
cells and glutamate are
close and calcium must be supplied by vitamin A in the diet
hyperpolarization released from the
levels drop inside
of off-center cell
the cell - Deficiency of all-trans retinal can lead to night
bipolar cells
blindness

OPHTHA Posterior Segment Problems Page 4 of 14

 - The recycling of rhodopsin is critically important for
maintaining the light sensitivity of photoreceptors. Even
under intense levels of illumination, the rate of
regeneration is sufficient to maintain a significant
number of active photopigment molecules.

SYMPTOMS OF RETINAL DISEASE

1. Blurring of vision – may be central (e.g. Age-related
macular degeneration/AMD) or peripheral (Retinitis
pigmentosa/RP)

Fig 11. Fovea is poorly appreciated. Notice the lines covering the
macula.

3. Scotoma – a blind area in the visual field

Fig 8. Central and Peripheral blurring of vision

 Central blurring:
o Age related macular degeneration
 “Greyish spot that always covers the center of
my vision”
 “The letters disappear when I try to look at them”
 “Floaters”

Fig 12. Patient will tell you “nawawala ung gitna” of their visual field.
 Macular hole:
o “Images or letters jump around”
o “Line is broken”
o “There are missing parts”

Fig 9. AMD

2. Metamorphopsia – wavy distortion of vision (not present in

optic neuropathy). Once encountered, think of retina right
away!

Fig 13. Macular hole. There is absence of tissue in the center.

4. Micropsia – decrease in image size caused by spreading

apart of foveal cones
 Central serous choroidopathy
o “The images are smaller compared to the other
Fig 10. Notice that the vertical columns in the center are wavy. eye”

 Cellophane maculopathy:
o “Distorted letters”
o “The lines are not the same”

Fig 14. There is fluid accumulation.

OPHTHA Posterior Segment Problems Page 5 of 14
5. Macropsia– increase in image size caused by crowding 8. Flashes – when the vitreous rubs or pulls on the retina it
together of foveal cones creates a sensation of flashing lights

Fig 15. Amsler grid of patient with micropsia and macropsia

6. Photopsia – appearance of sparks or flashes of light within

the eye due to retinal irritation
Fig 18. Flashes

TESTS THAT MEASURE RETINAL FUNCTION

Vision testing
 Corrected visual acuity (VA) – most important test of
macular function, particularly for near vision
 For patients with macular disease, VA is frequently worse
when the patient looks through the pinhole

Color vision (Read it, no need to memorize it)

 A function of 3 populations of retinal cones each with a
specific sensitivity (blue/tritan, red/protan, green/deuteron)
o Normal person requires all these primary colors
match within the spectrum
 Color desaturation is not present in mild macular disease
Fig 16. Sparks of light but is common in early optic nerve disease
 Color vision tests include:
7. Floaters – moving images in the visual field due to vitreous o Ishihara test – most common test
opacities o Hardy-Rand-Ritler
o Farnsworth-Munsell 100-hue test – a complex test in
which the patient is asked to arranged colors.
o Farnsworth D15 hue discrimination test

Visual field
1. Central visual field
 Amsler grid testing – evaluates the 10 degrees of the
visual field surrounding fixation
o Useful for screening and monitoring macular
disease
2. Peripheral visual field
 Confrontation testing
 Automated perimetry

Fig 17. Floaters
 Posterior vitreous detachment:
o “Spots that float”
o Movement – may remind them of a fly in motion
o Usually seen against a bright background – e.g.
the sky, a white page
 Vitreous hemorrhage:
o A small amt of bleeding can still produce a haze
effect which impairs vision
o Vitreous hemorrhage can give rise to profound
loss of vision if the macula is obscured
Fluorescein angiography
 Fluorescein – an orange water-soluble dye (sodium
fluorescein) that when injected IV, remains largely IV and
circulates in the bloodstream
 ***The dye outlines the retinal and choroidal vascular
system and is picked up by a special fundus camera
 Gives us an idea of any abnormal circulation within the eye,
any leaks, or anything that might be blocking the circulation
of the dye.
 Steps:
o Pupils dilated
o Patient is seated in front of the fundus camera
o Red-free photos taken
o Dye (5 mL) is injected IV
o Photographs taken at 1-second intervals – Shows how
the blood flows through the retina
o 5 to 30 secs after injection there is a coroidal flush
(prearterial phase)
o Late photographs may also be taken (10 and 20
minutes after injection)

OPHTHA Posterior Segment Problems Page 6 of 14

 Optical coherence tomography (OCT)
 Uses the optical backscattering of light to rapidly scan the
eye and describe a pixel representation of the anatomic
layers within the retina.
 It is basically a non-invasive procedure in which a light is
shine inside the eye and reflections are being interpreted.
Interpretations are based on assigned colors.

Fig 20. (Top Photo) Normal OCT – a depression (macula) is seen;

(Middle photo) Retinal Detachment; (Bottom photo) Retinoschisis –
abnormal splitting of the retina‟s neurosensory layers

Fig 21. Interpretations of retinal layers (From the internet) No need to

study or memorize.

Conditions and their typical appearance

1. Retinal neovascularization
- Begins in the plane between the ILM of the retina
and the posterior hyaloids of the vitreous
- Most common locations:
o Along the vascular arcades and the optic disc
o Border of perfused and non-perfused retina
- Hallmark: abnormal new vessels can cross both retinal
arterioles and veins
- Fan-like growth: abnormal neovascularization, uses
the back of the hyaloid as framework for growth

Fig 19. Phases of Fluorescein Angiogram. (Top photo) from

the lecture; (Bottom photo) from the internet - Normal fluorescein
angiogram. A and B represent preinjection photographs; C-E are the
transit (early) phase of the angiogram; and F-I are the recirculation
("mid" and "late") phase. A. (preinjection) With exciter and barrier in
place, the featureless black control photograph reveals either the
presence or absence of auto- and pseudofluorescence. B. (0 secs after
injection) The transit phase begins with choroidal filling. C. (10 secs)
Described as patchy, the transit phase is simultaneous with the filling of
cilioretinal arteries. D. (12 secs) The retinal arteries are infused. E. (15
secs) the dye returns via the retinal veins. Note the laminar flow during
the arteriovenous phase (inset). F. (about 30 secs) The angiogram is
brightest and microvasculature most visible. G-I. (5 and 10 mins) As the
fluorescein dye diffuses through the tissue, contrast decreases and the
optic nerve head stains.

Fig 22. Neovascularization (arrow), It usually starts at the optic disc.

2. Venous dilatations
- May appear as beading or sausage-like dilatation
- May appear as generalized dilatations of vessel

OPHTHA Posterior Segment Problems Page 7 of 14

 Fig 26. Choroidal neorovascularization

6. Intraretinal hemorrhages
Fig 23. Notice the rosary beadings. - Flame-shaped: superficial, bright red, located in nerve
fiber layer (NFL)
3. Microaneurysms - Dot/blot: round, dark red, located deeper, more
- Located in the inner nuclear layer vertically oriented layers of the retina
- Focal dilatations of retinal arterioles that appear as tiny,
round, red dots. They can be mistaken for dot
hemorrhages.
- On angiogram, presents as tiny hyperfluorescent dots.
This differentiate it from dot hemorrhages.

Fig 27. Flame-shaped hemorrhages with dot hemorrhages.

7. Pre-retinal hemorrhage
- Blood anterior to the retina but posterior to the
Fig 24. On angiogram, there are hyperfluorescent dots or they appear posterior hyaloid of the vitreous
as focal dilatations - Bright red and obscures the retinal vessels beneath it
- Blood tends to form a level
4. Capillary nonperfusion - Boat-shape appearance, also known as boat
- Also known as capillary drop-out hemorrhage
- Ischemic areas
- Blacked-out areas: capillaries are destroyed so no
dye goes inside

Fig 28. Preretinal hemorrhages in a patient with proliferative diabetic

retinopathy. Shaped like boat hemorrhages.

PATHOLOGIES OF THE RETINA

Fig 25. The arrows show hypoflourescence from capillary Opacities of the central retina
nonperfusion
 Cotton wool spots
- Small area of superficial retinal whitening
5. Choroidal neovascularization
- Results from an ischemic insult to the NFL
- Disruption of the Bruch‟s membrane/RPE complex,
- Represents interruption of axoplasmic flow
allowing vessels from the choriocapillaries to grow into
- “Soft exudates”
the subretinal space. This begins ARMD.
- Seen in Purtscher‟s retinopathy (Angiopathia retinae
- Clinically seen as grayish-green subretinal lesion
traumatic and HIV retinopathy
(You’ll know that it is subretinal when intact retinal
vessels are seen on top)
- Associated with subretinal fluid, hemorrhage, and lipid
exudation

Fig 29. Soft exudates

OPHTHA Posterior Segment Problems Page 8 of 14
 Lipid exudates – has well defined edges
- Referred to as “hard exudates”
- Either intraretinal or subretinal
- Tend to be localized around a given area of pathology
forming a circiniate pattern
- Large amounts may accumulate at sites distant from
the abnormality
- Seen in Diabetic retinopathy and Coat‟s disease
Fig 30. (Left photo) Lipid exudates in patients with DR. (Right Photo)
Coat‟s disease.
 Epiretinal membrane proliferation
- Proliferations of glial tissue that produce mechanical
distortion of the macula that may or may not be
associated with visual symptoms
- Forms a scar
- Most common form is idiopathic
- Seen in Cellophane maculopathy (see figure 10)
Disturbances in position of sensory retina
 Retinal detachment (RD) – separation of the sensory retina
- 3 types:
o Rhegmatogenous RD – most common
 With full-thickness break in the sensory
retina, vitreous traction, passage of liquefied
vitreous through the retinal defect into the
subretinal space
 Risk factors: myopia, aphakia, lattice
degeneration, ocular trauma
Fig 31. Posterior retinal break resulting to RD
o
nd
Traction RD – 2 most common
 When there is proliferation of membranes that
can contract and pull the retina.
 With concave surface, more localized
 Most commonly due to diabetic retinopathy,
PVR, ROP, ocular trauma
Fig 32. Traction RD in a patient with DR
o Exudative RD – due to collection of fluid
beneath sensory retina
 Caused primarily by disease of the RPE and
choroid
 May be associated with systemic vascular
and inflammatory disease
OPHTHA Posterior Segment Problems
Fig 33. Exudative RD In a patient with a pulmonary metastasis. The
presence of a mass increased fluid production.
DISEASES OF THE RETINA
Diabetic retinopathy (DR)
 Risk factors
- Duration of diabetes
o After 10 years (50%)
o After 30 years (90%)
- Metabolic control
- Miscellaneous factors: pregnancy, HPN, renal disease,
anemia
 Pathogenesis
- Microangiopathy affecting retinal and precapillary
arterioles, capillaries and venules
- Larger vessels may also be involved
- Has features of both microvascular occlusion and
leakage
o Occlusion and leakage disrupt the flow in retina,
causing the retina to perceive under-perfusion.
Thus, it forms abnormal vessels.
 Signs of Non-proliferative diabetic retinopathy (NPDR)
- Hemorrhage, exudates, cotton wool spots, vascular
abnormalities
 Signs of Proliferative diabetic retinopathy (PDR)
- All of NPDR + neovascularization
- Vitreous hemorrhage
- Fibrous proliferation
- Retinal detachment
*The book will show you stages of NPDR and PDR but what you
only need to know is the difference of the two.
 Features of DR
1. Microaneurysms – earliest clinically visible changes of
DR
- Localized capillary dilatations which are usually
saccular (round)
- Small red dots which are often in clusters
- Do not affect vision; they are one of the features of
background DR
2. Intraretinal hemorrhages – may be “dot”, “blot”, or
flame-shaped depending on their location within the
retina
- Hemorrhage within the NFL tends to be flame-
shaped, following the divergence of axons
- In the inner layer, hemorrhage is aligned at right
angles to the retinal surface and is consequently
viewed end-on when using an ophthalmoscope;
these hemorrhages appear dot- or blot-shaped
- The clinical differentiation between dot
hemorrhages and microaneurysms is difficult and
of little consequence since both are changes of
background retinopathy. Again, order fluorescein
angiogram!
3. Hard exudates – distinct yellow-white intra-retinal
deposits which can vary from small specks, circinates,
or large confluent plaques
- Extracellular lipid which has leaked from abnormal
retinal capillaries often associated with retinal
edema
4. Cotton Wool spots – grayish white patches of
discoloration in the nerve fiber layer which have
indistinct (fluffy) appearance. Once you see CW spots,
the patient more likely has an advanced retinal disease,
usually severe or very severe.
Page 9 of 14
 5. Venous abnormalities – venous dilatation, beading and
duplication occur as retinal ischemia progresses
- Beading is a useful sign of diffuse retinal ischemia
- Venous dilatation is seen early in DR but is rather
a subjective diagnosis
6. Intraretinal microvascular abnormalities (IRMAs) – are
areas of capillary dilatation and intraretinal new
vessel formation. To differentiate it from other
neovascularization, order angiogram.
- They arise within ischemic retina and when they
are present in numbers, it is a feature of pre-
proliferative retinopathy
7. Neovascularization – as retina becomes more ischemic,
new blood vessels may arise from the optic disc or in Fig 37. PDR: Here, there are membranes all over. When you
the periphery of the retina see membranes, it suggests PDR because membranes don’t
- Fine tufts on the surface of the disc or from the develop without developing vessels.
vessels of the major arcades
- The new vessels are fragile and bleed easily
leading to vitreous hemorrhage, hence the
importance of PDR. So if you see vitreous
hemorrhage, think of proliferative changes.
8. Retinal detachment (usually a late complication) – as
the new vessels mature, connective tissue and fibrosis
(gliosis) occurs
- Allowing the vitreous to exert traction which may
cause retinal detachment
9. Vitreous hemorrhage – can give rise to profound loss
of vision if the macula is obscured
- A small amount of bleeding can still produce a Fig 37. Neovascularization w/ Vitreous hemorrhage.
haze effect which impairs vision
 Treatment of DR – blood sugar control, laser treatment
(For those who have severe PDR), vitrectomy (for those
with hemorrhage and RD)
- Do not treat the central area

Panretinal Photocoagulation (Laser treatment)

The goal of this treatment is to kill off the peripheral
retina so that the retina is convinced that it is not in hard
time obtaining oxygen. Decrease amount of tissue will
decrease O2 demand. Hence, angiogenic factors are
prevented from being produced. SIDE EFFECT: NIGHT
BLINDNESS. Once central portion of retina is involved,
patient will experience blurring of vision. Therefore, don’t hit
the CENTER!
Fig 34. Vitreous hemorrhage

10. Macular edema – when the leak is centered on the

macula, the macula thickens, causing a decrease in
vision

Fig 38. A fundus photo of a patient with DR showing areas treated with
scatter laser surgery or PRP.

Hypertensive retinopathy (HR)

Fig 35. Macular edema
 General features:
Pictures of Diabetic Retinopathy: - Narrowing of the retinal arterioles
- Fundus picture:
o Vasoconstriction
o Leakage
o Arteriosclerosis
 May look like DR. Thus, history taking is important!!
 An assessment of hypertensive retinopathy signs may
provide important info for vascular risk stratification
 The 3-year survival of persons with grade 1 HR was 70%;
the survival was only 6% in those with grade 4 HR
 Classification of HPN
o Grade 1 – mild arteriolar attenuation
o Grade 2 – attenuation plus AV crossing defects and
increased vascular reflex
Fig 36. Severe NDPR: Note the hemorrhages and CW spots. o Grade 3 – retinal arteriole narrowing, AV nipping,
flame-shape and blot hemorrhages, cotton wool spots,
and hard exudates
o Grade 4 – all grade 3 findings + papilledema
o Important to note here is when you see papilledema!

OPHTHA Posterior Segment Problems Page 10 of 14

Retinal artery occlusion (RAO)
 Central RAO:
- Manifestations:
o White retina from cloudy swelling
o Cherry-red spot at the macula
- Causes:
o Cholesterol emboli (Hollenhorst plaque)
o Fibrinoplatelet emboli
o Calcific emboli
- Risk factors: HBP, arteriosclerosis, DM, glaucoma,
increasing age, blood dyscrasias, inflammatory
disease Fig 41. “Blood and thunder appearance”

Branch retinal vein occlusion

 Same changes with CRVO but confined to one area
(FOCAL)

Fig 39. Whitened retina with cherry red spots
- Ischemic necrosis results, and the retina becomes
opacified and yellow-white in appearance
- The foveola assumes a cherry-red spot because of a
combination of 2 factors:
o The intact RPE and choroid underlying the fovea
o The foveolar retina is nourished by the
choriocapillaries
- 25% of eyes with acute central RAO have cilioretinal
artery
Fig 42. More often occurs at the arteriovenous intersection in the
superotemporal quadrant.
Central serous chorioretinopathy (CSCR)
 Self-limited localized serous retinal detachments of the
 Usually in young individuals, M>F (8:1)
 Typically unilateral
 Common associations: stress, type A personality traits,
HPN, headach
 Most commonly idiopathic
 Patient presents with blurring of vision, distortion, micropsia,
area of visual darkening (positive scotoma)
 50% of patients retain better than 20/30 visual acuity
 Serous detachment seen on OCT

Fig 43. Color: Blister of fluid on the macular area. Typical smoke-
Fig 40. Acute central retinal artery occlusion with cherry-red spot stack appearance of the leak on angiogram.
(arrow) and preserved retina due to cilioretinal arterial supply
(arrowheads).
Age-related macular degeneration (AMD)
- The visual acuity generally returns to 20/50 or better in  A degenerative disorder of the macula, seen in patients 50
80% of eyes over a 2-week period years and older
 Symptoms: reduced central visual acuity, central scotoma,
Other conditions with cherry-red spot metamorphopsia
 Tay-Sach‟s disease (Remember this! It is a favorite exam  Leading cause of blindness among people over age 50 in
question) the western world
 Niemann-Pick disease  Prevalence expected to triple over the next 25 years
 Sandhoff‟s disease  Etiology:
 Generalized gangliosidosis - Etiology is unknown
 Sialidosis - Only definitive risk factor: Aging
- The older the patient, the higher the risk for AMD
Central retinal vein occlusion (CRVO) - Possible risk factors:
o *Gender: women > men
 Risk factors: same sa central RAO (HBP, arteriosclerosis,
o *Race: White > Black or Hispanic
dm, glaucoma, inc age, blood dyscrasias, inflammatory
 *for Neovascular AMD
disease)
o HPN or CV disease
 Ophthalmoscopy o Family history
- Dilated and tortuous veins o Ocular conditions (light iris color, lens opacities,
- Flame-shaped hemorrhages aphakia, hyperopia)
- Soft exudates o Cigarette smoking
- Retinal edema o Exposure to blue light or sunlight
- Cotton wool spots o Nutrition (low levels of Carotenoids)
o Elevated cholesterol

OPHTHA Posterior Segment Problems Page 11 of 14

 2 forms: Retinitis pigmentosa
- Non-neovascular AMD – dry type
o Vision loss is not as severe as the wet or
neovascular type
o May cause severe vision loss due to a geographic
atrophy in the fovea
o 10 to 20% may progress to the neovascular form

- Neovascular AMD – exudative type

o leading cause of severe vision loss
o Characterized by choroidal neovascularization
(CNV)
o New vessels are fragile and leak blood and fluid
that can lead to detachment of the RPE or
neurosensory retina, scar formation, and loss of
outer retinal tissue
 Causes of vision loss in AMD:
- CNV (80 to 90%)
- Atrophy of RPE (<5%)
- Serous RPE detachment (5 to 10%)
 Early characteristics (80% of AMD cases):
- Discrete yellow spots at the macula (drusen)
- Hyperpgmentation of the RPE
- Sharply demarcated areas of RPE depigmentation
Fig 44. Hard (Left) and Soft (Middle) Drusen, Geographic Atrophy
(Right) - Macular area is thinned out so that the underlying choroidal
vessels are seen.
Fig 46. Notice the pigmentation
 Progressive retinal dystrophy
 Inherited disorder in which abnormalities of the
photoreceptors RPE lead to progressive visual loss
 Defective dark adaptation or nyctalopia (Patients will
complain of night blindness)
 Reduction of the peripheral visual field (“tunnel vision”)
 Loss of central vision late in the disease
 Progressive degeneration of the photoreceptor cells
 A rod-cone dystrophy
 Genetic defects cause cell death (apoptosis) predominantly
in the rod photoreceptors and less commonly, the cone
photoreceptors
 Decreased vision at night or in low light
 Bone spicule pigmentation
 Waxy pallor of the optic nerve head
 Attenuation of the retinal vessels
 Other problems: Cellophane maculopathy, Cystic macular
edema, Posterior subcapsular cataract
 Diagnosis:
- Fundoscopy
- Electroretinography (ERG)
- Visual field testing

 Late characteristics
- Geographic atrophy of the RPE
- Pigment epithelial detachment
- Subretinal or sub-RPE neovascularization
- Fibroglial scar tissue, hemorrhage, and exudates

Fig 45. Subretinal fluid, blood and exudates. When it dries out it forms
Disciform Scar

 Detection and dx – via direct and indirect ophthalmoscopy

or fluorescein angiography
 Treatment:
- Non-exudative
o Vit A, C, E, Zn, lutein (ARED study)
o Low-vision consult/aids
- Exudative Fig 47. ERG in RP. Measures the ___ produce by the cells as it
o Intra-vitreal anti-VEGFs (ranibizumab, fire inside the retina. (Inset) Biphasic waveform of the ERG of a
bevacizumab, pegaptanib) – PIER, ANCHOR, normal patient.
MARINA studies
o Photodynamic therapy (verteporfin) – TAP study  Treatment
o Argon laser treatment – MPS study (Old treatment - Low vision consult
that is not done anymore because it produces - Vitamin A?
large scar) o 15,000 IU/day of vitamin A palmitate has possible
o Low-vision consult/aids slowing effect on changes in retinal function
o Problem: Toxicity
o Vitamin E: may have adverse effects on the
course of RE, DO NOT GIVE!
- Treat other conditions as needed
o EOR
o Cataract, epiretinal membranes, macular pucker

