OPTHALMOLOGY – EYE ANATOMY, PHYSIOLOGY, BASIC EYE EXAM FOR 3RD YEAR – SY 2014-2015

ANATOMY AND PHYSIOLOGY

OF THE EYE

THE EYEBALL

• Thin transparent mucous membrane which covers the

eye

-Normally the adult globe is spherical with AP diameter of 22- • Bulbar conj – anterior surface of the sclera
24 • Palpebral conj – posterior surface of the eyelid / when
-Volume 30cc you flip your upper eyelid, the one covering it is the
palperal conj ( sometimes FB can be lodge in this
area)
Layers of the Eye • (3) Foniceal conj – where the palpebral/bulbar meet
• Outer Layer • (6) Marginal conj – at the eyelid margin
– Cornea • Located at you inner canthus is the semilunar fold –
– Sclera this is a rudundant or thickened fold of the bulbar
– Corneo-Scleral Junction (limbus) conj.
• Middle Layer • Composed of 2-5 layers of stratified columnar
– Iris epithelial cells.
– Choroid • Contains glands/goblet cells that secretes mucin
– Ciliary Body which help in ocular lubrication
• Inner Layer
– RPE
– Sensory Retina
TENON’S CAPSULE

CONJUNCTIVA • A fibrous membrane

that envelopes the
globe from the limbus
to the optic nerve
• Continuous with the
EOM’s
• Thickens to form
check ligaments

The structure was named after Jacques-René

Tenon (1724–1816),[1] a French surgeon and pathologist.

• The fascia bulbi is a thin membrane which envelops

the eyeball from the optic nerve to the limbus,
separating it from the orbital fat and forming a socket
in which it moves.
• Adjacent to the limbus, these facia the conj and
episclera are fused together.

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OPTHALMOLOGY – EYE ANATOMY, PHYSIOLOGY, BASIC EYE EXAM FOR 3RD YEAR – SY 2014-2015

• Its inner surface is smooth, and is separated from the

outer surface of the sclera by the periscleral lymph CORNEA
space. • Transparent tissue which accounts for most of the
• The fascia is perforated behind by the ciliary vessels refractive power of the eye
and nerves, and fuses with the sheath of the optic • 11-12mm horizontal; 10-11mm vertical
nerve and with the sclera around the entrance of • Thicker at the limbus, and thinner at the center
the optic nerve. • Devoid of blood vessels
• In front it adheres to the conjunctiva • Gets nutrition from vessels of the limbus, aqueous
• Check ligaments, regulate the direction of the eom and tears, atmosphere
and act as their functional mechanism • Transparency of the cornea is due to its uniform
structure, avascularity and deturgescence.
The cornea is the clear front surface of the eye. The cornea-air interface actually
SCLERA provides the majority of the eye’s refractive power. Giving a 40D So remember, we
have several refrative media of the eye but he cornea is the main refractive medium
of the eye.
• Fibrous outer protective covering The cornea is avascular and gets its nutrition from tears on the outside, aqueous
of the eye fluid on the inside, and from blood vessels located at the peripheral limbus.
– It is strong, opaque, inelastic
– Serves to maintain the form of the
eye CORNEA
– 1 mm thick
– Posteriorly, it is pierced b the optic
nerve and that part is known as the
LAMINA CRIBROSA
• The sclera per se has scanty 5 layers of the Cornea:
vascular supply, but the episcleral • Epithelium
tissue contains numerous vessels
• Layers of the sclera: • Bowman’s layer
– Episclera • Corneal stroma
– Sclera proper • Descemet’s layer
– Lamina fusca • Endothelium

• The sclera (from the Greek skleros, meaning hard),

*Dua’s layer
also known as the white of the eye, is the opaque,
fibrous, protective, outer layer of the eye containing
mostly collagen
• the sclera forms the posterior five-sixths of the of
the globe. Where it is continuous with the cornea
anterirly and dural sheath of the optic nerve • On cross section, the cornea contains five distinct
posteriorly. It maintains the shape of the globe, layers. Although recently, they have discovered
provides an attachment for the extraocular another layer of the cornea which is the DUA’s layer.
muscle insertions. The thickness of the sclera varies The outside surface layer is composed of stratified
from 1mm at the posterior pole to 0.3 mm just behind squamous non keratinized epithelial cells that are
the rectus muscle insertions. This are of the sclera is easily abraded. Though epithelial injuries are painful,
the most common site of rupture in cases of trauma. this layer heals quickly and typically does not scar.