OPHTHA Posterior Segment Problems Page 12 of 14

 MANAGEMENT OF RETINAL DISEASE Summary
Indications for vitreous surgery Anatomy
 Removal of vitreous opacities  Layers of the retina – 10 layers
 Vitreous biopsy  Macula - With 2 or more layers of ganglion cells and with
 Vitreous clean-up for endophthalmitis xanthophyll
 Retinal detachment surgery  Fovea – devoid of blood vessels
 Removal of IOFB, dropped lens/IOL  Photoreceptors
 Macular pucker surgery o Rods- for dim-light vision, 100 millions
 Subretinal surgery o Cones – for bright-light and color vision; for patter
recognition, 5 millions
 Macular translocation and sclera imbrication
 Vitreous – 80% of the globe; Synchisis – physiologic
Cryosyrgery, photocoagulation, diathermy collapse of vitreous at 45-50
 Blood supply
 Sterile inflammation of the tissue to create chorioretinal o Choriocapillaris (Outer third) and Branches of the
scars to seal retinal tears or holes central retinal artery (inner two-thirds)
 Cryosurgery: uses intense cold  Blood retina barrier
 Photocoagulation: uses laser (argon diodie, etc) wherein o Inner (fenestrated endothelium) and outer ((in the
light is converted to heat RPE)
- mainstay of DR treatment  Embryonic origin of the retina: Neural ectoderm
 Diathermy: uses high temperature
 Cryopexy Symptoms of Retinal Disease
 Scleral buckling – put a silicone band around the eye to  Blurring of Vision: Central or peripheral; in AMD
support the sclera to seal the break and fix RD  Metamorphopsia – wavy distortions; in Cellophane
 Pneumatic retinopexy – maculopathy
- Indications:  Scotoma – blind area
o Retinal break confined to the superior 8 clock-hrs  Macropsia – increase in image size, crowding of foveal
o Retinal break/s with 1 to 2 clock-hrs cones
o Absence of PVR grade C or D  Micropsia – decrease in image size; due to spreading of
o Ability to maintain head position foveal cones
o Clear media  Photopsia – sparks of light
- Injection of an expansile gas (“pneumatic”), which
 Floaters – moving images
stay inside the eyes for 3-4 weeks and creation of
 Flashes – flashing of light
choroid-retinal adhesion (“retinopexy”) using laser
retinopexy or cryopexy
Tests that measure retinal functional
- Create an intraocular tamponade of the retinal breaks
to allow sufficient time for subretinal fluid to be  Visual acuity – important for macular disease
resorbed and a chorioretinal adhesion to form around  Color vision testing - function of 3 populations of retinal
the break cones sensitivity is measured
- Patient in prone of face down position  Amsler grid – for central visual field
- Gas displaced superiorly  Fluorescein angiography - dye outlines the retinal and
choroidal vascular system; detects abnormal circulation
Vitrectomy in the eye
 Optical coherence tomography (OCT) - rapidly scan the
 Most common procedure
eye and describe a pixel representation of the anatomic
 Removal of part or the whole of the vitreous body and its
layers within the retina.
replacement with balanced salt solution
 Indications: Pathologies of the Retina
- Vitreous hemorrhage o Vascular abnormalities
- Traction of the retina by vitreous strands  Retinal Neovascularization – fan-like growth of new
- Macular hole vessels at the optic disc
- Giant retinal breaks  Venous dilatation – appear as beading or sausage-
 Vitreous substitutes: like
- Intraocular gases  Microaneurysms – appears as tiny red dots. On
- Perfluorocarbon liquids angiogram, it appears as hyperfluorescent dots.
- Silicone oil  Capillary nonperfusion – ischemic areas
 Choroidal neovascularization – disruption of RPE;
Anti-VEGFs subretinal lesion
 Inhibit vascular growth  Intra retinal hemorrhages – flame-shaped or
 The role of VEGF in the growth of both regular and dot/blot hemorrhages
abnormal blood vessels was identified in the 1980s, and  Pre retinal hemorrhages – boat hemorrhages
agents that could block the angiogenic cascade first came
on the scene for cancer treatments in the early 1990s o Opacities of the sensory retina
 Usually a treatment for Macular degeneration  Cotton wool spots –ischemic insult to nerve fiber
 Examples: layer, soft exudates
- Macugen (pegaptanib sodium)  Lipid exudates – hard exudates, circinate patter
- Avastin (bevacizumab)  Epiretinal membranes - Proliferations of glial tissue
- Lucentis (ranibizumab) that produce mechanical distortion of the macula

END OF TRANS. o Disturbances in the position of the retina

 Retinal detachment
Transcribers‟ Note: The PPT was not provided. Since the photos shown  Rhematogenous – full-thickness retinal break
in the lecture were detailed and the pictures taken were not clear  Traction – pulling of retina due to
enough, we lifted most of the photos included in this trans from the neovascularization
websites provided by Doc, from google or from the book. Many of them  Exudative – involves RPE and choroid, due to
are the exact photo. If not, we made sure they are almost the same. If collection of fluid
you want a copy of the PPT pictures, just approach us.  Thanks.

http://pediaview.com/openpedia/Phototransduction: where the part on

Physiology and Biochemistry of Vision was mostly taken, with
supplemental info from http://www.ncbi.nlm.nih.gov/books/NBK10806/
Columbia University pictures: http://dro.hs.columbia.edu/vr2.htm

OPHTHA Posterior Segment Problems Page 13 of 14

  Diseases of the retina
o DM Retinopathy
 Non-proliferative DR - Hemorrhage, exudates,
cotton wool spots, vascular abnormalities
 Proliferative DR – NPDR + neovascularization
 Treatment – usually laser treatment or PRP
o HPN Retinopathy - Narrowing of the retinal
arterioles,
 Grade 4 - retinal arteriole narrowing, AV
nipping, flame-shape and blot hemorrhages,
cotton wool spots, and hard exudates +
Papilledema
o CRVO – flamed-shaped hemorrhages + soft
exudates; blood and thunder appearance
o CRAO – pale retina w/ cherry red spots, can be
found in patient‟s with Tay Sach‟s disease
o CSCR – usually found in male, unilateral; blister of
fluid around the macular and smoke-stack
appearance
o AMD - degenerative disorder of the macula, seen in
patients 50 years and older
 Dry type – non-neovascular
 Wet type – characterized by choroidal
neovasculariation
o RP - Inherited disorder in which abnormalities of the
photoreceptors RPE lead to progressive visual loss;
Defective dark adaptation or nyctalopia

Management of intra-retinal disorders

 Indications for vitreous surgery
o Removal of vitreous opacities
o Vitreous biopsy
o Vitreous clean-up for endophthalmitis
o Retinal detachment surgery
o Removal of IOFB, dropped lens/IOL
o Macular pucker surgery
 Cryosyrgery, photocoagulation, diathermy
o Cryosurgery: uses intense cold
o Photocoagulation: mainstay of diabetic
retinopathy treatment; uses laser
o Cryopexy
o Scleral buckling –silicone band around the eye to
support the sclera to seal the break
o Pneumatic retinopexy – injection of gas resulting
to intraocular tamponade eventually leading to
resorption of extra fluid
 Vitrectomy – most common procedure done; Removal
of part or the whole of the vitreous body and its
replacement with balanced salt solution
 Anti-VEGFs – inhibit vascular growth

OPHTHA Posterior Segment Problems Page 14 of 14

   OPHTHALMOLOGY LEC
Red eye and Teary Eye Module 03
 
5TH PERIODICAL Dr. Lim Bon SIong
Monday, January, 6, 2014
TP03
D - 09266994320
JM - 09272508243

OUTLINE:
I. Basic Concepts
II. Acute Viral Conjunctivitis
III. Bacterial Conjunctivitis
IV. Allergic Conjunctivitis
V. Keratitis
VI. Phlyctenulosis
VII. Scleritis
VIII. Pinguecula
IX. Pterygium
X. Subconjunctival Hemorrhage
XI. Anterior Uveitis
XII. Tearing

*Exam is lecture based according to the lecturer. We

apologize for some of the pictures, we tried to look for
alternative pictures but apparently sometimes, nothing
• Mainly involves the conjunctival vessels, scleral
compares. J Malabo lang yung kuha ng cam naming sa lec. J
vessels, iris vessels
 Additional notes from book
• Characterized by Conjunctival congestion and ciliary
injection
Objectives o Difference:
• To understand the concepts and definitions of red eye § Conjunctival injection has a more
and tearing diffuse redness
• To know the common etiologies of red eye and § Ciliary injection is concentrated
tearing around the cornea or limbus
• To formulate diagnosis and differential diagnosis of
eye disorders with redness/or tearing based on Important things to ask in the history of the patient
History and PE • Age, gender and occupation
• To know the principles of management • Time of onset and duration of redness
• Acute, recurrent, chronic
Basic Concepts • Any associated signs such as: pain, discharge,
• Blurring of vision is the most common chief tearing, BOV, itching, lid swelling, mass photobia,
complaint for ophthalmologic consults foreign body sensation
• Redness, Tearing, Discharge are major reasons for • Exposure to similar illness
consult • History of trauma, eye disease, eye surgery and
contact lens wear
Differentials for Red eye and Teary Eye • Systemic illnesses like URTI and TB
Red Eye Tearing • Use of any eye drops, eye medications and its effects
• Infectious/allergic/ • Irritative/foreign o Indigenous eyedrops include your urine
chemical/irritative body/trauma wash and breast milk
conjunctivitis • Nasolacrimal • Sexual practice history
• Blepharitis duct obstruction o Chlamydial conjunctivitis
• Keratitis • Dry Eye Disease
• Phylctenulosis Possible diagnosis when red eye is associated with
• Scleritis different signs and/or symptoms
• Pterygium and pinguecula • Conjunctivitis – red eye + tearing/discharge
• Subconjunctival • Allergy – red eye + itching
Hemorrhage • Blepharitis – red eye + lid margin/lash lesions
• Anterior uveitis • Keratitis – red eye + corneal lesion
• Others: Contact lens • Scleritis – red eye + tenderness
related, Stevens Johnson, • Uveitis – red eye + photophobia
Acute Glaucoma, • Pterygium/pinguecula – red eye + conjunctival mass
Arteriovenous fistula, • Phlyctenulosis – red eye + limbal nodules
medications, • Red eye + no symptoms – subconjunctival
*The lecture mainly discussed all these hemorrhage
• Severe alkali burns causes severe ischemia of the
conjunctiva THE NORMAL CONJUNCTIVA
THE RED EYE
• Redness is an essential sign of ocular pathology
• A red eye is always abnormal but a white eye is not
always normal
• It is a key sign of inflammation where the eye
becomes red due to vascular dilation and congestion,
and/or hemorrhage/bleeding

OPHTHA Red eye and Teary eye Page 1 of 9

 
 • Consists of:
o Bulbar - conjunctiva lining the globe itself
o Forniceal – conjunctiva lining the junction
o Palpebral – lines the back part of the eyelid
§ Marginal – closer to the lid margin
§ Tarsal -
§ Orbital

Conjunctivitis
• Inflammation of the conjunctiva is the most common
eye disease worldwide
 Varies from a mild hyperemia with tearing to
a severe conjunctivitis with copious purulent
discharge
 
Clockwise: Serous, Mucous, Mucopurulent, Purulent/pus-like
 Case is usually endogenous
• Etiologies: IMPORTANT TABLE!
o Infectious (viral, bacterial, chlamydial) Serous Mucoid Mucopurulent Purulent
o Allergic Viral + - - -
o Chemical/toxic Chlamydia - + + -
• Associated signs: Bacteria + +
o Discharge Allergic + + - -
o Papillae – refer to dilated vessels Toxic + + +
o Follicles – result from proliferation of the
lymph nodes ACUTE VIRAL CONJUNCTIVITIS
 Seen in most cases of viral
conjunctivitis, chlamydial inclusion
conjunctivitis, parasitic conjunctivitis
and in some toxic conjunctivitis
 These should be suspected for when
they are located on the tarsi
(especially the upper tarsus)

 Acute usually benign and self

limited, lasting no more than 14
days
Note in the picture: Bilateral eye redness, serous/watery discharge, lid swelling.
If these three are present, it almost makes the diagnosis certain

• Adenoviruses are the most common cause of acute

follicular conjunctivitis worldwide
• Commonly known as “sore eyes”
• Acute in onset, highly contagious (hand to eye
contact), usually bilateral
• Affects all ages and sexes
• Symptoms:
o Redness, tearing, irritation and burning, lid
swelling, follicles, papillae, membranes, pre
auricular node, keratitis
• Self limiting (7-10 days)

Recall: pharyngoconjunctival fever

 Usually caused by adenovirus 3 and sometimes 4 and
7
 Characterized by Pharyngitis, fever and conjunctivitis
 Nontender preauricular lymphadenopathy is
  characteristic
(UP) Follicles (DOWN) Papillae
 Other possible associated findings
o Pseudomembranes and membranes BACTERIAL CONJUNCTIVIS
§ Result of an exudative process • May be:
differing only in degree o Hyperacute - peaks 1-2 days after onset of
o Pseudomembrane – coagulum on the redness);
surface of the epithelium and when it is § May be caused by N. gonorhoea
removed, the epithelium remains intact § May cause blinding due to corneal
o Membranes – coagulum involving the entire damage or loss of the eye
epithelium o acute – peaks in 2-4 days
§ If removed, a raw, bleeding surface § usually benign and self-limiting
remains § does not last for more than 15 days
o Phlyctenules – represent a delayed § can be treated using topical
hypersensitivity reaction to microbial antigen antimicrobials
• Types of discharge: o chronic - if already longer than 2 weeks
o Serous/watery  usually secondary to eyelid or
o Mucous/stringy nasolacrimal duct abnormalities
o Mucopurulent • Redness, tearing, burning, chemosis, lid edema,
o Purulent/pus-like mucopurulent or purulent discharge, inflammatory
membranes, keratitis in some
• N. gonorrhoeae, H. influenza, S. pneumonia, C.
trachomatis

OPHTHA Red eye and Teary eye Page 2 of 9

 
Neisseria gonorrhoeae conjunctivitis
• Characterized by Hyperacute, copious purulent
papillary conjunctivitis with severe lid swelling and
chemosis
• Most hyperacute of them all
• Other associated findings:
o Membranes
o Papillae
o pre-auricular node
• Invades intact corneal epithelium and cause
ulceration and perforation thus leading to damage
 Thus any person with a very copious amount
of discharge should undergo evaluation and
be treated properly
 This can also serve as a route for more
serious infection such as meningitis and
sepsis
•
th
In neonates it usually appears in less than 5 day of
life
• In adult it is a result of either auto-inoculation or
sexual activity appearing after 1-2 days of inoculation
• Diagnosis: presence Gram negative intracellular
coffee bean diplococcic
o Can be diagnosed even without asking, just
observe
o “cheese whiz” - K
• Treatment: Ceftriaxone 500 mg to 1 g IM
Haemophilus influenza conjunctivitis
• Characterized by a muco-purulent discharge with
papillary conjunctivitis, matting of lashes, lid swelling,
chemosis, redness
• Occurs in children with an associated history of URTI
and usually lasts for 7-10 days
• Diagnosis: made by detecting small fine gram
negative rods
• Treatment: topical antibiotics (aminoglycoside)
Streptococcus pneumonia conjunctivitis
• Characterized by muco-purulent discharge with
papillary conjunctivitis
o Very similar to Haemophilus
• Other associated features: redness, matting of lashes,
crusting, formation of membranes
• acute to chronic conjunctivitis in adults that is usually
associated with naso-lacrimal duct obstruction
• Diagnosis: S. pneumoniae are gram positive lancet
shaped diplococci
• Treatment: topical/systemic antibiotics
o Penicillin
Chlamydial conjunctivitis
• Most common cause of sexually transmitted
chronic follicular conjunctivitis
• Can be adult or neonatal inclusion conjunctivitis
OPHTHA Red eye and Teary eye
• Characterized by redness, crusting, tearing, mucoid to
muco-purulent discharge, prominent follicles and
papillae, limbal swelling, micropannus,
preauricular nodes
• Consultation is done at 1 -2 weeks after the onset of
redness or in children, 5-7 days after birth
NEONATAL CHLAMYDIAL CONJUNCTIVITIS
• Beefy red papillary conjunctivitis with
mucopurulent discharge occurring 5-7 days after birth
o compared to Neisserial conjunctivitis which
th
occurs before the 5 day of life
• sanguinous discharge due to the presence of
membranes
o remember when you peel of membranes,
they are raw and bleed
o “bleeding tears”
• Diagnosis: Giemsa stain will show basophilic
particles within the conjunctival epithelial cells which
represent the bacteria
• Treatment: systemic macrolides
ADULT CHLAMYDIAL CONJUNCTIVITIS
• In the first picture, note the very large follicular
conjunctivitis along with the mucoid discharge
 Herbert’s pits: pathognomonic cicatrical
remains of these follicles
§ Small depressions in the connective
tissue at the limbocorneal junction
covered by epithelium
• On the second one, note that there is limbal swelling
and congestion
• Does not heal spontaneously in several weeks unlike
in viral conjunctivitis
 All signs of trachoma are more severe in the upper
than in the lower conjunctiva and cornea
th
• Treatment: 4 generation fluoroquinolones, systemic
antibiotics (tetracyclines, macrolides)
 If not treated properly may lead to
conjunctival scarring, destruction of the
accessory lacrimal glands and obliteration of
the ductules of the lacrimal gland
§ May cause corneal scarring or
damage as an end result
Allergic conjunctivitis
• Itching is a cardinal symptom
o NO ITCH, NO ALLERGY
• History of atopy (asthma, rhinitis, eczema)
• Occur in all ages and sexes
Page 3 of 9
 • Symptoms:
o Mild redness, chemosis, serous,
mucoid/stringydischarge, mild papillary
conjunctivitis
o Redness is not as prominent as in infectious
etiologies
§ Aqueous red congestion
• Types:
o Seasonal
o Perennial Moraxhella
o Vernal • As shown in the first picture, this is characterized by
o Giant papillary conjunctivitis maceration and redness of the lid angles.
• Treatment approach: • Congestion and crusting can also be observed like in
o Avoidance and elimination of allergen the second picture.
o Topical/systemic antihistamines • Irritation and burning sensation with keratitis are also
o Mast cell stabilizers observed
• Aside from these, it can be characterized as a chronic
VERNAL ALLERGIC CONJUNCTIVITIS follicular and papillary conjunctivitis with mucopurulent
 Also known as "spring catarrh" and "seasonal discharge
conjunctivitis" or "warm weather conjunctivitis," • Treatment approach
o lid hygiene and lid scrub
o antibiotic eye drops

Ulcerative blepharoconjunctivitis

• Characterized by tarsal conjunctiva with cobblestone

papillae and ropy discharge as shown in the first
picture
o usually the upper lid is more involved
• Limbal giant papillae are also seen as shown in the
second picture
• Caused by severe allergy and is usually seen in • caused by S. aureus and other bacteria from the lids
prepubertal age and in children • causes ulceration into the skin itself and even
o more common in males and may occur for 5- cause secondary bacterial conjunctivitis
10 years
• characterized by lid margin redness, crusting, burning
• There is also damage to the corneal epithelium as sensation, matting of eye lashes and keratitis
well as conjunctival scarring o mats of fibrin are present
 Patients often complain of severe itching and
• acute to chronic papillary conjunctivitis with muco-
ropy discharge
purulent discharge
 May be associated with keratoconus
• Treatment approach
 Treatment:
o lid hygiene and lid scrub
o The disease is a self-limited disease, it must
o antibiotic eye drops
be recognized that the medication used to
treat the symptoms may provide short-term
benefit but long-term harm. Chemical conjunctivitis
o Short term treatments may include
§ Topical steroids to relieve itching
• Highly damaging (may
cause glaucoma and
cataract)
o Antihistamines
o Cold compresses, and ice packs are helpful,
and sleeping (and, if possible, working) in
cool, air-conditioned rooms can keep the
patient reasonably comfortable.
   
• Due to acid/alkali or topical medications
o Most commonly due to chemical burn
Summary from Vaughan:
• Characterized by Patchy redness and patchy
whiteness due to ischemia and edema due to
damage to the cornea

Book trans:
• In acid burns, the acids denature the tissue proteins
and the effect is immediate
• On the other hand, alkalis do not denture proteins but
tend to penetrate the tissues deeply and rapidly
o They tend to linger in the conjunctival tissue
and cause damage there for several days
§ As a result, adhesion between the
bulbar and palpebral conjunctiva
(symblepharon) and corneal
scarring are more likely to occue
• Pain, injection, photophobia and blepharospasm are
the principal symptoms
• Immediate treatment: Immediate and profuse
irrigation of the conjunctival sac with water or saline
solution
BACTERIAL KERATOCONJUNCTIVITIS o Removal of any solid object

OPHTHA Red eye and Teary eye Page 4 of 9

 
 • Etiologic agents: S. pneumonia, Pseudomonas,
KERATITIS Moraxella liquefasciens, Streptococcus,
Staphyloccocus are the most common
MICROBIAL KERATITIS • They are acute in onset with a rapid progression (2-5
days)
• Characterized by redness, pain, blurring of vision,
photophobia and tearing
• Diagnosis can be made by history, slit lamp exam,
gram stain and culture
• Treatment: intensive topical broad spectrum
antibiotics, systemic antibiotics, keratoplasty
 Pseudomonas corneal ulcer:
o begins as a gray or yellow
infiltrate at the site of a
break in the corneal
epithelium
o severe pain with rapid
progression due to
proteolytic enzymes
o infiltrate may be bluish
green
 Moraxella liquefaciens
Clockwise: Pseudomonas, HSV, Proteus, Aspergillus keratitis o Indolent oval ulcer that
• Recall that keratitis is suspected when there is usually affects the inferior
redness and a corneal lesion cornea
• Many types of bacterial corneal ulcers look alike and o Orogresses into the deep
vary only in severity. stroma over a period of
• At this point, doc did not discuss the pictures but days
proceeded to Herpes keratitis, which he mentioned o No hypopyon usually
we should be familiar about o Surrounding cornea is
clear
Herpes Keratitis o Usually in patients with
• Can be primary or recurrent alcoholism or DM
• Important as it is the most common cause of unilateral  Group A Strep
corneal blindess in the USA with the causative agent o No identifying features
usually being HSV – 1
• Lesions are characterized as: FUNGAL KERATITIS
o Dendritic/geographic-epithelial
§ Most characteristic
 branching, linear pattern with
feathery edges, and has terminal
bulbs at its ends
 geographic refers to a dendritic
pattern that is broader
o Disciform stromal
o Keratouveitis
• Other symptoms are: Redness, photophobia, foreign • Usually seen in farmers and agricultural workers
body sensation o Associated with trauma with organic matter
• Worsens with steroids
• Symptoms are similar to bacterial keratitis
o “It is important to differentiate bacterial from
fungal since treatment would differ
substantially.”
• Indolent and slow growing process (1-2 weeks)
• Difficult to treat once if caught late in its course
• Diagnosis: History, slit lamp exam, giemsa stain,
culture
• Treatment: debridement, topical natamycin,
amphotericin B, and keratoplasty.