The sclera is perforated by many nerves and vessels (long and • Under this lies Bowman’s layer ( ant limiting
short ciliary artery and nerves) passing through the posterior membrane of the cornea which provides protection to
scleral foramen, the hole that is formed by the optic nerve the stroma.
The sclera's blood vessels are mainly on the surface. The
outer surface of the anterior sclera is covered by a thin layer of • The corneal stroma makes up 90% of the corneal
tissue, this is the episclera which contains blood vessles that thickness, a transparent layer composed of a
nourishes the sclera. regularly arranged collagen fibers. Once this layer is
• The brown pigment layer on the inner surface of the damaged this can lead to scar formation.
sclera is the lamina fusca which forms the outer layer
of the suprachoroidal space • The new found corneal layer is the DUA’s layer, a
very thin layer which is very strong and impervious to
air.

• The next layer is Descemet’s membrane, which is

really the basal lamina of the endothelium, (post
limiting membrane)

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OPTHALMOLOGY – EYE ANATOMY, PHYSIOLOGY, BASIC EYE EXAM FOR 3RD YEAR – SY 2014-2015

• The endothelium is one cell layer thick and works as a

pump to keep the cornea dehydrated. Unlike the
corneal epithelium the cells of the endothelium do not
CILIARY BODY
regenerate. Instead, once damaged they stretch to
compensate for dead cells which reduces the overall • Extends from the choroid Composed of two parts:
cell density of the endothelium, which has an impact to the iris a. Ciliary muscle (muscle
• It is triangular in shape of accommodation)
on fluid regulation. If the endothelium can no longer
with a narrow base b. Ciliary process (secrete
maintain a proper fluid balance, stromal swelling due
directed forward giving aqueous humor)
to excess fluids and subsequent loss of transparency origin to the iris
will occur and this may cause corneal edema and • Divided into the pars
interference with the transparency of the cornea and plicata and pars plana
thus impairing the image formed. • Point of suspension of the
lens
• Produces aqueous humor
THE UVEAL TRACT
• The ciliary body is a part of the eye that includes
the ciliary muscle, which controls the shape of the
lens, and the ciliary epithelium, which produces
the aqueous humor. The ciliary body joins the ora
serrata of the choroid to the root of the iris
• Accomodation
• Aqueous production
• The inner iris flows back and becomes the ciliary
We now move to the middle layer of the eye body.
The iris, ciliary body, and the choroid plexus are all continuous with each
other and are collectively called the uvea. This is an important term, as many • The ciliary body has two functions: it secretes
people can present with a disease termed“uveitis”
This it the pigmented layer of the eye
aqueous fluid and it controls the shape of the lens.
The ciliary body contains sphincter muscles that
change the lens shape by relaxing the zonular fibers
that tether to the lens capsule.

IRIS The choroid, also known as the choroidea or choroid coat, is

• Flat anterior extension of the ciliary body

CHOROID the vascular layer of the eye, containing connective tissue, and
lying between the retina and the sclera.
The choroid provides oxygen and nourishment to the outer layers
• Has a central round aperture known as the pupil of the retina.
• Divides the anterior from the posterior chamber Along with the ciliary body and iris, the choroid forms the uveal
• Muscle of the iris tract.
– Sphincter pupillae muscle
• Posterior segment of the
– Dilator pupillae muscle uveal tract in between the
• Blood supply retina and sclera
– Major circle of the iris • Joins the ciliary body
The iris is the colored part of the eye and its primary function is to anteriorly
control the amount of light hitting the retina.
• Consists mainly of blood
Sympathetic stimulation of the pupil leads to pupil dilation and vessels united by
parasympathetic stimulation leads to constriction. connective tissue with
numerous pigmented
Functions of the iris: cells
• Regulate amount of light entering the eye
• Separates anterior and posterior chamber • Choroidal blood vessels
• Cut off marginal rays of light that interfere with the sharpness of nourish outer portion of
retinal image the retina
• Layers of the choroid (of furthest away from the retina
to closest)

a. Suprachoroid
b. Layer of large vessels (Hallers)
c. Layer of medium sized vessels (Sattlers)
d. Layer of Choriocapillaries
e. Lamina Vitrea (Bruch’s membrane-synonyms:
Lamina basalis, Complexus basalis, Lamina vitra)

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OPTHALMOLOGY – EYE ANATOMY, PHYSIOLOGY, BASIC EYE EXAM FOR 3RD YEAR – SY 2014-2015