PHLYCTENULOSIS

upper leftt: dendritic, UR, discoid, Lower: keratouveitis

• Treatment
o Debridement
o Trifluridine
o Acyclovir, gancyclovir
o Keratoplasty • Due to a Type IV hypersensitivity reaction to
o Control trigger mech microbial proteins including:
o Tuberculosis
Bacterial keratitis o Staphylococcus
• Risk factors: trauma, contact lens use, epithelial o Moraxella
erosion, nasolacrimal duct obstruction, DM, o Haemophilus
immunosuppression, corneal surgery

OPHTHA Red eye and Teary eye Page 5 of 9

 
  According to the book: phlyctenule begins as a
small lesion that is hard, red, elevated, and
surrounded by a zone of hyperemia
• May be seen as limbal, corneal, and conjunctival
lesions.
• Presents with redness, photophobia, white lesions,
and vascular fronds.
• Treatment: Topical corticosteroids
SCLERITIS
• Gradual and progressive encroachment on the cornea
 If the pterygium encroaches on the pupillary
area, it should be removed surgicaly along
with the superficial clear cornea beyond the
encroachment.
• May arise from a preexisting pinguecula
• Can recur if excised L
SUBCONJUNCTIVAL HEMORRHAGE

• Inflammation of the episclera or sclera
• Can either be immune-mediated or infectious
• Can present as diffuse or nodular lesions
• Associated with arthritis, Tb, and Herpes Zoster
• Manifests as deep red discoloration, dilation of
subconjunctival vessels, elevated nodules with
tenderness and pain
• “Since this is not conjunctivitis, you will not see any
discharge, follicle, or papilla.”
• Treatment: Corticosteroids – Unless the indection is
due to bacteria other than Tb or fungi.
DEGENERATIVE DISEASES OF THE CONJUNCTIVA
• Common condition wherein there is rupture of the
small conjunctival blood vessels
o This may occur spontaneously or may be a
result of trauma, rubbing, coughing, Valsalva,
anti-coagulants, conjunctivitis, or blood
dyscracia (in which case, it is bilateral).
• Aside from the appearance, subconjunctival
hemorrhages typically lack clinical symptoms
• Reassurance is the best plan of management as
subconjunctival hemorrhages would normally resolve
spontaneously after 2 to 3 weeks.
• Application of warm compress may also help in
resolution.

PINGUECULA ANTERIOR UVEITIS

• Inflammation of the uveal structures:
o Iris
o Ciliary body
o Choroid
• Anterior: Iritis, iridocyclitis
• Immune-mediated or infection-associated
• Etiologies:
o Idiopathic
o Tb related
o HLA-B27 related
• May present as a single episode, recurrent, or
chronic; unilateral or bilateral
• Conjunctival damage/degeneration secondary to • Clinical manifestations:
exposure to the environment o Blurring of vision
o Actinic/UV degeneration – occurs in o Photophobia
individuals who live in areas with high o Ciliary injection
exposure to sunlight (UV) o Miotic pupil
• Manifests as localized, raised, yellowish areas in the o Keratic precipitates
conjunctiva o Hypopyon – accumulation of white blood
o Commonly affects the interpalpebral portion cells in the anterior chamber (Wikipedia)
of the bulbar conjunctiva – Nasal location o Iris nodules
• Typically takes several years to develop o Posterior synechiae
o Therefore, it is not seen in infants and o AC cells
younger children o Flare
• May become inflamed EPISODICALLY • Treatment:
• Rarely excised o Corticosteroids
• Treatment: Decongestant or mild steroid o Immune-suppressants
o Mydriatics
PTERYGIUM

• Actinic/UV degeneration of the substancia propia

• Easily recognizable as a triangular, fleshy mass that
most commonly originates from the nasal side of the
affected eye.

OPHTHA Red eye and Teary eye Page 6 of 9

 

Hypopyon (upper left); Keratic precipitates (right); Iris nodules (lower
left)
Tearing
• Non-specific sign of ocular surface irritation or
lacrimal apparatus pathologies
• Definition of terms:
o Lacrimation – increased reflex tearing
o Epiphora – failure of tears to drain properly
• May combine with other signs and symptoms like
burning sensation, redness, pain, itching, discharge,
photophobia etc.
Important things to ask in the history of the tearing patient
1. Presence of associated symptoms such as: itchiness,
foreign body sensation, redness, pain, discharge, or
swelling of the medial canthal area
2. Duration and aggravating factors:
• Worse in the morning/evening, while in air-
conditioned room
• Tearing is an important Sx of Dry Eye
Disease
3. History of trauma: injury ot the lacrimal drainage
system; foreign bodies, abrasion, or chemicals
4. History of surgery: exposed sutures
Lacrimation – increased aqueous tear production
The Tear Film
• Current model
o Superficial lipid layer
o Aqueous layer
o Mucin layer creating a gel gradient
Functional Unit of the Healthy Eye
• “Normal tearing depends on a feedback loop system
that involves efferents from the trigeminal innervation
of the ocular surface to the pterygopalatine ganglion.
Afferent signals carried by the post-ganglionic fibers
innervate the lacrimal glands, nasopharynx, and
vessels of the orbit to initiate tearing and maintain the
integrity of the ocular surface.”
OPHTHA Red eye and Teary eye
Lacrimal Functional Unit
• Trigeminal sensory fibers from ocular surface run to
the superior salivary nucleus in the pons
• Efferent fibers from the intermedius go to the
pterygopalatine ganglion
• Post ganglionic fibers innervate the lacrimal glands,
nasopharynx, and vessels of the orbit
• Blink Reflex: CN V (afferent); CN VII (efferent)
• Sympathetic innervation to the epithelium and blood
vessels of glands and ocular suface
The Tear Production
• Average of 1.2 µL per minute
• Too much/ excessive production may be caused by
irritation of the cornea or primary hypersecretion of
the lacrimal gland
o Crocodile tears: in facial nerve (CN VII)
palsy is due to damage and subsequent
aberrant nerve regeneration
• Too little/ inadequate production may suggest an
aqueous deficiency dry eye
• Poor quality of produced tears on the other hand is
characteristic of tear instability dry eye.
Normal Tear Composition
• Tears – a complex mixture of proteins, mucin, and
electrolytes
o Antimicrobial proteins: lysozymes and
lactoferrins
o Growth factors and suppressors of
inflammation: EGF, IL-1RA
o Soluble mucin 5AC secreted by goblet cells
provide viscosity
§ Membrane-bound mucins1 and 4
help sterilize tear film
o Electrolytes for proper osmolarity
Normal components present in a drop of tear
Causes of Lacrimation
• Corneal or conjunctival foreign bodies
• Corneal or conjunctival abrasion or trauma
• Corneal epitheliopathy: keratitis, microcystic edema
etc
• Chemical or infectious conjunctivitis
• Ocular surface irritation: trichiasis
• Reflex tearing in Dry Eye Disease
• Emotional stimulation
Epiphora
• Blockage of lacrimal drainage or tear overflow
Page 7 of 9
Anatomy of the Lacrimal Drainage System

• Puncta: 0.3mm in diameter, 1 medial to the end of the

tarsal plate, inferior punctum more lateral
• Canaliculus: vertical and horizontal portions, in 90%
forms a common canaliculus (ampulla of Maier)
• Lacrimal Sac: 15 mm in length, anterior: anterior
lacrimal crest, medial canthal tendon, medial: lacrimal
maxillary suture and anterior ethmoidal air cells,
inferior: IO and angular vein
• Nasolacrimal duct (intraosseous): nasofrontal process
of the maxilla, angulated posteriorly, inferiorly and
laterally

Nasolacrimal Duct Obstruction

• Common cause of tearing in newborns and adults
• Congenital NLDO: blockage of valve of Hasner at the
inferior meatus of the inferior turbinate
o 90% resolves by 1 year of age
o Manage by probing
• Acquired NLDO: blockage of the intraosseous portion
of the NLD
o Usually seen in females
o Managed by doing a DCR Dry Eye signs: abnormal tear break up time/TBUT (upper left); positive
(dacryocystorhinostomy) Rose Bengal/ Lissamine Green dye test (upper right); abnormal
Schirmer’s test (bottom)
• Note that the dye localizes to areas of damage

END OF TRANS.

Congenital NLDO (left); Acquired NLDO with Dacryocystitis (right)

Probing and Irrigation

Dry Eye Disease

• DEWS definition (2007)
o Dry eye disease is a multi-factorial disease
of the tears and ocular surface that result in
symptoms of discomfort, visual disturbance
and tear film instability with potential damage
to the ocular surface.
o It is accompanied by increased osmolarity of
the tear film and inflammation of the ocular
surface
OPHTHA Red eye and Teary eye Page 8 of 9

 
 Summary
Possible diagnosis when red eye is associated with
different signs and/or symptoms
• Conjunctivitis – red eye + tearing/discharge
• Allergy – red eye + itching
• Blepharitis – red eye + lid margin/lash lesions
• Keratitis – red eye + corneal lesion
• Scleritis – red eye + tenderness
• Uveitis – red eye + photophobia
• Pterygium/pinguecula – red eye + conjunctival mass
• Phlyctenulosis – red eye + limbal nodules
• Red eye + no symptoms – subconjunctival
hemorrhage
IMPORTANT TABLE!
Serous Mucoid Mucopurulent Purulent
Viral + - - -
Chlamydia - + + -
Bacteria + +
Allergic + + - -
Toxic + + + -
•Signs and symptoms of Conjunctivitis
o Discharge
o Papillae – refer to dilated vessels
o Follicles – result from proliferation of the
lymph nodes
o Pseudomembranes and membranes
§ Result of an exudative process
differing only in degree
o Pseudomembrane – coagulum on the
surface of the epithelium and when it is
removed, the epithelium remains intact
o Membranes
o Phlyctenules – represent a delayed
hypersensitivity reaction to microbial antigen
Herpes Keratitis
• Lesions are characterized as:
o Dendritic/geographic-epithelial
o Disciform stromal
o Keratouveitis
FUNGAL KERATITIS
• Usually seen in farmers and agricultural workers
o Associated with trauma with organic matter
• Worsens with steroids
• Symptoms are similar to bacterial keratitis
• Diagnosis: History, slit lamp exam, giemsa stain,
culture
• Treatment: debridement, topical natamycin,
amphotericin B, and keratoplasty.
PHLYCTENULOSIS
 According to the book: phlyctenule begins as a
small lesion that is hard, red, elevated, and
surrounded by a zone of hyperemia
• Treatment: Topical corticosteroids
SCLERITIS
• Inflammation of the episclera or sclera
• Treatment: Corticosteroids – Unless the indection is
due to bacteria other than Tb or fungi.
OPHTHA Red eye and Teary eye
DEGENERATIVE DISEASES OF THE CONJUNCTIVA
PINGUECULA
• Conjunctival damage/degeneration secondary to
exposure to the environment
• Manifests as localized, raised, yellowish areas in the
conjunctiva
• Treatment: Decongestant or mild steroid
PTERYGIUM
• Actinic/UV degeneration of the substancia propia
• Easily recognizable as a triangular, fleshy mass that
most commonly originates from the nasal side of the
affected eye.
TEARY EYE
• Definition of terms:
o Lacrimation – increased reflex tearing
o Epiphora – failure of tears to drain properly
Important things to ask in the history of the tearing patient
• Presence of associated symptoms such as: itchiness,
foreign body sensation, redness, pain, discharge, or
swelling of the medial canthal area
• Duration and aggravating factors:
• History of trauma: injury ot the lacrimal drainage
system; foreign bodies, abrasion, or chemicals
• History of surgery: exposed sutures
The Tear Film
• Current model
o Superficial lipid layer
o Aqueous layer
o Mucin layer creating a gel gradient
The Tear Production
• Average of 1.2 µL per minute
• Too much/ excessive production may be caused by
irritation of the cornea or primary hypersecretion of
the lacrimal gland
Normal Tear Composition
• Tears – a complex mixture of proteins, mucin, and
electrolytes
o Antimicrobial proteins: lysozymes and
lactoferrins
o Growth factors and suppressors of
inflammation: EGF, IL-1RA
o Soluble mucin 5AC secreted by goblet cells
provide viscosity
§ Membrane-bound mucins1 and 4
help sterilize tear film
o Electrolytes for proper osmolarity
Normal components present in a drop of tear
Epiphora
• Blockage of lacrimal drainage or tear overflow
Nasolacrimal Duct Obstruction
• Congenital NLDO: blockage of valve of Hasner at the
inferior meatus of the inferior turbinate
o 90% resolves by 1 year of age
o Manage by probing
• Acquired NLDO: blockage of the intraosseous portion
of the NLD
Page 9 of 9

  OPHTHALMOLOGY LEC
Systemic Ophthalmology 01

 
6TH PERIODICAL Dr. Lee Verzosa
Monday, February 3, 2014
TP02
Jaque Arsenal 09258837527
Miggy Patrocinio 09176951741

OUTLINE: • Other causes of blepharitis:

I. Inflammatory Conditions o Rosacea
a. Infectious o Herpes simplex dermatitis
i. Staphylococcal Anterior Blepharitis o Varicella zoster dermatitis
ii. Hordeolum/Stye o Molluscum contagiosum
iii. Chalazion o Allergic or contact dermatitis
iv. Dacryocystitis o Seborrheic dermatitis
v. Preseptal and Orbital Cellulitis o Staph dermatitis
vi. Staphylococcal Endophthalmitis o Parasitic infections – demodex
vii. Streptococcal Keratitis o Irritants like smoke, fumes and other
viii. Gonococcal Conjunctivitis chemicals
ix. Chlamydia Conjunctivitis
x. TB Uveitis HORDEOLUM/STYE
xi. Leprosy Cataract and Corneal Scarring
xii. Adenovirus (Viral Conjunctivitis)
xiii. Herpes Simplex Virus
xiv. Herpes Zoster Ophthalmicus
xv. Rubella (German Measles)
xvi. Cytomegalovirus in AIDS
xvii. Toxocara canis
xviii. Toxoplasmosis
xix. Lice
xx. Keratomycosis
xxi. Fungal Orbital Cellulitis
b. Non-infectious
i. Rheumatoid Arthritis
ii. Ankylosing Spondylitis
iii. Stevens-Johnson Syndrome
iv. Lupus
II. Non-inflammatory Conditions
a. Cardiovascular
i. Capillary Hemangiomas
ii. Retinal Hemangiomas
iii. Hypertensive Retinopathy
b. Endocrine
i. Grave’s Disease
ii. Diabetic Retinopathy
c. Blood Disturbances
i. Polycythemia Vera
ii. Anemia
iii. Leukemia
d. Nutritional Figure 2. (Top image) Stye on gross examination
i. Vitamin A Deficiency (Bottom image) The location of hair follicle and Gland of Zeis in the
III. Summary anterior lamella, which are infected in styes

Italicized – lecture notes • Symptoms: lid swelling, pain, tenderness, FB

& - book trans sensation
• Infection of hair follicle and/or gland of Zeis
INFLAMMATORY CONDITIONS • Trivia (The Myth of Peeping Tom’s Stye): Styes were
INFECTIOUS probably associated with voyeurism because in the
olden days, when houses were made of nipa, those
who peep through the small spaces on the walls get
STAPHYLOCOCCAL ANTERIOR BLEPHARITIS their eyelids irritated and subsequently infected.
• Treatment: spontaneous resolution, warm compress,
antibiotic (and steroid) ointments, oral antibiotics,
incision and curettage (I & C)
o I & C is not usually done, especially in simple,
uncomplicated styes because even if you put
anesthesia, patients will still complain of
severe pain during the procedure
o Pulling out the infected hair follicle can also
work because the stye may start draining,
which will clear up the infection

 
Figure 1. Crusting of the lids seen in Staphylococcal anterior
blepharitis

• Symptoms: burning, itching, foreign body (FB)

sensation, red eyes, red lids
• Treatment: warm compress, lid shampoo, lid
scrubbing with antibiotic ointments

OPHTHA Systemic Ophthalmology Page 1 of 15

   
CHALAZION

Figure 3. (L) Chalazion, (R) Incision & curretage (the eyelid with
anesthesia is everted, then an incision is made on the area of the Figure 5. Illustration of dacryocysto rhinostomy.
chalazion where the granulomatous contents are curetted)
PRESEPTAL AND ORBITAL CELLULITIS
• Symptom: Lid mass usually painless
• Painless granuloma of the meibomian glands (not
due to an infectious process like styes)
• Treatment: Incision and curettage, systemic
antibiotics (Tetracycline group)
o Tetracycline is given at a low dose for a
prolonged period (20 days to a month) to
regulate the oil glands
o Spontaneous resolution may also be an
option if the chalazion is not too big (patient
feels it but not grossly conspicuous)

DACRYOCYSTITIS

Figure 6. Characteristic lid swelling in preseptal/orbital cellulitis

• Symptoms: Lid swelling, pain, discharge

• Difference between preseptal and orbital
cellulitis: there is pain on movement of the
eyeball in orbital cellulitis because of spread
of bacterial infection posteriorly to the
extraocular muscles
• Due to Staphylococcus epidermidis
• Treatment: oral antibiotics, intravenous antibiotics,
topical antibiotics/steroids, oral anti-inflammatory
agents

Figure 4. Dacryocystitis. Located between the eyes and nose ridge STAPHYLOCOCCAL ENDOPHTHALMITIS

• Symptom: mass near the nasal area, periorbital

cellulitis, tearing/discharge
• Infection of the lacrimal sac
o Usually starts as nasolacrimal duct
obstruction, which impairs normal tear flow
to the nose and lead to pooling and
stagnation of tears in the lacrimal sac,
promoting bacterial infection
• Epiphora (excessive tear production), swelling
lacrimal sac
• Treatment: Oral antibiotics , dacryocystorhinostomy
o Since dacryocystitis tends to be recurrent,
treatment used to involve opening the skin
and making a new passageway for the tears Figure 7. Hypopyon (presence of pus in the anterior chamber)
o Dacryocystorhinostomy – a less invasive
procedure where laser probe is inserted, new • Occurs post surgery, presents with pain, swelling,
opening is created from the blocked sac blurring of vision
directly into the nose to bypass the • Treatment: Oral, IV, intravitreal antibiotics, vitrectomy,
obstruction without having to break the skin topical and intravitreal steroids
§ Involves fistulization of the lacrimal o One of the dreaded complications of
sac into the nasal cavity to alleviate intraocular operations because it is difficult to
epiphora and swelling (Medscape) treat
• Staph Infections
o chronic blepharitis,
o glands of Zeis infections (hordeolum/stye)
o meibomian gland infections ( chalazion)
o corneal ulcers
o dacryocystitis
o preseptal and orbital cellulitis
o endophthalmitis

OPHTHA Systemic Ophthalmology Page 2 of 15

   
STREPTOCOCCAL KERATITIS Chlamydia trachomatis Trachoma

Figure 8. Corneal opacity seen in Streptococcal keratitis

• Symptoms: FB sensation (since the cornea is
involved), eye redness, blurring of vision if visual axis
is affected
• Usually seen in contact lens users, especially those
who do not remove it before sleeping
• Treatment: topical antibiotics, cycloplegics, topical
steroids to control uveitis

GONOCOCCAL CONJUNCTIVITIS Figure 11. Trachoma

• Not endemic to the Philippines (seen more in

India or Africa where there is poor sanitation)
• Trachoma is produced by scarring due to
prolonged inflammation of the lids and
conjunctiva
• Treatment: Oral Tetracycline, Doxycycline,
Erythromycin, Azithromycin

Figure 9. Mucopurulent discharge seen in gonococcal

conjunctivitis

& Appears immediately after or within 2-5 days after

birth; earlier with premature rupture of membranes
• Caused by Neisseria gonorrrheae
• Present with mucopurulent discharge, lid edema and
chemosis
Figure 12. Corneal Scarring, Neovascularization and Opacification
• Treatment: topical, oral, IV antibiotics

CHLAMYDIA CONJUNCTIVITIS • Corneal involvement is due to frequent blinking from

prolonged inflammation, which leads to diminished
tear production, formation of new vessels and
opacification

TB UVEITIS

Figure 10. Red eye in chlamydia conjunctivitis

• Usual presentation: chronic red eyes, non-purulent

discharge, not responsive to eyedrops
• Common in the younger population who are sexually
active, thus asking the sexual history is important
• Treatment : Single dose Azithromycin, Doxycycline,
Erythromycin, Ofloxacin Figure 13. (L) Granulomatous uveitis; (R) Choroiditis
• Plus topical Moxifloxacin or Gatifloxacin, Erythromycin
• Tuberculous choroidal granuloma
• Symptoms: red eye, hypopyon (uveitic in nature)
• Ask for history of tuberculosis, intake of 6-month drug
regimen, joint pains
• Treatment: send the patient to a pulmonologist
because treatment of TB will also cure the eye
infection

OPHTHA Systemic Ophthalmology Page 3 of 15

   
LEPROSY CATARACT AND CORNEAL SCARRING HERPES SIMPLEX VIRUS

Figure 16. Presence of dendritic ulcer in HSV infection

& HSV 1 ocular while HSV 2 is genital

Figure 14. Cataract formation and corneal scarring (more severe & Most common extraocular sign: cold sore on the lips
on the right eye) • Dendritic corneal ulcer - branching linear pattern with
feathery edges and terminal bubs
• Not common in the Philippines • Treatment: oral and topical Acyclovir
• Caused by Mycobacterium leprae • NO STEROIDS
• Treatment: Rifampicin, Dapsone, and Clofazimin
• Cataract surgery, Corneal transplant (from a donor) HERPRES ZOSTER OPHTHALMICUS
o Corneal transplant is used in severely
scarred corneas with prominent blood
vessels
o However, more blood vessels in the cornea
lowers the chances of survival of the
transplanted one because the vessels may
invade the new cornea and cause scarring
once more
o Fortunately, there are artificial corneas which
can be sutured to the host cornea without
risk of recurrent scarring

ADENOVIRUS (VIRAL CONJUNCTIVITIS)

Figure 15. Red eyes and watery discharge of viral conjunctivitis

• Symptoms: red eye, watery discharge, itching and

burning, lid swelling
o Remember our case in Clin Integ: transfer of
infection is through fomites; avoid rubbing
eyes and sharing personal items; observe
frequent handwashing
• Pharyngoconjunctival Fever (PCF) – serotypes 3 & 7
• Epidemic Keratoconjunctivitis (EKC) – serotypes 8 &
19
o Review: EKC mostly manifests with eye Figure 17. Periorbital rash seen in Herpes zoster
symptoms (conjunctival hyperemia, watery ophthalmicus
discharge, lid swelling) while PCF presents
with a triad of fever, sore throat and bilateral • Reactivation chicken pox (HHV3) in the
conjunctivitis ophthalmic division of the trigeminal nerve
& Symtoms: rash, conjunctivitis, keratitis, episcleritis,
uveitis
• Treatment : Oral and topical acyclovir
• Steroids may be given (in drops)

OPHTHA Systemic Ophthalmology Page 4 of 15

 
 
RUBELLA (GERMAN MEASLES)
Figure 18. Cataract on the right eye (characteristic of Rubella)
• Child is born with cataract
• Caused by measles infection of the mother in the first
trimester
• Causes severe congenital defects
• Congenital cataract and retinitis most common
ocular disorders
• Cataract should be removed before 3 months of age
because this is the time when the infant starts to
fixate; otherwise nystagmus will ensue because the
eye will look for something to focus on
CYTOMEGALOVIRUS IN AIDS
Figure 19. (Above) Retinitis and (Below) Venous sheathing
(whitish silhouette covering the vessels)
& Florid necrotizing retinitis with arteriolar occlusion,
hemorrhage and edema
• Treatment: Intravenous antivirals (gancyclovir) – not
available in the Philippines
Figure 20. Retinitis with hemorrhage
OPHTHA Systemic Ophthalmology
TOXOCARA CANIS (ROUNDWORM OF DOGS)
Figure 21. Elevated granuloma (large white circles), which is the
most common finding in Toxocariasis
• Symptoms: severe blurring of vision (e.g. 20/200),
scarring or granuloma formation in the macula
• Usually affect dog owners who are licked by or kisses
their pets (not limited to stray dogs but even
pedigreed ones/house pets that have been dewormed
may still be a source of infection)
• Visceral larva migrans
• Treatment with steroids or vitrectomy
• Poor prognosis in most cases
TOXOPLASMOSIS (TOXOPLASMA GONDII)
Figure 22. Ophthalmologic findings of toxoplasmosis (not
discussed)
• Intracellular protozoan, cats as definitive host
& Focal choroidtis, posterior uveitis, chorioretinitis
& Congenital: in utero infection, commonly in the 3
rd
trimester; treated with topical corticosteroid and
cyclopegics
& Acquired: with hepatosplenomegaly, lymphadenopathy,
sore throat; treated with IgG and IgM antibodies
• Treatment: Steroids, Clindamycin, Cotrimoxazole,
lasers, cryotherapy, vitrectomy
LICE
Figure 23. Eyelash lice
• From Wikipedia; Demodex spp. (folliculorum or
brevis) infection; can cause blepharitis
• Cut off lashes one by one
• Not so common
Page 5 of 15
KERATOMYCOSIS & More common in women
& Peripheral corneal melting in severe cases
• Common associated systemic disease causing
scleritis
• Treatment: topical NSAIDs, steroids

Scleromalacia perforans
& Scleritis with vasculitis à scleromalacia perforans
• In cases of chronic scleritis, the sclera may thin
out and the uveal tract may be visualized already,
which may eventually perforate
• Treatment: put patch of donor sclera

Figure 24. Fungal corneal ulcer

• Usually caused by an agricultural ocular injury

• Aspergillus or Fusarium species
• Treatment with systemic and topical antifungals
• Usually poor prognosis; even with medical treatment,
the patient will need corneal transplant eventually

FUNGAL ORBITAL CELLULITIS

Figure. 26 Scleromalacia perforans. There is already

perforation of the sclera in this picture; the conjunctiva is just
holding back the contents

ANKYLOSING SPONDYLITIS

Figure 24. Orbital cellulitis with abscess and discharge

• A more severe case of keratomycosis

• The fungus has affected the whole orbit

NON-INFECTIOUS Figure. 27 Anterior iritis on slit-lamp biomicroscopy

RHEUMATOID ARTHRITIS • Chronic, idiopathic, inflammatory arthritis

• More common in males, 16-40 years old
• Positive for HLA-B27
• Acute iritis as ocular manifestation
• Treatment: steroids, cycloplegics

STEVENS-JOHNSON SYNDROME

Figure 25. Localized area of inflammation (on the left side of both
images) with normal gross findings in rest of the eye
Figure 28. Conjunctivitis (above); crusted lips and mouth ulcers
(below) in SJS
OPHTHA Systemic Ophthalmology Page 6 of 15

 
 
 • Severe mucocutaneous, vesiculobullous disease
disease that primarily occurs in young healthy
individuals
• Common cause is a hypersensitivity reaction to
drugs (allopurinol, sulfadrugs [Cotrimoxazole],
penicillin, dilantin, NSAIDs)
• Poor tear function (due to occlusion of the lacrimal
gland ducts), scarring of the conjunctiva
& In severe cases: corneal ulcers, perforation,
panophthalmitis
• Treatment: Steroids, tear supplements, punctal
occlusion
• Poor prognosis
& Common complication: secondary infection with
Staphylococcus aureus
LUPUS
Figure 29. Cotton wool spot (black arrows) and hemorrhage (blue
arrow) in SLE
• Can cause discoid lupus-type rash over the eyelids,
dry eye syndrome, corneal erosion, scleritis and
retinal disease (Sivaraj et al, 2007, Rheumatology)
• Treatment: oral steroids
• Refer to rheumatologist or immunologist
NON-INFLAMMATORY CONDITIONS
CARDIOVASCULAR
CAPILLARY HEMANGIOMA
Figure 30. Capillary hemangionma covering the right lid (top
image) and extending to the scalp, pre- and post-auricular area
OPHTHA Systemic Ophthalmology
• Treat if sight threatening; intra-lesional / systemic
steroids, pulsed dye laser treatment
o Most cases regress when the child gets
older
o Only treated when it gets large enough that it
closes the eyelid à lazy eye or amblyopia
§ Seen with anisometropia where
there is a grade difference of > 200
between the eyes
§ Often not detected because the
patient can see well on one eye
§ Only when the patient gets older,
an eye exam is conducted or when
the patient is rubbing the normal
eye that the discrepancy is noticed
§ Even with full correction, the patient
will still not be able to have a clear
20/20 vision – denotes a
developmental problem of the
visual cortex because it was not
stimulated enough by the lack of
utilization of the amblyopic eye
§ Should be detected before 8 years
old à correct lazy eye with the
appropriate grade and put a patch
on the GOOD EYE so the patient
will be forced to use the bad eye,
thereby speeding up the
development of the visual cortex
• Propranolol – results in faster regression of the
hemangioma
• Pulsed dye laser – targets the vessels which will
make the hemangioma regress
RETINAL HEMANGIOMA
Figure 31. Cavernous retinal hemangioma
Figure 32. Racemose retinal hemangioma
• No treatment required
TRANSCRIBERS’ NOTE: In Dr. Verzosa’s powerpoint, the top
image is identified as cavernous while the bottom image is
labeled racemose. However, upon verifying with credible
sources online (Expert Consult, JAMA Ophthalmology),
cavernous retinal hemangioma was described as grape-like
clusters of dark intraretinal venular aneurysms while racemose
was defined as congenital vascular malformation in which
some or all of the retinal vessels are dilated, often to the point
that the arterial system cannot be distinguished from the
venous system. Comparing this with the info from the
powerpoint, it seems that image-caption mismatch may have
Page 7 of 15
occurred. Nonetheless, this part was not discussed thoroughly
and was just skimmed through by the lecturer, which could
mean that the differentiating the two is not a must-know.

HYPERTENSIVE RETINOPATHY

Figure 35. Grade 4 Hypertensive Retinopathy with Disc Swelling

and Macular Star (yellowish streaks on the right side of the image,
marked by the black star)

ENDOCRINE
• Grading:
Grade 1 Mild arteriolar attenuation GRAVE’S DISEASE
Grade 2 More severe arteriolar constriction, vein • Autoimmmune disorder caused by excess secretion
deflection at AV crossings (nicking)
of thyroid hormones
Grade 3 Copper wiring of arterioles, flame shaped
• Women more than men; 8:1 ratio
hemorrhages, cotton wool spots and hard
• Hypertrophy of extraocular muscles
exudates
• Proliferation of orbital fat
Grade 4 Grade 3 plus silver wiring of arterioles and
o Since the orbit is made of bone, there is no
disc swelling
place for the eyeball to go but forward in
cases of EOM hypertrophy and orbital fat
proliferation, hence the characteristic
exophthalmos in Grave’s disease
• Cellular infiltration of interstitial tissue with
lymphocytes, plasma cells, macrophages and mast
cells
• Classification:
1. Eyelid retraction
2. Soft tissue involvement
3. Proptosis
4. Optic neuropathy
5. Restrictive Myopathy

Figure 33. Grade 2 Hypertensive Retinopathy with AV nicking

(encircled)

Figure 36. Lid retaraction (Dalrymple’s sign). Normally, the upper

part of the cornea should be covered by the lids.(L) Notice the
difference between the normal right eye and the retracted lid on
the left eye. (R) Both her eyelids retracted and corneas are fully
exposed.

Figure 34. Grade 3 Hypertensive Retinopathy with Hemorrhages

(blue arrow) and Cotton wool spots (black arrows)

Figure 37. Lid lag on downgaze (Von Graefe’s sign). Normally, lids
should still cover part of the cornea even when you look down
OPHTHA Systemic Ophthalmology Page 8 of 15
   
 • Defect due to fibrotic contraction

Figure 42. Tight inferior rectus, left eye. Increased IOP on upward
Figure 38. Staring and frightened appearance (Kocher’s sign) gaze due to inferior rectus muscle being tethered

Figure 43. Tight medial recti, right eye

Figure 39. Soft tissue involvement (Chemosis) Characterized by
DIABETIC RETINOPATHY
conjunctival balloon, which may also be seen in allergic patients

• Microangiopathy affecting retinal precapillary

arterioles, capillaries, and venules
• The consequence is retinal ischemia and hypoxia
causing intraretinal microvascular abnormalities
(IRMA) and neovascularization.
• Release of vascular endothelial growth factor
(VEGF) causes new vessel formation
& Type 1 DM has more severe retinopathy than Type 2
DM

Case:
54-year-old male came for a check up . The patient had no
visual complaints and stated that his blood sugar normally
reads about 155mg/dl, with an occasional reading of 200mg/dl.
His last eye exam was about two years ago.
Figure 40. Proptosis
Best-corrected visual acuity (BCVA) was 20/25 O.U.
Tonometry revealed intraocular pressure (IOP) of 12mm Hg
O.D. and 15mm Hg O.S. Pertinent biomicroscopy findings
included no rubeosis; mild cataract development O.U.; and,
most importantly, exudates and hemorrhages within 500
microns of the fovea O.D.

Figure 41. EOM enlargement in Grave’s disease

Dysthyroid Optic Neuropathy

• Due to direct compression of the optic nerve
• 5% affected
• Symptoms include a slowly progressive impairment
of central vision associated with defective red green
color perception Figure 44. Exudates and hemorrhage
Restrictive Thyroid Myopathy
• Muscles affected in order of frequency
1. Inferior rectus
2. Medial rectus
3. Superior rectus
4. Lateral rectus
OPHTHA Systemic Ophthalmology Page 9 of 15
   
 Figure 48. Background Stage of DM Retinopathy
Figure 45. Macular edema on fluorescin angiography (FA). White
spots in the middle denote edema. • Pre proliferative – ischemic changes; vascular
changes, dark blot hemorrhages, cotton wool spots
Two years later, VA counting fingers at five feet O.D. and
20/60-2 O.S. (patient has deteriorating vision)

Figure 46. More diffuse hemorrhages and exudates.

Figure 49. Preproliferative Stage. With areas of nonperfusion (blue

arrows on the bottom image)

• Proliferative – neovascularization, vitreous

Figure 47. Worsening edema and neovascularization on FA. Areas hemorrhage and fibrosis
of nonperfusion will eventually release VEGF

Stages:
• Background – microaneurysms, hemorrhages, hard
exudates, retinal edema

 
Figure 50. Neovascularization in Proliferative Phase. Notice the
small fine vessels forming near the optic disc

OPHTHA Systemic Ophthalmology Page 10 of 15

 

Figure 51. Neovascularization in Proliferative Phase on FA.
Prominent new vasculature is seen on the entire field; in normal
patients, only the bigger vessels are visualized.
Figure 52. Vitreous Hemorrhage. Since the new vessels are fragile,
it can rupture and result in hemorrhage.
Figure 53. Fibrotic tissue with beginning traction. Results from
chronic hemorrhage and can pull the retina and cause detachment.
Treatment of diabetic retinopathy
• Panretinal photocoagulation (PRP) – former gold
standard
• Anti VEGF intravitreal injections – used a lot
nowadays especially in the earlier stages of DM
retinopathy (with macular edema, hemorrhage and
exudates)
o Anti VEGF was first used in ophthalmology
for macular degeneration (wet-type), where it
was seen to cause regression of new
vessels and subsiding of edema
o Proven to be effective later on in other cases
of macular edema aside from macular
degeneration, such as DM
OPHTHA Systemic Ophthalmology
• Argon laser
Figure 54. Laser treatment (PRP). The white spots (middle) are
laser marks; non-perfused or ischemic retinal parts are vaporized
so that there is decreased demand for blood supply, resulting in
less neovascularization. After about 3 months, all that will be left
are scarred tissues (R). The macular area is spared (L), since the
area of most acute vision is the fovea. Areas between laser marks
are functional retina so vision is more or less preserved.
BLOOD DISTRURBANCES
POLYCYTHEMIA VERA
Figure 55. Engorged vessels seen in polycythemia vera
& Chronic clonal disorder characterized by elevated red
cell mass, normal arterial oxygen saturation,
leukocytosis, thrombocytosis and splenomegaly
& SSx due to slowing of blood flow and formation of
thrombosis as a result of increased viscosity.
& Dilation of retinal arteries and veins, hemorrhages,
microaneurysms, and areas of capillary closure
ANEMIA
Figure 56. Hemorrhages with Roth’s spots (light blue arrows) in
anemia
From the Internet:
• Roth’s spots – white centered hemorrhages that
probably reflect microinfarcts
• Common in anemia for uncertain reasons; theorized
to be due to hypoxia from the low oxygen-carrying
capacity of the blood, thus triggering small occlusions
Page 11 of 15
LEUKEMIA
Figure 57. Orbital involvement in Acute Myelogenous Leukemia
(AML)
From Bidar et al, 2007, Ophthal Plast & Reconstr Surg:
• Occur most commonly in the first decade of life
• Painful proptosis and limitied ocular motility;
homogenous masses along the orbital walls
NUTRITIONAL DEFICIENCIES
VITAMIN A DEFICIENCY
Figure 58. Bitot’s spot (demarcated by the black circle). White
keratinized conjunctiva surrounded by areas with vasculature
Figure 59. Xerophthalmia. Severe dryness with loss of
“shimmer” of the cornea
QUESTIONS RAISED IN CLASS
Difference between exophthalmos and proptosis:
• Proptosis – more generalized term to describe
forward protrusion of the eyeball e.g. when there is a
tumor behind the eyes
• Exophthalmos – specific for Grave’s disease
Difference between Xerophthalmia and Dry eye syndrome:
• Xerophthalmia – more severe presentation where
you don’t see the normal shimmer of the cornea
• Dry eye syndrome – patient will complain of
symptoms but the eye still looks well
OPHTHA Systemic Ophthalmology
Use of Vitrectomy
• Removal of the vitreous layer is only indicated, i.e. in
cases of endophthalmitis, when the patient reaches a
certain visual acuity score; otherwise do a
conservative management (intravitreal injections, IV
or oral medications)
o Intravitreal injections are used even in the
setting of infection because the vitreous
cavity is conducive for bacterial growth and
you want to directly treat it. Because there is
still the posterior capsule separating the
anterior chamber from the posterior chamber,
oral or IV medications may not be as
effective in reaching the vitreous cavity
hence direct injections are done.
• Vitrectomy may also be performed to treat advanced
(proliferative) stages of DM retinopathy in order to
clear the hemorrhage and fibrotic tissue so retinal
detachment will not occur. Thereafter, you can still
administer the anti-VEGF injections.
o Remember that anti-VEGF is more
recommended during the earlier stages
(when there is only macular edema), but it
may also be used as post-operative
treatment for proliferative cases
Limit to amount of retinal tissue targeted in PRP
• In the beginning, keep about 50% then you can do
another round of PRP on the same area or just
adjacent to it
• If the disease is still progressive, it may be more
prudent to take out the majority of retina and only
spare the macula
• In terms of number of spots, approximately 2000 is
used, but it also depends on the spot size
o Formerly marked one by one in the retina;
nowadays the newer lasers that are used in
SLMC can make patterns where 25 shots
can be done in one hitting, which can cut the
operative time by more than half
Diagnostic Procedures
• History and fluorescein angiography – for diagnosis of
DM retinopathy
• Gram stain and culture – in cases of cornea ulcer and
before starting antibiotic therapy, do scraping first
Reminder from Dr. Verzosa: DM retinopathy is probably most
common cause of retinal disorders, so advise your relatives
who have DM to have their eyes checked twice a year.
END OF TRANS.
References:
• Lecture
• Powerpoint slides
• Vaughan & Asbury’s General Ophthalmology
• Bidar M et al. Clinical and imaging characteristics of
orbital leukemic tumors. Ophthal Plast & Reconstr
Surg. 2007 Mar-Apr;23(2):87-93. (supplemental info
for leukemia)
• Sivaraj RR et al. Ocular Manifestations of systemic
lupus erythemtosus. Rheumatology. 2007;
46(12):1757-1762 (supplemental info for lupus)
• Other internet sources (Medscape, Wikipedia)
Page 12 of 15
 SUMMARY

INFLAMMATORY - INFECTIOUS
Disease Presentation Cause/Important Characteristic Treatment
Staphylococcal Burning, itching, foreign body (FB) Warm compress, lid shampoo, lid
Anterior sensation, red eyes, red lids scrubbing with antibiotic ointments
Blepharitis

Hordeolum/Stye Lid swelling, pain, tenderness, FB Infection of hair follicle and/or Spontaneous resolution, warm
sensation gland of Zeis compress, antibiotic (and steroid)
ointments, oral antibiotics, incision and
curettage (I & C)
Chalazion Lid mass usually painless Painless granuloma of the Incision and curettage, systemic
meibomian glands antibiotics (Tetracycline group)
Dacryocystitis • Mass near the nasal area, Infection of the lacrimal sac Oral antibiotics, dacryocystorhinostomy
periorbital cellulitis,
tearing/discharge
• Epiphora, swelling lacrimal
sac
Preseptal and Lid swelling, pain, discharge Due to Staph. epidermidis Oral antibiotics, intravenous antibiotics,
Orbital Cellulitis topical antibiotics/steroids, oral anti-
inflammatory agents

Staphylococcal Pain, swelling, blurring of vision Occurs post surgery Oral, IV, intravitreal antibiotics,
Endophthalmitis vitrectomy, topical and intravitreal
steroids
Streptococcal FB sensation, eye redness, Associated with contact lens use Topical antibiotics, cycloplegics, topical
Keratitis blurring of vision steroids to control uveitis

Gonococcal Mucopurulent discharge Neisseria gonorrheae infection Topical, oral , IV antibiotics

Conjunctivitis

Chlamydia Chronic red eyes, non-purulent Common in the younger • Single dose Azithromycin,
Conjunctivitis discharge, not responsive to population Doxycycline, Erythromycin,
eyedrops Ofloxacin
• Plus topical Moxifloxacin or
Gatifloxacin, Erythromycin
Trachoma Produced by scarring due to Oral Tetracycline, Doxycycline,
prolonged inflammation of the Erythromycin, Azithromycintrac
lids and conjunctiva
TB Uveitis Red eye, hypopyon (uveitic in Tuberculous choroidal granuloma Refer to pulmonologist
nature)
Leprosy Caused by Mycobacterium • Rifampicin, Dapsone, and
Cataract and leprae Clofazimin
Corneal Scarring • Cataract surgery, Corneal
transplant

Adenovirus Red eye, watery discharge, itching • Transfer through fomites
(Viral and burning, lid swelling • Pharyngoconjunctival Fever
Conjunctivitis) (PCF) – serotypes 3 and 7
• Epidemic
Keratoconjunctivitis (EKC)
– serotypes 8 and 19
• Supportive management
• Avoid rubbing eyes and sharing
personal items; observe frequent
handwashing

Herpes Simplex • Dendritic corneal ulcer HSV 1 infection • Oral and topical Acyclovir
Virus • Extraocular symptom: cold • NO STEROIDS
sore on the lips
Herpes Zoster Periorbital rash, conjunctivitis, Reactivation chicken pox (HHV3) • Oral and topical acyclovir
Ophthalmicus keratitis, episcleritis, uveitis • Steroids may be given (in drops)

Rubella (German Congenital cataract and retinitis Cataract should be removed before 3
Measles) months of age
Cytomegalovirus Retinitis and venous sheathing on Intravenous antivirals (gancyclovir)
in AIDS fundoscopy
Toxocara canis • Severe blurring of vision (e.g. Visceral larva migrans • Steroids or vitrectomy
20/200) • Poor prognosis in most cases
• Scarring or granuloma
formation in the macula
Toxoplasmosis Focal choroidtis, posterior uveitis, Intracellular protozoan, cats as Steroids, Clindamycin, Cotrimoxazole,
chorioretinitis definitive host lasers, cryotherapy, vitrectomy

Lice Itching, blepharitis Demodex spp Cut off lashes one by one

Keratomycosis • Usually caused by an Treatment with systemic and topical

agricultural ocular injury antifungals
• Aspergillus or Fusarium
species

OPHTHA Systemic Ophthalmology Page 13 of 15

 
Fungal Orbital • More severe presentation than
Cellulitis keratomycosis; with abscess
and discharge
• Whole orbit is affected

 
INFLAMMATORY – NON-INFECTIOUS
Disease Presentation Cause/Important Characteristic Treatment
Rheumatoid Common associated systemic More common in women Treatment: topical NSAIDs, steroids
Arthritis disease causing scleritis

Scleromalacia perforans Thinning of sclera and Put patch of donor sclera

perforation
Ankylosing • Chronic, idiopathic, • More common in males, 16- Steroids, cycloplegics
Spondylitis inflammatory arthritis 40 years old
• Acute iritis as ocular • Positive for HLA-B27
manifestation

Stevens- • Severe mucocutaneous, • Primarily occurs in young Steroids, tear supplements, punctal
Johnson vesiculobullous disease healthy individuals occlusion
Syndrome • Poor tear function, scarring of • Common cause is a
the conjunctiva hypersensitivity reaction to
drugs (allopurinol, sulfadrugs
[Cotrimoxazole], penicillin,
dilantin, NSAIDs)

Lupus Cotton wool spot and hemorrhage Oral steroids

 
NON-INFLAMMATORY
Disease Presentation Cause/Important Characteristic Treatment
Cardiovascular
Capillary May cause lazy eye or amblyopia • Await spontaneous regression in
Hemangiomas most cases
• Treat if sight threatening (before 8
years old)
• Intra-lesional / systemic steroids,
pulsed dye laser treatment,
propanolol
Retinal Present as either cavernous or No treatment required
Hemangiomas racemose

Hypertensive • Grade 1: Mild arteriolar

Retinopathy attenuation
• Grade 2: More severe
arteriolar constriction, vein
deflection at AV crossings
• Grade 3: Copper wiring of
arterioles, flame shaped
hemorrhages, cotton wool
spots and hard exudates
• Grade 4: Grade 3 + silver
wiring of arterioles and disc
swelling

Endocrine
Grave’s Disease • Hypertrophy of extraocular o Autoimmmune disorder
muscles caused by excess secretion
• Proliferation of orbital fat of thyroid hormones
• Cellular infiltration of interstitial o Women more than men;
tissue with lymphocytes, 8:1 ratio
plasma cells, macrophages
and mast cells
• Classification:
o Eyelid retraction
(Dalrymple’s sign, Von
Graefe’s sign, Kocher’s
sign)
o Soft tissue involvement
(Chemosis)
o Proptosis
o Optic neuropathy
o Restrictive Myopathy
(Inferior > Medial >
Superior > Lateral)

 
OPHTHA Systemic Ophthalmology Page 14 of 15
 
 Disease Presentation Cause/Important Characteristic Treatment
Diabetic • Retinal ischemia and hypoxia Due to microangiopathy affecting • Panretinal photocoagulation (PRP)
Retinopathy causing intraretinal retinal precapillary arterioles, – former gold standard
microvascular abnormalities capillaries, and venules • Anti VEGF intravitreal injections –
(IRMA) and more commonly used nowadays
neovascularization • Argon laser
• Stages:
o Background –
microaneurysms,
hemorrhages, hard
exudates, retinal edema
o Pre proliferative –
ischemic changes;
vascular changes, dark
blot hemorrhages, cotton
wool spots
o Proliferative –
neovascularization,
vitreous hemorrhage and
fibrosis

Blood Disturbances
Polycythemia Engorged vessels
vera

Anemia Hemorrhages with Roth’s spots

Leukemia Orbital involvement in AML

Nutritional
Vitamin A Bitot’s spot - white keratinized
Deficiency conjunctiva

Xerophthalmia - severe dryness

with loss of “shimmer” of the
cornea
 

OPHTHA Systemic Ophthalmology Page 15 of 15

 
   OPHTHALMOLOGY LEC
Ocular Trauma and Emergencies 02
  Tin Cruz  09194136152
6TH PERIODICAL Dr. Versoza
Monday, February 11, 2014
TP15
Pia Sandoval 09064077352

OUTLINE: conjunction with a slit lamp or

• Introduction operating microscope to gain a view
o Statistics of the iridocorneal angle, or the
o History anatomical angle formed between
o PE the eye's cornea and iris.
o Diagnostics § The importance of this process is in
• Ocular Emergencies diagnosing and monitoring various
o Acute angle closure glaucoma eye conditions associated with
o Retinal detachment glaucoma. (web)
o Foreign body • Fundoscopic Exam
o Lid lacerations, corneal abrasions, o Intraocular foreign body
lacerations, ulcers o Vitreous hemorrhage
o Chemical injuries o Retinal detachment or tears
o CRAO
o Blunt trauma Diagnostics
o Penetrating injuries • B-scan ultrasound
*Exam will be lecture-based according to Doc Versoza. o A diagnostic test used in optometry and
ophthalmology to produce a two-dimensional,
INTRODUCTION cross-sectional view of the eye and the orbit.
Statistics and Demographics It is otherwise called brightness scan (web)
nd o Opaque media
• 2 leading cause of visual impairment in US
o Minimal globe pressure
• 2.4 million eye injuries in the US annually
o Defer if obvious rupture
• 1 million permanently visually impaired
• CT scan
• Males have 9 times greater risk o Axial and coronal cuts
• Primary age under 30 years old o Bones and IOFB
• 16% injuries work related • MRI
• 95% male o Good for wood and plastic
• Construction is leading reported occupation o Poor for bone and metal
• Many injuries preventable o Contraindicated with metallic IOFB
• 78% did not wear protective eye gear
OCULAR EMERGENCIES
History A. Acute angle closure glaucoma
• How did the injury occur? B. Retinal detachment
• When did the injury occur? C. Foreign body
• Work-related? D. Lid lacerations, corneal abrasions, lacerations, ulcers
• Protective eye gear? E. Chemical injuries
• Emergency measures taken? F. CRAO
• Globe rupture possible? Intraocular foreign body? G. Blunt trauma
• When did patient last eat? H. Penetrating injuries
o In many cases, patient may be required to
be under general anesthesia. Gastric ACUTE ANGLE CLOSURE GLAUCOMA
contents may cause aspiration. Local • Not necessarily an injury but an ocular emergency
anesthesia (retrobulbar) may reduce the • History: Acute onset, higher risk in far-sighted
pressure and increase bleeding or allow the • Symptoms:
eye contents to come out. If the patient is o Pain
awake, blood pressure and intraocular o Halos (around lights)
pressure may go up (Normal IOP: 10-21 o Decreased vision
mmHg) and cause vessel rupture and o Nausea/vomiting – because of the pain
pushing out of eye contents.
• Signs:
o Conjunctival injection
Physical Examination
o Corneal edema
• Examine both eyes o Mid-dilated, fixed pupil
• Caution during exam o Increased IOP (usually 50s and 60s)
• Visual acuity – to determine deterioration
• APD
• External exam
• Orbit or facial bony abnormalities
• Crepitus
• Entry wounds
• Hypoesthesia
• EOMs
• Slit Lamp Exam
o Entry wound
o Conjunctiva, sclera, cornea
o Hyphema – blood in the anterior chamber Figure 1. Cornea is normally crystal clear unlike in these
o Cells & flare photos. Pupillary action is also slower and weaker.
o Iris damage
o Cataract • Aqueous humor produced by ciliary body, enters the
o IOP anterior chamber, drains via the trabecular meshwork
o Gonioscopy – skip if globe rupture is at angle to enter canal of Schlemm
suspected
§ Describes the use of a goniolens
(also known as a gonioscope) in
OPHTHA Ocular Trauma and Emergencies Page 1 of 12
   
 • In acute angle closure glaucoma (AACG), the iris
obstructs the trabecular meshwork by closing off the
angle
• Optic nerve damage secondary to increased
intraocular pressure

Figure 4. Laser beam applied to iris to create a small hole to

allow flow of aqueous humor. It’s like making a bypass. It
doesn’t have to pass the pupil anymore. Before the advent of
lasers, we do it surgically. (google image)

o Trabeculectomy
§ In most cases, we still end up with
Figure 2. Normal anatomy doing a trabeculectomy which is
making a new hole through the
sclera. It’s also like a bypass
procedure.

Figure 3:Left – Normal flow of aqueous humor. (Google image)

Right – In acute angle closure glaucoma, the iris sticks to the
trabecular meshwork so the angle closes and the fluid cannot
go through anymore and pressure increases. In other cases,
what happens is a pupillary block, such as in advanced
cataract where the anterior-posterior diameter of the lens can
increase, it can block the flow of aqueous humor through the
pupil causing build up in the posterior area. This will push the
iris forward. At pressures 60 to 70mmHg, complete vision loss
would ensue within one month. At 20mmHg, it will take a few
years before vision is gone.

• Medical Treatment
o Reduce production of aqueous humor
§ Topical beta-blocker (timolol 0.5% -
1- 2 gtt)
§ Carbonic anhydrase inhibitor
(acetazolamide 500mg iv or po)
§ Systemic osmotic agent (mannitol
1-2 g/Kg IV over 45 min)
o Or increase outflow
§ Topical apha-agonist Figure 5. Trabeculectomy. A glaucoma filtration procedure.
(phenylephrine 1 gtt) (google image)
§ Miotics (pilocarpine 1-2%)
o We usually also give an anti-inflammatory RETINAL DETACHMENT
§ Topical steroid (prednisolone • Signs and symptoms
acetate 1%), 1 gtt Q15-30 min x 4, o “curtain coming down (or from the side) over
then Q1H visual field”
o Question from the class: Why are alpha o bright flashes of light (photopsia)
agonists given when they can cause o increasing floaters
mydriasis which is contraindicated in acute o decreased visual acuity
open angle glaucoma? Answer: A mydriatic o distortion of objects (metamorphopsia)
may be given only in cases of pupillary block o +APD (afferent papillary defect) on exam.
to increase the pupillary diameter resulting in • Risk factors
increased outflow. It can also increase o Increasing age
uveoscleral outflow. o History of posterior vitreous detachment
o Myopia (nearsightedness) – because they
• Surgical Treatment have long eyeballs that grow longer through
o Laser peripheral iridectomy time. Since the retina does not change in
size, the tendency is that it is just stretched
and stretched, eventually causing it to break
at about grade -5.
o Trauma
o Diabetic retinopathy
o Family History
OPHTHA Ocular Trauma and Emergencies Page 2 of 12
   
 o Cataract surgery CORNEAL FOREIGN BODIES
• Diagnosis • Signs and symptoms: foreign body sensation, tearing,
o Direct ophthalmoscopy red, or painful eye. Pain often relieved with the
§ Direct ophthalmoscopy is not very instillation of anesthetic drops.
effective at visualizing periphery • Most common case you’ll see here in the Philippines
where most RD’s occur. would be people who are grinding or hammering.
§ Instead of ROR, the reflex is gray Thus, it’s important to were protective eyewear.
on the affected area.
o Indirect ophthalmoscope – especially if the
lesion is peripheral
• Treatment
o Scleral buckling
§ A scleral buckle is performed for
retinal detachment to reestablish
the geometric proximity of
separated layers in the retina. (web)

Figure 6. A scleral buckle is a piece of silicone sponge, rubber,

or semi-hard plastic. In scleral buckling surgery, the buckle is Figure 8. Slit lamp or Loupe (magnifier) is needed to remove,
placed against the outer surface of the eye and sewn onto the or a microscope if you’re in the operating room.
eye to keep it in place. The buckle pushes the sclera toward
the middle of the eye, relieving the pull on the retina and
allowing the tear to settle against the wall of the eye. (web)

o Vitrectomy, GFX (gas-fluid exchange), Laser

Photocoagulation
§ Vitrectomy is the surgical removal
of the vitreous gel from the middle
of the eye camera. It provides
better access to the back of the eye.
(web)
§ GFX - injection of air into the eye to Figure 9. Linear epithelial defects suggestive of foreign body
remove the intraocular fluid from (FB) under the eye lid. A glass FB would be difficult to visualize.
the posterior segment of the globe
while maintaining intraocular Management
pressure to temporarily hold the • Anesthetize eye
retina in place or seal off holes in • Remove FB
the retina. (web) o Cotton swab (Don’t use if FB is embedded
§ Laser photocoagulation - burns because it will not work and just worsen the
small areas of the retina and the abrasion!)
abnormal blood vessels beneath o Kimura spatula
the macula forming scar tissue that o +/- needle tip of a tuberculin syringe
seals the blood vessels, keeping • Antibiotic drops and +/- patch
them from leaking under the macula. • 1-2 day follow-up with eye doc. (Usually, the
(web) epithelium would have healed by that time.)
o Prognosis is dependent on how soon
intervention (e.g. surgery) is performed.
Remember that the retina gets its blood
supply from the choroid. Thus, if it is
detached, it will slowly become non-
functional.

Figure 10. Equipment for corneal foreign body removal

Figure 7. Retinal Detachment (Left – Retina shows a tear in

which fluid may accumulate and cause retinal detachment.
Right – The only normal retinal is the central dark brown area.)

OPHTHA Ocular Trauma and Emergencies Page 3 of 12

 
 

Figure 11. Not like this. You may puncture the eyeball in case
the patient moves.
Figure 12. A rust ring may appear a day after FB removal. You
also have to take this off because this also has iron in it.
Figure 13. Burr, a diamond-tipped equipment. Correct way of
holding the instrument. Reminder: Limit depth near the pupil
(Center: ~0.3 to 0.5mm, Periphery ~1mm)
INTRAOCULAR FOREIGN BODIES (IOFBs)
• Severe inflammatory reaction
o Magnetic: iron, steel
o Nonmagnetic: copper, plant matter
• Mild inflammatory reaction
o Magnetic: nickel
o Nonmagnetic: aluminum,mercury, zinc
• Inert foreign bodies
o carbon, coal, glass, lead
o plaster, platinum, porcelain,
o rubber, silver, stone, brass
Figure 14. IOFBs (intraocular FB, specifically in the retina). The
right has a worsening reaction because the FB wasn’t removed
immediately.
• Determine visual acuity
• Examine for global integrity and degree of damage
• Do fundus examination
• Place shield (not patch) over eye
o If you think there is globe rupture or a risk of
it, don’t put an eye patch because it will just
increase the pressure in the eye and cause
the release of its contents. Just put a shield
OPHTHA Ocular Trauma and Emergencies
so that the patient will not be able to rub the
eye.
• Refer to ophthalmologist
LID AND CONJUNCTIVAL LACERATION
Figure 15. Dog bite resulting in lacerations.
• When you repair lid lacerations, you have to do it
precisely and by layer. Start from inside but don’t
suture it through-and-through. Do not go through the
mucosa because you might abrade the cornea.
Tarsusà orbicularis muscleà skin.
CORNEAL INJURIES
Figure 16. Remember the 5 layers ABCDE (A-“a”pithelium, B-
Bowman’s layer, C-corneal stroma, D-Descemet’s membrane,
E-endothelium)
• Abrasions, lacerations, ulcers
• Symptoms:
o Tearing, foreign body sensation
o Extreme eye pain, relieved with lidocaine
drops.
o Visual acuity usually decreased, depending
on location of injury in relation to visual axis
(esp. if at the center).
o Inflammation leading to corneal edema can
decrease VA.
• Diagnosis: fluorescein staining to see epithelial
defect.
• Seidel’s test for aqueous leakage to diagnose
lacerations.
o If there is a puncture and you’re in doubt,
you perform this test. This also makes use of
fluorescein stain. If you see a little river, then
it means there is aqueous leakage.
o A fluorescein strip containing 10%
fluorescein is applied topically to the affected
area and is examined with a cobalt blue filter.
At this point, the fluorescein appears green
in color. Any changes in color or surface of
the fluorescence area indicate the presence
of corneal leakage.(web)
• Common cases include injury by fingernail or pages
of a magazine. Usually, it just involves the epithelium.
If the abrasion is deeper, such as involving the
Bowman’s layer or the stroma, the erosions may be
recurrent. The epithelium is attached to the Bowman’s
layer, thus, when the Bowman’s layer is damaged,
even though the epithelium grows over, eventually it
will slough off because it does not have a good
foundation or basement membrane.
Page 4 of 12
 Figure 22.Seidel’s test. Use concentrated fluorescein
Figure 17. Corneal Abrasion.

Figure 18. Stain with fluorescein (L) and illuminate with cobalt
blue fluorescent light (R) to effectively see corneal epithelial Figure 23. Positive Seidel’s Test. Left is a pinpoint leak. Right
defects. is leaking filtering bleb.

Figure 19. Corneal abrasions

Figure 24. Penetrating corneal injury. Pupil shape is the clue.

The reason for the change in pupil shape is a portion of the iris
sticking out at the side of the pupil (red circles).

Figure 20. Fingernail damage

Figure 25. Fishing hook injury

Figure 21. Thorn puncture (Perforated or not? If in doubt, do

the Seidel’s Test.)

Figure 26. Sutured corneal laceration. Sutures used in the

10
cornea is 10-O. It is comparable to (½) of a 1-O suture or
th
1/7 of a hair strand.
OPHTHA Ocular Trauma and Emergencies Page 5 of 12
   
 CHEMICAL INJURIES
• Emergency!!! - Every minute counts
• Do not waste time on history and physical exam.
Rinse quickly!
• Alkali burns are more common and worse than
acid
• ALKALI
o Saponification – denatures collagen
o Household cleaners, fertilizers, drain
cleaners. The most dangerous household
agent is liquid sosa.
o Common cases involve workers in bottling
Figure 27. Iridodialysis (Internet: localized separation or tearing companies/factories because they usually
away of the iris from its attachment to the ciliary body.) use alkali in cleaning bottles.
• ACID
+
o Coagulation, H precipitates protein – barrier
o Industrial cleaners, batteries, vegetable
preservatives
• Management:
o Topical anesthetic
o Copious irrigation with BSS (balanced salt
solution), saline or Lactated ringers for at
least 30 minutes
o No neutralizing acidic or alkali solutions
o Irrigate until neutral pH
o Sweep fornices for retained material
Figure 28. L- Corneal puncture wound with abscess. § Once pH is stabilized, give the ff:
R- Treatment via conjunctival flap. Just release the • Cycloplegic – mydriatic; To
conjunctiva from the limbus and suture it to the cornea. We use prevent anterior chamber
the conjunctiva because it is highly vascular. We thus place it inflammatory reaction
over the affected area to take care of the abscess.
• Broad-spectrum antibiotic

Figure 33. Chemical injuries

Figure 29. 3 months after flap

Figure 30. Corneal ulcer Figure 34. Alkali Burn

CENTRAL RETINAL ARTERY OCCLUSION

• Narrow arterioles
• Optic disc and retinal pallor
• Cherry red spot at fovea (due to maintained perfusion
of cilio-retinal artery)
• Emboli seen – 20%

Figure 31. Corneal ulcer with hypopyon. Meaning, it is a

penetrating injury.

• Question from the class: How do you differentiate an

abscess from a hypopyon? Answer: A hypopyon has to
be located in the anterior chamber. Hypopyon may be
infectious or sterile. An abscess is due an infection. Figure 35. Pale retina with cherry red spot characteristic of
CRAO

OPHTHA Ocular Trauma and Emergencies Page 6 of 12

   
 • Etiology
o Emboli – cardiac, atherosclerotic, fat
o Vasculitis
o Coagulopathy
o Sickle cell

• Signs and Symptoms:

o Sudden onset severe monocular vision loss
over seconds
o It is painless, thus, patients may take it for
granted or delay consult and therefore it
results in irreversible vision loss.
o Usually preceded by amaurosis fugax
o 90% will have visual acuity of counting Figure 37. Subconjunctival hematoma
fingers or less If it’s massive, conjunctiva may bulge and it is now called a
o Dilate pupils immediately and perform hematoma. This may occur in patients taking aspirin and
fundoscopic exam anticoagulants because the bleeding won’t stop. Usually the
• Treatment increased pressure in the eye because the blood has nowhere
o Must have VERY high index of suspicion, to go causes the bleeding to stop.
especially in patients with appropriate risk
factors. Periorbital edema and Raccoon eye
§ Immediate referral to an
ophthalmologist. Retina can
become irreversibly damaged in
100 min.
§ Mannitol 0.25-2.0 g/kg IV or
acetazolamide 500 mg PO once to
reduce IOP.
§ Carbogen inhalation (95 percent
oxygen and 5 percent carbon
dioxide)
• Done by breathing into a
paper bag.
§ Oral nitrates – vasodilator
§ Lay the patient flat on his/her back
§ Massage orbit. This is thought to
help dislodge the clot from a larger
to smaller retinal artery branch, Figure 38. Periorbital hematoma/raccoon eye. Ask for history
minimizing area of visual loss. of blunt trauma such as a punch.
§ Ophthalmologist may perform
paracentesis of aqueous humor to Retrobulbar Hematoma
reduce IOP. • Acute orbital compartment syndrome 2° to blunt or
penetrating trauma
BLUNT TRAUMA • Hemorrhage into closed space of orbit, thus, the
• Subconjunctival hemorrhage / hematoma globe is pushed forward similar to exopthalmos of
• Periorbital hematoma Graves Disease.
• Retrobulbar hematoma • ↑ IOP leading to vision loss from optic nerve
• Globe rupture damage/compression or retinal ischemia
• Hyphema • Clinical diagnosis:
• Blow-out fractures o Ocular pain, APD, proptosis,
• Commotio retinae, Retinal tears/detachments ophthalmoplegia, diminished vision, ↑ IOP
• Glaucoma o Immediate lateral canthotomy and
• Cataract cantholysis indicated if IOP > 40mmHg or
• Dislocation of the lens vision loss

Subconjuctival Hemorrhage

Figure 39. Retrobulbar hematoma.

Figure 36. Subconjuctival hemorrhage

• In most cases, there are still areas that are white.

• Remember, in subconjunctival hemorrhage, there is a
vessel that ruptured, therefore, ask the patient for
history of trauma, straining (e.g. constipation),
hypertension or anything that involves Valsalva (e.g.
coughing, sneezing).
• Most important here is assurance. Tell the patient it’s
like a bruise under your conjunctiva. You don’t usually
do anything though you may put a warm compress. It
will usually regress in 1-2 weeks.

OPHTHA Ocular Trauma and Emergencies Page 7 of 12

 
 
Globe Rupture
Figure 40. Lens of the eye sticking out of the globe.
• If the vessels break under the retina, everything may
come out.
• This is a STAT OR. Make sure that the BP does not
increase. If only the lens is out and the retina is intact,
you can still save the eye.
Hyphema
• Rebleeding may happen in the first 5 days (critical
period) which is usually worse.
• Bedrest, avoid straining, coughing, sneezing
• Cycloplegics, topical steroids
• Monitor intraocular pressure
o RBC are relatively large particles to pass
through the trabecular meshwork. Thus,
tendency for blood is just to collect in the
anterior chamber and cause increased IOP.
• Common in badminton or tennis DOUBLES.
Figure 41.Top Left and Right.Grade 1. Bottom Left. Grade
2.Bottom Right. Grade 4
OPHTHA Ocular Trauma and Emergencies
Figure. Grading of hyphema (google image). According to Dr.
Versoza Grade 1 is below the pupil. Grade 2 starts from the
bottommost part of the pupil. Grade 3 is covering the upper
part of the pupil while Grade 4 is when you don’t see the iris
anymore.
Question from the class: In Grade 4 hyphema, how do we
manage the patient? Do we use cycloplegics only or do we
also aspirate? Answer: Most of the time, it’s just cycloplegics
then we observe daily if the blood subsides.Aspiration may be
considered in the absence of response to medical treatment.
However, if you try to aspirate, you are lowering the eye
pressure and chances are, you will have rebleeding.
Blowout Fracture with Muscle Entrapment
Figure 42. Orbital floor fracture. Observe sunken right eye.
Breakage of the inferior orbital wall resulting in the herniation of
the contents of the orbit into the maxillary sinus. The eyeball
will contract
Figure 43. Inferior rectus muscle entrapment of LEFT EYE
secondary to inferior orbital wall fracture. Patient will complain
of diplopia especially when looking upwards.
Page 8 of 12
 Optic Disc Hemorrhage

Figure 47: Optic disc Hemorrhage, not discussed

Retinal Tears
Figure 44. MRI blow out fracture. Blood and orbital contents fall
into the maxillary sinus.

Commotio Retinae
• Retinal edema from a counter coupe effect (pressure
transmitted to posterior portion of the globe)
• Decline in visual acuity

Figure 48. In most cases, tears are peripheral and occur in

shapes as shown above.

Figure 45. White spots. Secondary to blunt injury Retinal Detachment

Retinal Hemorrhage
• Vaughan and Asburys (not discussed): Result from
diapedeses from veins or capillaries, and the
morphologic appearances depend on the size, site,
and extent of damage to the vessel. May also be
caused by any condition that alters the integrity of the
endothelial cells:
o vessel wall disease (eg, hypertension,
diabetes)
o blood disorders (eg, leukemia, polycythemia)
o reduced perfusion (eg, carotid
artery/cavernous sinus fistula, acute blood
loss).
• Different types (Vaughan and Asburys, not
discussed):
o preretinal hemorrhages
o linear hemorrhages
o punctate hemorrhages
o subretinal hemorrhages Figure 49. Observe the retinal tear progressing to detachment.
o hemorrhages under the retinal pigment
epithelium
o white centered hemorrhages (Roth's spots)

Figure 46. Retinal Hemorrhage.

OPHTHA Ocular Trauma and Emergencies Page 9 of 12

   
Angle Recession Glaucoma Figure. Trauma can also dislocate the lens by breaking the
zonular fibers. Yellow arrows show the location of the zonular
fibers

PENETRATING INJURIES
• Penetrating trauma leads to corneal or scleral
disruption and extravasation of intraocular contents.
• Can lead to:
– Irreversible visual loss
– Endophthalmitis -inflammation of the
intraocular cavities

RUPTURED GLOBE MANAGEMENT

Figure 50. Normal anatomy
Patients who’ve had hyphema should be advised follow up
after 3 months and then monthly up to 6 months. This is
because blunt injury can cause the iris to move again further
down which can change the structure of the trabecular
meshwork. Outcome would be inefficient evacuation of
aqueous humor and consequently, increased IOP or glaucoma.
Treatment
• If pressure is not too high, give eye drops.
• If too high, surgery should be performed.
SYMPHATHETIC OPHTHALMIA
Traumatic Cataracts
• Stop the examination
• Cover with metal eye shield or styrofoam cup. DO
NOT PATCH.
• Refer to ophthalmology immediately
• Do not perform tonometry.
• CT head and orbit to evaluate for concomitant
facial/orbital injury.
• NPO – because patient will have to be under general
anaesthesia which requires minimum of 6-hour NPO
to prevent aspiration. Doing retrobulbar anaesthesia
will cause increased pressure inside the globe
resulting in worsening of globe rupture.
• Tetanus shot
• Antibiotics
• Antiemetics and analgesics decrease risk of Valsalva,
movement which could increase IOP and increase in
BP due to pain.
• Rare, granulomatous uveitis
• The ‘exciting’ (injured) eye becomes inflamed as does
the ‘sympathizing’(previously normal) eye.
• Auto immune reaction to the retinal S antigen
• When the uveal tract or retina is infected, the body
may produce antibodies against patient’s own uveal
tract or retina resulting in attack of normal cells.
• 0.2-0.5% post-open globe injury
• 10 days to decades post injury
• Examine ‘uninjured’ eye

END OF TRANS.

SUMMARY

OCULAR EMERGENCIES
Dislocation of the Lens/Ectopia Lentis A. Acute Angle Closure Glaucoma
• Ocular emergency
• History: Acute onset, higher risk in far-sighted
• Symptoms: Pain, halos, decreased vision, nausea
and vomiting
• Signs: Conjunctival injection, corneal edema, mid-
dilated fixed pupil, increased IPO
• Management:
o Reduce production of aqueous humor
§ Topical beta-blocker (timolol 0.5% -
1- 2 gtt)
§ Carbonic anhydrase inhibitor
(acetazolamide)
§ Systemic osmotic agent (mannitol
1-2 g/Kg IV over 45 min)
o Increase outflow
§ Topical alpha-agonist
(phenylephrine 1 gtt)
§ Miotics (pilocarpine 1-2%)
o Anti-inflammatory
§ Topical steroid (prednisolone
acetate 1%)
o SURGICAL: Laser peripheral iridectomy,
trabeculectomy

B. Retinal Detachment
• Signs and symptoms:
o curtain coming down (or from the side) over
visual field”
o bright flashes of light (photopsia)
o increasing floaters
o decreased visual acuity
OPHTHA Ocular Trauma and Emergencies Page 10 of 12
 
 o distortion of objects (metamorphopsia) G. Central Retinal Artery Occlusion
o +APD (afferent papillary defect) on exam. • Narrow arterioles, optic disc and retinal pallor
• Risk factors: • Cherry red spot at fovea (due to maintained perfusion
o increasing age of cilio-retinal artery)
o history of posterior vitreous detachment • Emboli seen – 20%
o myopia (nearsightedness) • Signs and symptoms
o trauma o Sudden onset severe monocular vision loss
o diabetic retinopathy over seconds
o family history o Usually preceded by amaurosis fugax
o cataract surgery o 90% will have visual acuity of counting
• Diagnostics: fingers or less
o Direct ophthalmoscopy o Dilate pupils immediately and perform
o Indirect ophthalmoscopy fundoscopic exam
• Management: • Treatment
o Scleral buckling o Immediate referral to an ophthalmologist.
o Vitrectomy Retina can become irreversibly damaged in
o Gas-fluid exchange 100 min.
o Lase photocoagulation o Mannitol 0.25-2.0 g/kg IV or acetazolamide
500 mg PO once to reduce IOP.
C. Corneal Foreign Bodies o Carbogen inhalation (95 percent oxygen and
• Signs and symptoms: 5 percent carbon dioxide)
o foreign body sensation o Oral nitrates
o tearing o Lay the patient flat on his/her back
o red o Massage orbit. This is thought to help
o painful eye dislodge the clot from a larger to smaller
§ Pain often relieved with the retinal artery branch, minimizing area of
instillation of anesthetic drops. visual loss.
• Risk factors: occupation (construction, etc) o Ophthalmologist may perform paracentesis
• Management of aqueous humor to reduce IOP.
o Anesthetize eye
o Remove FB H. Blunt Trauma
o Cotton swab (Don’t use if FB is embedded • Subconjunctival hemorrhage / hematoma
because it will not work and just worsen the o If massive, conjunctiva will bulge. This may
abrasion!) occur in patients taking aspirin and
o Kimura spatula anticoagulants.
o +/- needle tip of a tuberculin syringe • Periorbital hematoma – check history
o Antibiotic drops and +/- patch • Retrobulbar hematoma
o Acute orbital compartment syndrome 2° to
D. Intraocular Foreign Bodies blunt or penetrating trauma
• Severe inflammatory reaction o Hemorrhage into closed space of orbit
o Magnetic: iron, steel o ↑ IOP leading to vision loss from optic nerve
o Nonmagnetic: copper, plant matter damage / retinal ischemia
• Mild inflammatory reaction o Clinical diagnosis:
o Magnetic: nickel • Ocular pain, APD, proptosis,
o Nonmagnetic: aluminum, mercury, zinc ophthalmoplegia, diminished vision,
• Inert foreign bodies ↑ IOP
o carbon, coal, glass, lead • Immediate lateral canthotomy and
o plaster, platinum, porcelain, cantholysis indicated if IOP >
o rubber, silver, stone, brass 40mmHg or vision loss
• Management • Globe rupture
o Determine visual acuity o If the vessels break under the retina,
o Examine for global integrity and degree of everything may come out.
damage o This is a STAT OR. Make sure that the BP
o Do fundus examination does not increase. If only the lens is out and
o Place shield (not patch) over eye the retina is intact, you can still save the eye.
o Refer to ophthalmologist • Hyphema
o Rebleeding may happen in the first 5 days
E. Corneal Injuries which is usually worse
• Abrasions, lacerations, ulcers o Bedrest, avoid straining
• Symptoms: o Cycloplegics, topical steroids
o Extreme eye pain, relieved with lidocaine o Monitor intraocular pressure
drops. • Blow-out fractures
o Visual acuity usually decreased, depending • Commotio retinae, Retinal tears/detachments
on location of injury in relation to visual axis. o Retinal edema from a counter coupe effect
o Inflammation leading to corneal edema can (pressure transmitted to posterior portion of
decrease VA. the globe)
• Diagnosis: fluorescein staining to see epithelial defect. o Decline in visual acuity
• Seidel’s test for aqueous leakage to diagnose • Retinal Hemorrhage
lacerations. o Result from diapedeses from veins or
capillaries, and the morphologic
F. Chemical Injuries appearances depend on the size, site, and
• Emergency, do not prioritize history and PE extent of damage to the vessel. May also be
• Alkali worse than acid caused by any condition that alters the
o Alkali – saponification - denatures collagen integrity of the endothelial cells:
o Acid – coagulation, H+ precipitates protein – • Glaucoma
barrier o Patients who’ve had hyphema should be
• Management: Copious irrigation with BSS, saline or advised follow up after 3 months and then
LRS for at least 30 mins monthly up to 6 months.
o Sweep fornices for retained material once o This is because blunt injury can cause the
stabilized iris to move again further down which can

OPHTHA Ocular Trauma and Emergencies Page 11 of 12

 
 change the structure of the trabecular
meshwork.
o Outcome would be inefficient evacuation of
aqueous humor and consequently, increased
IOP or glaucoma.
o Treatment: eye drops/surgery
• Traumatic Cataract
• Dislocation of the lens

I. Penetrating Trauma
• Penetrating trauma leads to corneal or scleral
disruption and extravasation of intraocular contents.
• Can lead to:
o Irreversible visual loss
o Endophthalmitis -inflammation of the
intraocular cavities

RUPTURED GLOBE MANAGEMENT

• Stop the examination
• Cover with metal eye shield or styrofoam cup. DO
NOT PATCH.
• Refer to ophthalmology immediately
• Do not perform tonometry.
• CT head and orbit to evaluate for concomitant
facial/orbital injury.
• NPO
• Tetanus shot
• Antibiotics
• Antiemetics and analgesics

SYMPHATHETIC OPHTHALMIA
• Rare, granulomatous uveitis
• The ‘exciting’ (injured) eye becomes inflamed as does
the ‘sympathizing’(previously normal) eye.
• Auto immune reaction to the retinal S antigen
• 0.2-0.5% post-open globe injury
• 10 days to decades post injury
• Examine ‘uninjured’ eye

OPHTHA Ocular Trauma and Emergencies Page 12 of 12

 
   OPHTHALMOLOGY LEC
  The Pediatric Eye 03
6TH PERIODICAL Dr. Carlos Alberto
Monday, January 13, 2014
TP21
Belle Gavilan
Ogie Guerrero

OUTLINE:
I. The Pediatric Eye The American Academy of Opthalmology (AAO) gives
II. Amblyopia Preferred Practice Pattern for Pediatric Screening
III. Strabismus
IV. Retinoblastoma
V. Retinopathy of Prematurity

The Pediatric Eye

Normal Full Term Infant

• At birth the eye is ¾ that of adult size
• Postnatal growth is maximal within the first year and
rd
then decelerates until 3 year, continuing at a much
slower rate until puberty
• Anterior segment is relatively large at birth and growth
results in a more spherical eye
• Sclera is thin and translucent
• Cornea is relatively large (10mm) and attains adult size
by 2 years (12mm)
• Len is spherical compared to an adult (compensates for
the shortness)
• Fundus is less pigmented and the choroidal vasculature This is not really elaborated by Doc but he emphasized the text
is visible; at 4-6 months it nearly approximates the on the red circle: At 6 months to 1 year of age, referral to an
mature eye. ophthalmologist is recommended if an infant fails to object
equally to covering each eye in an alternate occlusion
screening test. Normal infant should be bothered when one
eye is being covered. If he is not bothered at all, then it is
abnormal.

Amblyopia

• Amblyopia is reduced visual acuity as a result of

Normal newborn fundus
• Earliest response to formed visual stimuli is the infant’s
regard for the mother’s face evident during feeding
• 2 weeks of age -- sustained interest in large objects
• 8-10 weeks – can follow an object 180 degrees
• 4-6 months – eye movements are coordinated and any
deviations should be examined
Developmental Milestones at 3 Months
• Watches faces intently
• Follows moving objects
• Recognizes familiar objects and people at a distance
• Starts using hands and eyes in coordination
Developmental Milestones at 6 Months
• Reaches for and grasps objects
o Depth perception (binocular vision)
• Develops full color vision
o Attracted to different colors and can tell them
apart
• Distance vision matures
• Ability to track moving objects improve
Common Problems (referred to the eye specialist by the
pediatrician or mother; these are usually the CC)
• Visual inattentiveness
o Learning or behavior deficits
• Leukocoria (white pupil reflex due to opacities of the
ocular media)
o Congenital cataract
o ROB (retinoblastoma)
o ROP (retinopathy of prematurity)
• Strabismus
defective central visual processing. It is a functional
disorder of visual development that is caused by an
optical, physical, or ocular alignment defect during early
childhood.
Basically it is a decrease in vision in an otherwise normal
eye that can be caused by an undetected problem during
early childhood.
• A decrease of vision, either unilaterally or bilaterally, for
which no cause can be found by physical examination of
the eye.
“Vision is learned”
Although the ocular system is well developed at 3 years of age,
the visual response is not.
• Develop from birth to age 9 years
• Most rapid progression – infancy
• Neuronal connections between the retina and visual
cortex are still developing
“For a limited time only”
• Visual problem during this critical period (eg. EORs,
strabismus) can mess up this developmental wiring
• The potential for amblyopia – age 9 years
o Plasticity of the visual pathways ceases after 9.
After this age, what you get is a permanent eye
problem
“Competitive Wiring”
• Use it or lose it
• The afferent nerve connections of the strong eye
become numerous while the weak (unused eye) nerves
atrophy and decrease in number
o Loss and atrophy of cells in the LGN (lateral
geniculate nucleus) associated with that eye
Causes of Amblyopia
Basically anything that interferes in the ability to see very well
• Pattern deprivation
o Media opacities such as a dense cataract,
uncorrected aphakia, severe blepharoptosis or a
dense corneal opacity

OPHTHA The Pediatric Eye Page 1 of 10

   
 • Optical defocus
o May be the result of a reflective error that
selectively removes fine details
§ Uni or bilateral, anisometropia
o Lid problems like hemangioma – astigmatism
o Irregular cornea or subluxated lens
• Strabismus or the misaligned eye

Errors of Refraction (EOR) in Children

• Newborns average 3 diopters (eye grade of +300) of
hyperopia
o May increase slightly in the first few months, but
then declines
o Average of 1 diopter of hyperopia by 1 year of
age
• Onset of myopia – 6-12 years
o Rate of progression is approximately 0.5 diopters
per year
o Normal eye = 0 diopters
• Not all EORs are at risk for the development of
amblyopia

Potential Amblyogenic Refractive Errors Warranting

Optical Correction or Monitoring in Infants and Young
Children
Condition Diopters
Isometropia (similar
refractive error both eyes)
Astigmatism ≥2.5
Hyperopia ≥4.5
Anisometropia (unequal
refractive error of eyes)
Astigmatism ≥1.5
Hyperopia ≥1.5
Myopia ≥3
In isometriopa, there is a risk for amblyopia if the grade of
the eye with astigmatism is equal or more than 2.5 or 250,
while risk for amblyopia with a hyperopic eye occurs when
the grade is 450 or more. In anisometria, if one eye has an
astigmatism of 150, (or has hyperopia of 150, or myopia of
300) and has a normal grade on the other eye, then the
affected eye has high risk for amblyopia.

Amblyoia and Strabismus

• Unilateral amblyopia is associated with strabismus in
50% of cases
• Amblyopia is a risk factor for the development of
strabismus and reduced binocularity, and strabismus is
a risk factor for the development of amblyopia

Other Risk Factors for Amblyopia

• Prematurity
• Developmental delay
• Family history (very significant!)
Prevalence Estimates: 1% to 5%

“Early diagnosis and management is best”

• The progression of amblyopia in early childhood is
inversely proportional to the child’s age – the younger
the child, the faster the progression
• The reversibility of the visual deficit is likewise inversely
Duction and Versions
proportional to the child’s age – younger children
• Duction – monocular rotations with no consideration
respond more rapidly and more completely to
of the position of the other eye
treatment so early detection is important!
o Adduction – inward rotation (Ad-in)
o Abduction – outward rotation (Ab-out)
Strabismus o Elevation or Supraduction (sursumduction) –
upward rotation
o Depression or Infraduction (deorsumduction)
– downward rotation
o Excycloduction (extorsion) – rotation of the
upper pole of the cornea templeward
o Incycloduction (intorsion) – rotation of the
upper pole of the cornea nasalward

OPHTHA The Pediatric Eye Page 2 of 10

 
 

• Version – movements of both eyes in the same
direction (eg, right gaze in which both eyes move to
the right)
Yoke Muscles
• Yoke muscles are the primary muscles in each eye
that accomplish a given version.
• Muscles that function together in a particular version
Fusion
What the alignment of the eye tries to accomplish is fusion.
And ultimately, binocular fusion. Fusion is formation of one
image from the two different images seen by the left and right
eye.
• Fusion – formation of one image from the two images
seen simultaneously by the two eyes
o Motor fusion (EOM control) – your eyeballs
have to work together to look at an object
(although from slightly different angle) so
that your brain can bring these images
together
o Sensory fusion (visual sensory integration of
the brain)
o Motor fusion is a prerequisite for sensory
fusion, but complete sensory fusion does
not always follow motor fusion. Seen usually
after strabismus surgery immediately post op
where patient initially complain of diplopia
because the sensory function has not yet
accommodated the new images that the
eyeball is seeing.
• With the successful binocular fusion – stereopsis
(the visual perception of depth)
Ocular Motility – Strabismus
• Under normal conditions, the image of the object of
regards falls simultaneously on the fovea of each eye,
when the eyes are in perfect alignment
• Any deviation from the perfect ocular alignment is
known as strabismus
OPHTHA The Pediatric Eye
Heteropia/Strabismus
• Manifest (can be readily seen or obvious) deviation
of the eyes that cannot be controlled by binocular
vision
o Esotropia – convergent manifest deviation
o Exotropia – divergent manifest deviation
o Hypertropia – manifest deviation of one eye
upward
o Hypotropia – manifest deviation of one eye
downward
Heterophoria
• Latent (able to maintain alignment initially but later on
deviates) deviation of the eyes held straight by
binocular vision
o Esophoria – tendency to turn inward
o Exophoria – tendency to turn outward
o Hyperphoria – tendency to deviate upward
o Hypophoria – tendency to deviate downward
Definitions of Other Terms (BE FAMILIAR WITH THESE
TERMS)
• Orthophoria – absence of any tendency of either eye
to deviate when fusion is suspended
• Prism Diopter – a unit of angular measurement used
to characterize ocular deviations (in percentiles)
• Torsion – rotation of the eye about its anteroposterior
axis
o Intorsion – 12 oclock meridian (the top of
conea) turing toward the midline
o Extorsion – 12 oclock meridian turning away
from midline
• Conjugate Movement – movement of the two eyes in
the same direction at the same time
• Vergence – movement of the two eyes in opposite
directions
o Convergence – the eyes turn inwards
o Divergence – the eyes turn outwards
Agonist, Synergist, and Antagonist EOMs
• Primary muscles that move an eye in a given direction
– agonist
• Muscle in the same eye same direction as the agonist
– synergist
• Muscles in the same eye opposite direction of agonist
– antagonist
• Example: ABDUCTION of the RIGHT eye
o Right lateral rectus muscles is the agonist
o Right superior and inferior oblique muscles
are the synergists
o Right medial, superior, and inferior recti are
the antagonists
• Sherrington’s Law states that an increased
innervations to any muscle (agonist) is accompanied
by a corresponding decrease in innervations to its
antagonists
o The antagonist relaxes as the agonist
contracts
o eg. The right eye’s right gaze would involve
a contraction of the right lateral rectus and a
relaxation of the right medial rectus
Strabismus Symptoms
• “Crossed eyes” or “walled eyes” (duling in Filipino
whether inward or outward)
• Learning/reading difficulties (amblyopia)
• Head tilt, turn, chin up, or chin down
Strabismus History
• Family history
• Age at onset (always important!)
• Type of onset (gradual, sudden, intermittent)
• Types of deviation (comitant or incomitant)
• Fixation (one eye or alternating)
Ocular Examination
• Visual acuity adapted for age
• Determination of refractive error
• Inspection
• Test for EOM function – 6 cardinal gazes
Page 3 of 10
Examination Specific for Ocular Motility Cover Test: Tropias
• Gaze positions – primary position and cardinal
positions
• Hirschberg Test (Corneal Reflex Test)
• Cover Test – Uncover Test
• Alternate Cover Test
• Krimsky Test
• Convergence Measurement
• Prism plus Cover Test
• Maddox Rod Test

Hirschberg test – looks for manifest deviations

Cover/Uncover test – looks for manifest deviations
Alternate cover test – looks for latent deviations

Hirschberg Test – Use your penlight to look for the corneal

reflex

Right eye shows esotropia. When you cover the left

eye, the right eye (abnormal) moves outwards to
fixate and reflex is centered; however on uncovering
the left eye, the abnormal right eye reverts back to
esotropia.

Alternate Cover Test (Eyes are initially aligned normally.

Hirschberg corneal reflex test – varying degrees of
esotropia show the corneal reflex becoming
progressively more temporal
Different tropias seen in Hirschberg test
Cover/Uncover Test
• The patient is asked to fix on a target
• The occlude is introduced over one eye
• Look at the uncovered eye
o Note any movement to take up fixation
(telling you that the eye has a manifest
deviation)
o Note the size, direction, and speed of
movement
o Note any nystagmus
• Repeat with the other eye
Then you break the fusion of the patient’s eyes by covering
one eye.)
• The patient is asked to fix on a target
• One eye is covered with the occluder
• The occluder is then switched to the other eye,
making sure that one eye is kept occluded at all times.
This way, the patient is not allowed to fuse and have
binocular vision
• This is repeated several times to fully dissociate
the two eyes
• Look at the covered eye as the occlude is
removed
o Note any movement, its direction and size
o Note whether the deviation increases with
dissociation
• When the occluder is removed completely at the
end, watch for a recovery movement as the
patient restores binocular vision
o The better eye fixates faster while the
weaker eye moves slower to fixate. This
slow movement of the weak eye to gain
fixation is what you see.
o Note the speed of recovery, and confirm that
binocular vision has been restored with a
cover/uncover test
Alternate Cover Test – Phoria
With removal of the cover, no movement is noted initially
Esophoria Exophoria

With removal of the cover, the deviated eye will move to fixate

OPHTHA The Pediatric Eye Page 4 of 10

   
Example: If upon removal of the occluder the eye moves
inwards to gain fixation, what do you have? EXOPHORIA

Adult strabismus which is already amblyopic on the affected

eye (left eye). Even if we do alignment surgery on this patient,
sometimes there will still be ocular misalignment later on
because there is no more center fusion. But still, surgery is still
recommended.

Causes of Strabismus (YOU CAN SKIP THIS)

• Restrictive strabismus
o Physically stuck (blowout fracture)
• Paretic strabismus
o One muscle is weak due to innervational
reasons
th
Krimsky test (JUST NICE TO KNOW) – we use prisms to o eg. 6 nerve palsy
measure actual deviations of the eye. Used in planning surgery • The most common cause of strabismus occurs
of the patient. without restriction or paresis
o The eyes can move normally in all directions
o Misalignment because one eye sees poorly
Review: eg. EOR
o Strabismus due to poor vision in one eye is a
subtype called sensory strabismus
o There is unexplained eye muscle imbalance
such that the brain and muscles are unable
to keep the eyes straight.

Surgical Management of Strabismus

• Resection – strengthening procedure (if the eye is
deviated inwards, cut short the lateral rectus to
strengthen it so it pulls the eyeball outwards)
o Cut short the muscle and advance the cut
edge
• Recession – weakening procedure
o Loosen the attachment and bring it back.

Squint Procedure (NICE TO KNOW)

However, beware of pseudostrabismus which occurs in

infants and toddlers whose facial features are not fully
developed. The bridge of their nose is wide and flat
creating telecanthus (increased distance between
medial canthus of both eyes). Facial asymmetry can also Retinoblastoma
produce pseudostrabismus, so it is important to always
look at the reflex. • Cancer of the eye that affects the retina
• Mostly affects children
• Presents after infancy as
o Leukocoria
o Esotropia
o Uveitis

Pseudostrabismus – commonly seen in the clinics

OPHTHA The Pediatric Eye Page 5 of 10

 
 

Retinoblastoma in infancy
• Most common intraocular malignancy in children
• Incidence ranges 1 in 15.000 to 1 in 18,000 live births
• Bilateral in about 25-35% of cases
• Average age at diagnosis is 18 months
o Unilateral cases being diagnosed at around
24 months
o Bilateral cases before 12 months
• Endophytic growth
o Growth breaks through the internal limiting
membrane – a whitish mass becomes visible
o Vitreous seeding (fragments become
separated from the main tumor)
§ May be seen floating in the vitreous
and anterior chamber and obscure
the view
• Exophytic growth
o Subretinal space – accumulation of
subretinal fluid and retinal detachment
o Cells may enter the choroid layer and
infiltrate blood vessels or ciliary nerves
• Diffuse infiltrating growth
o Rare
o A distinct tumor mass is absent although
tumor cells infiltrate the retina
Exophytic type -- white, vascualrized mass in the subretinal
space
Endophytic type – grows into the vitreous cavity and usually
produces vitreous seeding
Orbtial Retinoblastoma
• In untreated cases – extraocular spread primarily thru
optic nerve and sclera
• Developed countries – 6.3 to 7.6%
• Underdeveloped world – 18 to 40%
• Associated with increased in mortality and poor
prognosis
OPHTHA The Pediatric Eye
Orbital retinoblastoma
• Orbital invasion – 10 to 27 times higher risk of
metastasis
• The 5-year survival rates of orbital retinoblastoma
o In developed countries – 88-93%
o In developing countries – approximately 10-
50%
§ Late presentations compounded by
socioeconomic factors
ROB Management
• Early tumor recognition by direct ophthalmoscopy
• Enucleation – improved survival 81%
• External beam radiotherapy
• Chemoreduction
Retinopathy of Prematurity
• Retrolental fibroplasia
• A disease of pre-term infants where the immature
retina undergoes changes related to/caused by
ischemia and insufficient retinal vascularization
• Effects – mild peripheral retinal ischemia, vessel
turtuosity, severe exudative and tractional retinal
detachments
Risk Factors
• Decreasing gestational age
• Decreasing birth weight
• Supplemental oxygen
• Acidosis, apnea, patent ductus arteriosus, septicemia,
blood transfusions, intraventricular hemorrhage
International Classification of Acute Stages of ROP
• Stages 1-5
• Extent – specified as hours of the clock as observer
looks at each eye
• Plus disease – plus (+) is added when vascular
shunting is marked in the posterior pole
o Veins are enlarged
o Arteries are tortuous
Classification of ROP: Zones
• The zones are centered on the optic nerve
• Zone 1 – the circle with a radius extending from the
optic nerve to double the distance to the macula
• Zone 2 – is an annulus with the inner border defined
by zone 1 and the outer border defined by the radius
defined as the distance from the optic nerve to the
nasal ora serrata
• Zone 3 – the residual temporal crescent of the retina
Page 6 of 10
 Plus (+) disease

Stages of ROP

Stage 3 – extraretinal fibrovascular proliferation along the ridge

Stage 1 – thin white demarcation line between the

vascularized and avascularized retina

Stage 4 – subtotal retinal detachment macula sparing (4a) or

  involving (4b)
 
 
Stage 2 – line thickens and becomes elevated by additional
mesenchymal tissue to form a ridge

OPHTHA The Pediatric Eye Page 7 of 10

 
 

Stage 4B – retinal detachment with macular involvement
Stage 5 – total retinal detachment (finnel shaped) due to
contraction of fibrovascualr proliferation
Current Screening Recommendation
• AOG of 32 weeks or less or <1500 grams, as well as
selected infants with an unstable clinical course – at
least 2 fundus examinations
• Should be performed by an ophthalmologist with
sufficient regular experience and knowledge in the
examination of preterm infants
• First exam should normally be performed between 4-6
weeks of chronological age or, alternatively, within the
st rd
31 to 33 week of postconceptualor postmenstrual
age, whichever is later
• Treatment should generally be accomplished within
72 hours of determination of threshold ROP
• Threshold – stage 3+ ROP in 5 contiguous clock
hours or 8 cumulative clock hours in either Zone I or II
Treatment of ROP
• Retinal photocoagulation (laser treatment)
• Retinal cryotherapy
• Sclera bucking and vitrectomy in Stages 4 and 5
o Anatomical reattachment achieved in only
60% stage 1 demarcation line
END OF TRANS.
Reference: PPT and audio trans
OPHTHA The Pediatric Eye
SUMMARY
The Pediatric Eye
Normal Full Term Infant
• At birth the eye is ¾ that of adult size
• Postnatal growth is maximal within the first year and
rd
then decelerates until 3 year, continuing at a much
slower rate until puberty
• Anterior segment is relatively large at birth and growth
results in a more spherical eye
• Sclera is thin and translucent
• Cornea is relatively large (10mm) and attains adult size
by 2 years (12mm)
• Len is spherical compared to an adult (compensates for
the shortness)
• Fundus is less pigmented and the choroidal vasculature
is visible; at 4-6 months it nearly approximates the
mature eye.
• Earliest response to formed visual stimuli is the infant’s
regard for the mother’s face evident during feeding
• 2 weeks of age -- sustained interest in large objects
• 8-10 weeks – can follow an object 180 degrees
• 4-6 months – eye movements are coordinated and any
deviations should be examined
Developmental Milestones at 3 Months
• Watches faces intently
• Follows moving objects
• Recognizes familiar objects and people at a distance
• Starts using hands and eyes in coordination
Developmental Milestones at 6 Months
• Reaches for and grasps objects
o Depth perception (binocular vision)
• Develops full color vision
o Attracted to different colors and can tell them
apart
• Distance vision matures
• Ability to track moving objects improve
Common Problems (referred to the eye specialist by the
pediatrician or mother; these are usually the CC)
• Visual inattentiveness
o Learning or behavior deficits
• Leukocoria (white pupil reflex due to opacities of the
ocular media)
o Congenital cataract
o ROB (retinoblastoma)
o ROP (retinopathy of prematurity)
• Strabismus
Amblyopia
• Amblyopia is reduced visual acuity as a result of
defective central visual processing. It is a functional
disorder of visual development that is caused by an
optical, physical, or ocular alignment defect during early
childhood.
• A decrease of vision, either unilaterally or bilaterally, for
which no cause can be found by physical examination of
the eye.
“Vision is learned”
• Develop from birth to age 9 years
• Most rapid progression – infancy
• Neuronal connections between the retina and visual
cortex are still developing
“For a limited time only”
• Visual problem during this critical period (eg. EORs,
strabismus) can mess up this developmental wiring
• The potential for amblyopia – age 9 years
o Plasticity of the visual pathways ceases after 9.
“Competitive Wiring”
• Use it or lose it
• The afferent nerve connections of the strong eye
become numerous while the weak (unused eye) nerves
atrophy and decrease in number
o Loss and atrophy of cells in the LGN (lateral
geniculate nucleus) associated with that eye
Causes of Amblyopia
• Pattern deprivation
o Media opacities such as a dense cataract,
uncorrected aphakia, severe blepharoptosis or a
dense corneal opacity
Page 8 of 10
 Optical defocus
• Heteropia/Strabismus
o May be the result of a reflective error that
selectively removes fine details
§ Uni or bilateral, anisometropia
o Lid problems like hemangioma – astigmatism
o Irregular cornea or subluxated lens
• Strabismus or the misaligned eye
Errors of Refraction (EOR) in Children
• Newborns average 3 diopters (eye grade of +300) of
hyperopia
• Onset of myopia – 6-12 years
• Not all EORs are at risk for the development of
amblyopia
Potential Amblyogenic Refractive Errors Warranting
Optical Correction or Monitoring in Infants and Young
Children
Condition Diopters
Isometropia (similar
refractive error both eyes)
Astigmatism ≥2.5
Hyperopia ≥4.5
Anisometropia (unequal
refractive error of eyes)
Astigmatism ≥1.5
Hyperopia ≥1.5
Myopia ≥3
Amblyoia and Strabismus
• Unilateral amblyopia is associated with strabismus in
50% of cases
• Amblyopia is a risk factor for the development of
strabismus and reduced binocularity, and strabismus is
a risk factor for the development of amblyopia
Other Risk Factors for Amblyopia
• Prematurity
• Developmental delay
• Family history (very significant!)
Prevalence Estimates: 1% to 5%
“Early diagnosis and management is best”
• The progression of amblyopia in early childhood is
inversely proportional to the child’s age – the younger
the child, the faster the progression
• The reversibility of the visual deficit is likewise inversely
proportional to the child’s age – younger children
respond more rapidly and more completely to
treatment so early detection is important!
Strabismus
Duction and Versions
• Duction – monocular rotations with no consideration
of the position of the other eye
o Adduction – inward rotation (Ad-in)
o Abduction – outward rotation (Ab-out)
o Elevation or Supraduction (sursumduction) –
upward rotation
o Depression or Infraduction (deorsumduction)
– downward rotation
o Excycloduction (extorsion) – rotation of the
upper pole of the cornea templeward
o Incycloduction (intorsion) – rotation of the
upper pole of the cornea nasalward
• Version – movements of both eyes in the same
direction (eg, right gaze in which both eyes move to
the right)
Yoke Muscles
• Yoke muscles are the primary muscles in each eye
that accomplish a given version.
Fusion
• Fusion – formation of one image from the two images
seen simultaneously by the two eyes
• Motor fusion is a prerequisite for sensory fusion,
but complete sensory fusion does not always follow
motor fusion.
• With the successful binocular fusion – stereopsis
(the visual perception of depth)
Ocular Motility – Strabismus
• Under normal conditions, the image of the object of
regards falls simultaneously on the fovea of each eye,
when the eyes are in perfect alignment
• Any deviation from the perfect ocular alignment is
known as strabismus
OPHTHA The Pediatric Eye
• Manifest deviation of the eyes that cannot be
controlled by binocular vision
o Esotropia – convergent manifest deviation
o Exotropia – divergent manifest deviation
o Hypertropia – manifest deviation of one eye
upward
o Hypotropia – manifest deviation of one eye
downward
Heterophoria
• Latent (able to maintain alignment initially but later on
deviates) deviation of the eyes held straight by
binocular vision
o Esophoria – tendency to turn inward
o Exophoria – tendency to turn outward
o Hyperphoria – tendency to deviate upward
o Hypophoria – tendency to deviate downward
Definitions of Other Terms (BE FAMILIAR WITH THESE
TERMS)
• Orthophoria – absence of any tendency of either eye
to deviate when fusion is suspended
• Prism Diopter – a unit of angular measurement used
to characterize ocular deviations (in percentiles)
• Torsion – rotation of the eye about its anteroposterior
axis
o Intorsion – 12 oclock meridian (the top of
conea) turing toward the midline
o Extorsion – 12 oclock meridian turning away
from midline
• Conjugate Movement – movement of the two eyes in
the same direction at the same time
• Vergence – movement of the two eyes in opposite
directions
o Convergence – the eyes turn inwards
o Divergence – the eyes turn outwards
Agonist, Synergist, and Antagonist EOMs
• Primary muscles that move an eye in a given direction
– agonist
• Muscle in the same eye same direction as the agonist
– synergist
• Muscles in the same eye opposite direction of agonist
– antagonist
• Example: ABDUCTION of the RIGHT eye
o Right lateral rectus muscles is the agonist
o Right superior and inferior oblique muscles
are the synergists
o Right medial, superior, and inferior recti are
the antagonists
• Sherrington’s Law states that an increased
innervations to any muscle (agonist) is accompanied
by a corresponding decrease in innervations to its
antagonists
o The antagonist relaxes as the agonist
contracts
o eg. The right eye’s right gaze would involve
a contraction of the right lateral rectus and a
relaxation of the right medial rectus
Strabismus Symptoms
• “Crossed eyes” or “walled eyes” (duling in Filipino
whether inward or outward)
• Learning/reading difficulties (amblyopia)
• Head tilt, turn, chin up, or chin down
Strabismus History
• Family history
• Age at onset (always important!)
• Type of onset (gradual, sudden, intermittent)
• Types of deviation (comitant or incomitant)
• Fixation (one eye or alternating)
Ocular Examination
• Visual acuity adapted for age
• Determination of refractive error
• Inspection
• Test for EOM function – 6 cardinal gazes
Examination Specific for Ocular Motility
• Gaze positions – primary position and cardinal
positions
• Hirschberg Test (Corneal Reflex Test)
• Cover Test – Uncover Test
• Alternate Cover Test
• Krimsky Test
Page 9 of 10
 • Convergence Measurement
• Prism plus Cover Test
• Maddox Rod Test
Hirschberg test – looks for manifest deviations
Cover/Uncover test – looks for manifest deviations
Alternate cover test – looks for latent deviations
Hirschberg Test – Use your penlight to look for the corneal
reflex
Cover/Uncover Test
• The patient is asked to fix on a target
• The occlude is introduced over one eye
• Look at the uncovered eye
• Repeat with the other eye
Alternate Cover TestThe patient is asked to fix on a target
• One eye is covered with the occluder
• The occluder is then switched to the other eye,
making sure that one eye is kept occluded at all times.
This way, the patient is not allowed to fuse and have
binocular vision
• This is repeated several times to fully dissociate
the two eyes
• Look at the covered eye as the occlude is
removed
o Note any movement, its direction and size
o Note whether the deviation increases with
dissociation
• When the occluder is removed completely at the
end, watch for a recovery movement as the
patient restores binocular vision
o The better eye fixates faster while the
weaker eye moves slower to fixate. This
slow movement of the weak eye to gain
fixation is what you see.
o Note the speed of recovery, and confirm that
binocular vision has been restored with a
cover/uncover test
Surgical Management of Strabismus
• Resection
• Recession
Retinoblastoma
• Cancer of the eye that affects the retina
• Mostly affects children
• Presents after infancy as
o Leukocoria
o Esotropia
o Uveitis
• Most common intraocular malignancy in children
• Incidence ranges 1 in 15.000 to 1 in 18,000 live births
• Bilateral in about 25-35% of cases
• Average age at diagnosis is 18 months
o Unilateral cases being diagnosed at around
24 months
o Bilateral cases before 12 months
• Endophytic growth
o Growth breaks through the internal limiting
membrane – a whitish mass becomes visible
o Vitreous seeding (fragments become
separated from the main tumor)
• Exophytic growth
o Subretinal space – accumulation of
subretinal fluid and retinal detachment
o Cells may enter the choroid layer and
infiltrate blood vessels or ciliary nerves
• Diffuse infiltrating growth
o Rare
o A distinct tumor mass is absent although
tumor cells infiltrate the retina
Orbtial Retinoblastoma
• In untreated cases – extraocular spread primarily thru
optic nerve and sclera
• Developed countries – 6.3 to 7.6%
• Underdeveloped world – 18 to 40%
• Associated with increased in mortality and poor
prognosis
• Orbital invasion – 10 to 27 times higher risk of
metastasis
• The 5-year survival rates of orbital retinoblastoma
o In developed countries – 88-93%
OPHTHA The Pediatric Eye
oIn developing countries – approximately 10-
50%
ROB Management
• Early tumor recognition by direct ophthalmoscopy
• Enucleation – improved survival 81%
• External beam radiotherapy
• Chemoreduction
Retinopathy of Prematurity
• Retrolental fibroplasia
• A disease of pre-term infants where the immature
retina undergoes changes related to/caused by
ischemia and insufficient retinal vascularization
• Effects – mild peripheral retinal ischemia, vessel
turtuosity, severe exudative and tractional retinal
detachments
Risk Factors
• Decreasing gestational age
• Decreasing birth weight
• Supplemental oxygen
• Acidosis, apnea, patent ductus arteriosus, septicemia,
blood transfusions, intraventricular hemorrhage
International Classification of Acute Stages of ROP
• Stages 1-5
• Extent – specified as hours of the clock as observer
looks at each eye
• Plus disease – plus (+) is added when vascular
shunting is marked in the posterior pole
o Veins are enlarged
o Arteries are tortuous
• The zones are centered on the optic nerve
• Zone 1 – the circle with a radius extending from the
optic nerve to double the distance to the macula
• Zone 2 – is an annulus with the inner border defined
by zone 1 and the outer border defined by the radius
defined as the distance from the optic nerve to the
nasal ora serrata
• Zone 3 – the residual temporal crescent of the retina
Stage 1 – thin white demarcation line between the
vascularized and avascularized retina
Stage 2 – line thickens and becomes elevated by additional
mesenchymal tissue to form a ridge
Stage 3 – extraretinal fibrovascular proliferation along the ridge
Stage 4 – subtotal retinal detachment macula sparing (4a) or
involving (4b)
Stage 5 – total retinal detachment (finnel shaped) due to
contraction of fibrovascualr proliferation
Current Screening Recommendation
• AOG of 32 weeks or less or <1500 grams, as well as
selected infants with an unstable clinical course – at
least 2 fundus examinations
• Should be performed by an ophthalmologist with
sufficient regular experience and knowledge in the
examination of preterm infants
• First exam should normally be performed between 4-6
weeks of chronological age or, alternatively, within the
st rd
31 to 33 week of postconceptualor postmenstrual
age, whichever is later
• Treatment should generally be accomplished within
72 hours of determination of threshold ROP
• Threshold – stage 3+ ROP in 5 contiguous clock
hours or 8 cumulative clock hours in either Zone I or II
Treatment of ROP
• Retinal photocoagulation (laser treatment)
• Retinal cryotherapy
• Sclera bucking and vitrectomy in Stages 4 and 5
Anatomical reattachment achieved in only 60% stage 1
demarcation line
Page 10 of 10

  OPHTHALMOLOGY LEC

  Neuro Ophtha 04
6TH PERIODICAL Dr. Carlos Alberto
Monday, January 13, 2014
TP21
Ogie 09275805272
Belle 09266433331
OUTLINE:
History o Sudden-onset visual loss with little recovery
Chief complaint – ischemic event
- Blurring of vision o Sub-acute visual loss associated with pain
- Diplopia but with recovery of vision after several
Neuro-Ophthalmic examination weeks or months – optic neuritis.
- Pupils o Slowly progressive visual loss – compressive
o Pupil examination optic neuropathy.
o Pupil pathology o Visual loss with headache in an elderly
§ Acute oculomotor nerve palsy patient – giant cell arteritis.
§ Tonic/Adie’s Pupil
§ Argyll Robertson Pupil Diplopia
§ Horner’s Syndrome • Monocular or binocular, relative orientation of the
§ Pharmacologic Pupil Pathology separated images
- Visual Field • Frequency, activity that enhances the diplopia
o Terminologies and some generalities • Ptosis or known dysthyroidism
o Anatomy of the visual field afferent system
o Visual field defects o Monocular diplopia improves with pinhole –
§ Homonymous Hemianopsia EOR, optical aberrations of the media, retinal
§ Bitemporal Hemianopsia disorders that distort the fovea.
- Other Ophtha-Neuro Problems o Monocular diplopia the improves with
o Third Nerve disorder blinking – dry eyes
o Fourth Nerve disorder o Binocular diplopia with horizontal separation
o Sixth Nerve disorder that is worse in the distance suggests CN VI
o Papilledema palsy.
o Optic Atrophy o Variability or worsening of the diplopia as the
day progresses with associated ptosis
History suggests myasthenia gravis
Patient’s Age, Sex, Race, Occupation
Hand dominance: esp in patients with stoke Neuro-Ophthalmic Examination
Symptom onset: acute chronic insidious 1. Best corrected visual acuity
Duration a. Using either a Snellen acuity chart at 20 ft. or
Course of condition: static progressive relapsing remitting a near card equivalent for each eye (OD =
Lateralization or binocularity of visual deficits Right eye; OS = Left eye)
Associated features of the patient’s visual symptoms 2. Pupil Examination
Pain, headache, nausea, vomiting, weakness, 3. Visual Field examination
seizures 4. Extraocular motility examination
Medical History: 5. Funduscopic examination
• Trauma (motor vehicle accidents) and cancer
• Past surgery, previous consults Pupils
• Previous therapeutic intervention and the response to Constriction and Parasympathetic Input
those treatments
• Whenever feasible, personally review the patient’s CT
scans and MRIs
Family History
• Optic neuropathies
• Glaucoma
• Multiple sclerosis
• Unexplained blindness
• Diabetes
Social History
• Patient’s occupation
• Alcoholism
• Travel
• Previous transfusions, the patient’s sexual habits, use
of intravenous recreational drugs

A complete history often defines the clinical problem

and allows the examiner to proceed with a complete but
focused neuro-ophthalmic examination.
Unexplained visual loss is common in neuro-
ophthalmic consult.

Chief Complaint: Blurring of Vision

• Monocular, bilateral
• Homonymous or heteronymous defect
• Distance, near or both

o Transient visual obscurations that last for

seconds may be due to increased
intracranial pressure 1. Stimulus (light)
o Painless unilateral visual loss that lasts 2. Photoreceptors stimulated
several minutes may be embolic (amaurosis 3. Pupil motorfibers are also stimulated - transmitted
fugax) via the optic nerves; hemi-decussation at the chiasm
OPHTHA Neuro-Ophtha Page 1 of 7

 
 4. Exit from optic tracts before reaching the Lateral
Geniculate body
5. Enter brainstem via brachium of superior culliculus,
synapses in the pretectal area
6. Then distributed to both IPSI and CONTRAlateral
EDINGER WESTPHAL nuclei
7. Efferent pupillary fibers via CN III synapse in the
ciliary ganglia
8. Short ciliary nerves then go to the IRIS SPHINCTER
and ciliary body.
Dilation: Sympathetic Input
-less well defined
1. originates in the hypothalamus
2. descends uncrossed, to the level of C8-T2
3. exits from the spinal cord via the perivertebral
sympathetic chain
4. synapses in the superior cervical ganglion
5. follows carotid plexus to join the ophthalmic division
of the trigeminal nerve
6. reaches the ciliary body and the dilator of the iris,
via the long ciliary nerves
Schematic of the sympathetic nervous system (SNS) and
the parasympathetic nervous system (PSNS) pathways.
The SNS pathway begins in the hypothalamus, descends
through the brain stem and cervical spinal cord to synapse in
the ciliospinal center of Budge; it then exits the nerve root and
travels to the superior cervical ganglion (preganglionic). The
postganglionic pathway travels via the ophthalmic nerve to the
pupil dilator muscle, resulting in pupil dilation.
For the PSNS, the afferent pathway initiates after a light
stimulus and travels from the retina to the optic chiasm to the
pretectal nucleus in the midbrain. The PSNS efferent pathway
begins in the Edinger–Westphal nucleus in the dorsal midbrain.
The preganglionic neuron travels via the oculomotor nerve
(cranial nerve III) to the ciliary ganglion. Then, the
postganglionic signal travels to the iris sphincter muscle,
resulting in pupil constriction.
Examination of the Pupils
1. note the size and shape in darkness and in light
2. check for the light reflex in each eye individually
3. look for a afferent pupillary defect (RAPD or
Marcus Gunn Pupil)
a. the Swinging Flash Light Test
b. the pupils must react to light in order to
perform the test
c. not a test of the pupil per se – but we look at
the pupils when we do the test
d. TESTS the optic nerve function
4. Check for the near reflex by bringing the patient’s own
finger toward his nose – CONVERGENCE
5. Recording the pupils examination
a. Record the actual size of the pupil OD and
OS
b. i.e. pupils in darkness 8mm OU (both eyes).
In light 3mm OD and 2.5 mm OS. Each pupil
is briskly reactive to light. No relative afferent
pupillary defect (no RAPD). Good near reflex.
OPHTHA Neuro-Ophtha
Swing flash light test
Focus on the AFFERENT illustration (it was the one shown in
the lecture)
- unequal light conduction of the afferent visual
pathway
- examine in dim light with distant fixation
- the lesion can be anywhere from the retina to the
optic tract before the lateral geniculate body
- optic neuritis or ischemic causes
Clinical Rule about MARCUS-GUNN pupils
- you never see APD with ocular media opacities (i.e.
cataract)
- you never see APD with functional amblyopia of
childhood
- an optic neuropathy of any cause will result in an
APD, often disproportionate to the level of visual
acuity
- bilateral APD’s do not exist
o one functioning pathway is required to
determine if an APD is present
o if both afferent pathways are dysfunctional
then pupil response is equal
Pupil Pathology
- lesions of the parasympathetic system – dilated pupil
(greater anisocoria in light)
- Dilated pupil with other signs of acute motility
disturbances and ptosis – an acute third nerve palsy –
compression of the third nerve due to a posterior
communicating artery aneurism.
- An isolated dilated pupil does not usually signify a III
nerve palsy
- Light-near dissociation can be seen in lessions in
the mid-brain
o Light-near dissociation is used as a generic
term that includes not only Argyll Robertson
pupils
- Argyll Robertson pupils are miotic pupils with irregular
shape
- Tertiary syphilis is the most common cause of Argyll
Robertson pupils
Dilated Pupil associated with Acute Oculomotor Nerve (CN
III) Palsy
- Anisocoria with acute onset of third-nerve palsy and
associated with headache or trauma –
neurosurgical emergency
o Complete or partial palsy
o With or without pupil involvement
o Complete or partial ptosis
o Diplopia
- Sudden onset of painful third-nerve palsy with
pupil involvement and no history of trauma or
vascular disease – intracranial aneurysm
o Most common site is the posterior
communicating artery
Page 2 of 7
 Tonic Pupil or Adie’s Pupil
- Dilated pupil with very poor/ no light reaction and
tonic constriction to near and tonic redilation
- Damage is post-ganlionic (ciliary ganglion)
o There would be greater anisocoria in light
illumination than dark illumination
- Light and near reaction are intact
- Anhidrosis (decreased sweating) on the affected side
of the face
Vs ptosis associated with CNIII lesions – (more severe and
with a dilated pupil)

Right congenital Horner’s Syndrome. Miosis, mild ptosis,

hypochromic iris.

Anisocoria more prominent in light than dark illumination.

- The near-response is also slow but discernable vs.

the light response

Pharmacologic testing is used to confirm the diagnosis of

Horner’s syndrome and to determine the location of the lesion
in the sympathetic pupillary pathway
Upper picture: far focusing. Lower pic: near focusing. There is Cocaine test – 10% cocaine instilled will not dilate the eye
still pupillary constriction on both eyes. with a sympathetic defect, normal eye dilates
o Light-near dissociation: the dilated pupil Hydroxyamphetamine test – dilatation of a Horner’s eye
(pathologic eye) constricts slowly and means the lesion is preganglionic(before the superior
progressively until it becomes slightly smaller cervical ganglion). No dilatation if lesion is postganglionic
than the normal eye’s simultaneously
constricted pupil.
Pharmacologic Pupil Pathology
- Adie’s (tonic) Pupil
o Supersensitivity of the sphincter muscle to Pupil pathology can be Pharmacologic in nature
pilocarpine (constriction) - Can occur due to accidental or iatrogenic exposure of
o Pilocarpine has no effect on normal pupil/eye. the iris to a dilating agent (e.g. Jimson weed;
scopolamine patch, Atropine or tropicamine
during ocular examination)
Argyll Robertson Pupil
- Test with pupillary constricting drug – Pilocarpine 1%
- Pupils are small and irregular -- if no reaction – likely pharmacologic blockade
o They do not react to light but they
accommodate Pupil Light Near
- Stigma of tabes dorsalis: slow demyelination of the Anisocoria
anomalies reaction reaction
sensory nerves in the dorsal columns of the spinal
cord that carry information about proprioception, (-) or
Tonic pupil (+) d (+) but slow
vibration, and discriminative touch. minimal
- Diabetes mellitus and alcoholism can cause pseudo- Acute third-
(+) d (-) (-)
Argyll-Robertson’s pupils nerve palsy
- Not all light near dissociation are AR pupil!! Pharmacologic
(+) d (-) (-)
- VDRL and FTA dilatation
o Incidence of Syphilis: 0.20% Horner’s
(+) c (+) (+)
o Incidence of gonorrhea: 1.03% syndrome
o Incidence of chlamydia: 1.48% Argyll
(+) small
Robertson (-) (+)
irreg
Horner’s Syndrome pupils
- Lesions of the sympathetic system cause a small
pupil (increased anisocoria in darkness)
- Ptosis
- Slight elevation of the lower lid
- Enophthalmos (the impression that the eye is sunk )
- Miosis (constricted pupil) and dilation lag

OPHTHA Neuro-Ophtha Page 3 of 7

 
 Visual Fields
Automated perimetry - Automated perimetry uses a mobile
stimulus moved by a perimetry machine. The patient indicates
whether he sees the light by pushing a button. The use of a
white background and lights of incremental brightness is called
"white-on-white" perimetry. - Wiki

Terms

Hemianopsia (hemianopia) – partial blindness in the

visual fields of one or both eyes, and not necessarily
half-blindness as the etymology of the term may suggest.

Quadrantanopsia is a class of hemianopsia but

confined to visual field quadrant(s).

Scotoma is one or more islands of blindness within a

seeing zone. (ex. The physiological blind spot)

Homonymous implies correspondence and means (from

ancient Greek) “with the same same.” Can modify;
- Hemianopsia
- Quadrantinopsia
- Scotoma
and refers to:
- the corresponding visual fields of the two eyes, either
the right fields or the left fields (temporal and nasal’
fields)
- the correspondence parts of the visual pathways (i.e.
temporal and nasal’ hemiretinas – T and N’)

Heteronymus – implies a bilater defect of the non-

corresponding visual fields of an eye; seldom used

SOME GENERALITIES
- by convension, a field defect is named for the field
- when referring to a homonymous hemianopsia,
“right” or “ left” signify either the right or the left half of
the binocular visual field
- altitudinal hemianopsia refers to a field defect
above or below the equator with the blinded zone
extending across the prime meridian (midline)
- at the optic chiasm nasal fiber cross, temporal fibers A. Total blindness, right eye
do not. B. Nasal hemianopsia of the right eye (defect in the
nasal field of the right eye and not right nasal
Anatomy: visual field afferent system hemianopsia OR left hemianopsia of the right eye)
- retina C. Left homonymous hemianopsia
- optic disc a. With macular splitting
- optic nerve b. With either macular splitting or sparing
- optic chiasm D. Bitemporal (heteronymous) hemianopsia
- optic tract
- lateral geniculate body Homonymous Hemianopsia
- optic radiation 1. Post-chiasmal lesion
- occipital cortex 2. On the side of the brain opposite the compromised
o usually with macular sparing half
Is this a right or left homonymous hemianopsia?
Lesion is on what side of the brain?
Is there macular splitting? Macular sparing?

Macular splitting can occur in lesions both before and after

the LGB(lateral geniculate body or nucleus)
Macular sparing tends to occur with lesions beyond the
LGB.

OPHTHA Neuro-Ophtha Page 4 of 7

 
 Bitemporal Hemianopsia
- Tunnel vision
- The signals for the temporal fields are carried by
fibers from the nasal hemiretinas – crossed fibers
- The optic chiasm, where the crossed fibers (N + N’)
lie close together, is implicated
- Pituitary gland lesions.
Other Ophtha-Neuro Problems
Third Nerve Disorder
- Diplopia or ptosis
- Dilated pupils, the ptosis on the same side
- Ophthalmoplegia except for the LS and SO
- Sudden onset of a third nerve palsy: - aneurism?
- Brainstem or midbrain infarction
o Other neurologic findings such as ipsilateral
third nerve paresis with contralateral
hemiparesis (Weber’s syndrome)
- Ipsilateral third nerve paresis with contralateral
hemitremor – expanding mass in the temporal lobe
because the third nerve caught between the edge of
the tentorium cerebelli and the uncus of the temporal
lobe in Uncal Herniation Syndrome
- Cavernous sinus lesion and superior orbital
fissure masses can also cause third nerve lesions
Etiologies of Isolated third nerve palsy
1. Ischemic (DM) : DM neuropathy
2. Aneurysmal compression (look for pupil enlargement)
3. Trauma
4. Tumor (check for abberant regeneration)
5. Infection
6. Inflammation
7. Idiopathic
The III Nerve Pathway
- The oculomotor nerve arises from the anterior aspect
of midbrain
- There are two nuclei for the oculomotor nerve:
o Oculomotor nucleus originates at the level
of the superior colliculus
§ Ciliary muscle, and all
extraocular muscles except for
SO and LR
o Edinger-Westphal nucleus supplies the
parasympathetic fibers
§ Ciliary ganglion, and thus controls
the pupil constriction
(parasympa)
- On emerging from the brain, the nerve is invested
with a sheath of pia mater, and enclosed in a
prolongation of the arachnoid.
- Passes between the superior celebellar(below)
and posterior cerebellar arteries(above)
- Pierces the dura mater in front of and lateral to the
posterior clinoid process, passing between the free
and attached borders of the tentorium cerebelli
- Runs long the lateral wall of the cavernous sinus
o Receiving filaments from the cavernous
plexus of the sympathetic, and a
communicating branch from the ophthalmic
division of the trigeminal
OPHTHA Neuro-Ophtha
- It then divides into two branches, which enter the
orbit through the superior orbital fissure, between
the two heads of the lateral rectus
- Here the nerve is placed below the trochlear nerve
and the frontal and lacrimal branches of the
ophthalmic nerve, while the nasociliary nerve is
placed between its two rami:
o Superior branch of oculomotor nerve
o Inferior branch of oculomotor nerve
Fourth Nerve Disorder
Fourth Nerve Pathway
- Nucleus: in the periaqueductal gray
- It emerges on the dorsal surface of the brainstem
and passes around it
- Cavernous sinus – superior orbital fissure
- Supplies the superior oblique muscles (depressor
in adduction; rotator) (SO4)
- Longest course of any cranial nerve in the
subarachnoid space
Fourth nerve palsy
- Patient complains of vertical diplopia
- Trauma – long and very delicate nerve
- Isolated IV palsies
o Trauma: most common, even by small head
trauma
o Ischemic
o Masses (along the clivus)
Sixth Nerve Disorder
Sixth Nerve Pathway
- The abducens nerve nucleus lies underneath the
fourth ventricle
- Leaves the brainstem at the pontomedullary
junction
- Runs in the subarachnoid space along the base of
the pons
- Cavernous sinus – superior orbital fissure
Sixth Nerve Palsy
- Isolated sixth nerve palsies have no localizing value
- If they are associated with other neurologic signs
such as fifth nerve palsy, seventh nerve palsy, or
eighth nerve palsy, they may be of localizing value
- Chronic sixth nerve palsies should be evaluated
- Isolated VI nerve palsy:
o Idiopathic
o Ischemic
o Traumatic
o Inflammation
o Tumor
o Cavernous sinus thrombosis
Page 5 of 7
 PAPILLEDEMA
-Non-inflammatory passive swelling of the optic disc,
produced by raised intracranial tension (ICT)
- interrupted axoplasmic flow in the optic nerve due to
elevated cerebrospinal fluid pressure in the arachnoid
space
- venous congestion
Disc Edema vs. Papilledema
- optic neuropathy due to inflammation, infiltration,
ischemia or demyelination
o visual acuity is significantly diminished
- papilledema – disc edema resulting from elevated
intracranial pressure
o generally exhibits a minimal acuity deficit

UR and UL: optic atrophy

LR and LL: optic atrophy

UpperRight: papilledema, UpperLeft: magnified UR

LR: papilledema, LL: magnified LR

OPTHIC ATROPHY/Optic neuropathy

- death of retinal ganglion cell axons that comprise
the optic nerve
- pale optic nerve of fundoscopy
- end-stage that arises from myriad causes of optic
nerve damage anywhere along the path from the
retina to the lateral geniculate
- vision loss.
All are papilledema. Appreciate the bulging of the optic disc.
END OF TRANS.
Reference:
Doc’s PPT.
We used the pics of the slides since sabi ng clerks ngayon,
yung mga pic na yun ang pwedeng lumabas sa projection
exam, sorry it’s kinda hard to get the original images esp
for the fundoscopic images.

OPHTHA Neuro-Ophtha Page 6 of 7

 
Summary:

Chief complaint
- Blurring of vision
o Inc. ICP – transient, lasts for seconds
o Amaurosis fugax – painless, unilat, lasts for mins.
o Ischemic event – sudden, little recovery for weeks to months
o Optic neuritis – sub-acute, recovery after weeks to months
o Compressive optic neuropathy – slow progressive
o Giant cell artheritis – with headache in elderly
- Diplopia
o EOR – monocular, improve with pinhole
o Dry eyes – monocular, improve with blinking
o CN VI palsy – binocular, horizontal separation, worse in the distance
o Myasthenia gravis – worsening as the day progresses, with ptosis
Neuro-Ophthalmic examination
- Pupils
o Pupil examination
§ Size/shape in light, in dark
§ Light reflex
§ Afferent pupillary defect (RAPD/Marcus Gunn Pupil) – tests the optic nerve function
§ Convergence
§ OS (oculus sinister – left) OD (oculus dexter – right) OU (oculus uterque – both)
o Pupil pathology
rd
§ Acute oculomotor nerve palsy – anisocoria with acute onset 3 nerve palsy assoc with headache or trauma
rd
is a neurosurgical emergency. Sudden onset, painful 3 nerve palsy with pupil involvement, no history of
trauma or vascular disease – intracranial aneurysm. (post. Communicating artery)
§ Tonic/Adie’s Pupil – dilated pupil, very poor light reaction – post ganglionic damage – greater anisocoria in
light. Near-light dissociation - near focusing still with pupillary constriction. Abnormal supersensitivity to
Pilocarpine (constriction).
§ Argyll Robertson Pupil – small irregular pupil. (Stabes dorsalis)
§ Horner’s Syndrome – increased anisocoria in darkness. Ptosis, enophthalmos, meiosis, anhydrosis.
§ Pharmacologic Pupil Pathology
Pupil anomalies Anisocoria Light reaction Near reaction
Tonic pupil (+) d (-) or minimal (+) but slow
Acute third-nerve palsy (+) d (-) (-)
Pharmacologic dilatation (+) d (-) (-)
Horner’s syndrome (+) c (+) (+)
Argyll Robertson pupils (+) small irreg (-) (+)

0.125% Pilocarpine (+)

Pupil anomalies means increased 4% or 10% cocaine 1% hydroxyl amphetamine 1% pilocarpine
sensitivity to pilo
Tonic pupil (+) constriction No indication No indication No indication
rd
Acute 3 nerve palsy No indication No indication No indication (+) constriction
Pharmacologic dilatation No indication No indication No indication (-) constriction
st
(+) dilatation – 1 or 2nd
Horner’s syndrome No indication (-) dilatation order neurons (-) dilatation No indication
rd
– 3 order neuron
Argyll Robertson No indication No indication No indication No indication

- Visual Field
o Terminologies and some generalities
o Anatomy of the visual field afferent system
o Visual field defects
§ Homonymous Hemianopsia – post chiasmal lesion. Lesions beyond LGB (lateral geniculate body) can have
macular sparing. Macula splitting can occur both before and after LGB.
§ Bitemporal Hemianopsia – tunnel vision. Nasal hemiretina – pituary gland lesions usually implicated.
- Other Ophtha-Neuro Problems
o Third Nerve disorder – diplopia or ptosis, on the same side. ophthalmoplegia except for LS and SO (LS6 SO4).
rd
Aneurysm, brainstem/midbrain infarction. Weber’s syndrome – ipsi 3 nerve palsy +contra hemiparesis. Uncal
rd
Herniation Syndrome – ipsi 3 nerve palsy +contra hemitremor. Cavernous sinus lesion and superior orbital fissure
masses.
th
o Fourth Nerve disorder – vertical diplopia. Isolated 4 nerve palsy – trauma (most common), ischemic, masses along
clivus.
th
o Sixth Nerve disorder – isolated 6 nerve palsy has no localizing value.
o Papilledema – d/t inc ICP. Venous congestion. Minimal acuity deficit (disc edema – significant dec in visual acuity)
o Optic Atrophy – death of retinal ganglion cell axons – pale optic nerve. Vision loss.

OPHTHA Neuro-Ophtha Page 7 of 7