• Functions of the choroid is chiefly as nutrient organ

for the:
a. Retina VITREOUS
b. Vitreous
c. Lens • Clear, avascular, gelatinous
body
• Comprises 2/3 of the
LENS volume of the eye
• 99% water ; 1% hyaluronic
• Biconvex, avascular, acid and collagen
colorless and transparent • Firmly attached to the pars
structure plana and ora serrata
• Second most powerful
refractive tissue
• Held in place by suspensory
3 chambers in the eye
ligaments known as zonules
• Ant chamber – bounded ant by the cornea, posteriorly
• Accommodates to facilitate by the iris
near vision • Post chamber – front iris back lens
• Vitreous chamber
• Clear avascular body comprising 2/3 of the volume
and weight of the eye
• The lens is a magnifying glass inside our eye that • Fills the space bounded by the lens, retina and the
helps focus light. The lens sits behind the iris and is optic disc
unique in that it doesn’t have any innervation or • Hyaloid membrane which is the outer surface of the
vascularization. vit is in ntact with the post lens capsule,
• It gets its nourishment entirely from nutrients floating zonules,retina and optic nerve
in the aqueous fluid.
• The second refractive medium of the eye RETINA
• Thin, semitransparent, multilayered
• Though the lens may look solid, it actually has three sheet of neural tissue
layers in a configuration similar to a peanut M&M. • Lines the inner aspect of the
The outer layer is called the capsule. The capsule is posterior two thirds of the globe
thin with a consistency of saran wrap and holds the • Terminates anteriorly as the ora
rest of the lens in place. The middle layer is called the serrata
cortex, while the central layer is the hard nucleus. • Blood supply of the retina:
– Choriocapillaries (outer third of the
• Cataracts are described by where they occur - such retina)
as nuclear cataracts, cortical cataracts, and – Central Retinal Artery (inner two thirds
subcapsular cataracts. With cataract surgery the outer of the retina)
The retina is the sensory portion of the eye and contains layers of photoreceptors,
capsule is left behind and the artificial lens is placed nerves, and supporting cells.
inside this supporting bag.
Inner nuclear up to inner limiting membrane – central retinal artery
• The capsule is held in place by suspensory ligaments Outer portion of the inner nuclear down to RPE – choroidal circulation
called zonules that insert around the periphery and Ora serrata The ora serrata is the serrated junction between the retina and
connect to the muscular ciliary body. Contraction of the ciliary body.
the ciliary muscle causes the zonule ligaments to
relax (think about that for a minute), allowing the lens
to become rounder and increase its refracting power
for close-up reading.
• After age 40 the lens starts having difficulty "rounding
out" and people have problems focusing on near
objects. This process is called presbyopia. Almost
everyone over 50 needs reading glasses because of
this hardening of the lens

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OPTHALMOLOGY – EYE ANATOMY, PHYSIOLOGY, BASIC EYE EXAM FOR 3RD YEAR – SY 2014-2015

The optic disk is the entry and exit point

LAYERS OF THE RETINA OPTIC NERVE of the eye. The central retinal artery and
vein pass through here, along with the
ganglion nerves that form the optic
1. Internal limiting nerve. A physiologic divot or “cup” can
membrane be found here that will become
2. Nerve fiber layer important when we talk about glaucoma.
3. Ganglion cell layer
• Trunk of the optic nerve consist
4. Inner plexiform layer of about 1.2 million axons from
5. Inner nuclear layer the ganglion cells of the retina
6. Outer plexiform layer
7. Outer nuclear layer .
8. External limiting • 4 parts of the optic nerve:
membrane a. Intraocular – 1 mm
9. Photoreceptor layer (rods b. Intraorbital – 25 to 30 mm
and cones)
10. Retinal pigment c. Intracanalicular – 4 to 9 mm
epithelium d. Intracranial – 10 mm

• Histologically, many cell layers can be seen, so you

have to memorize these.
• The important ones include the photoreceptor layer, EXTRAOCULAR MUSCLES
which is located further out (towards the periphery),
and the ganglion nerve layer which lies most inward • Rectus Muscles
(toward the vitreous). – superior rectus
• The key point here is that for light to reach the – inferior rectus
photoreceptor it has to pass through many layers.
– medial rectus
After light reaches the photoreceptors the visual
signal propagates back up to the ganglion nerves. – lateral rectus
• These ganglion nerves, in turn, course along the • Oblique Muscles
surface of the retina toward the optic disk and form – Superior oblique
the optic nerve running to the brain.
– Inferior oblique
• Inner nuclear up to inner limiting membrane – central
retinal artery
• Outer portion of the inner nuclear down to RPE –
choroidal circulation
PHYSIOLOGY OF VISION

MACULA
• Center of the posterior
retina
• Responsible for fine central
vision
• Has yellow pigment
(xantophyll)
• Histologically empty space
tends to the accumulation
of extracellular material
that cause thickening
The macula is the pigmented area of the retina that is responsible for central vision.
Diameter 1.5mm
Within the central macula lies the fovea, which is a small pit that is involved with extreme
central vision.
The fovea is very thin and derives its nutrition entirely from the underlying choroid, making Physiology of vision is a complex phenomenon which is still
it especially susceptible to injury during retinal detachments. poorly understood.
The main mechanisms involved in physiology of vision are :
Initiation of vision (Phototransduction), a function of
photoreceptors (rods and cones),
Processing and transmission of visual sensation, a function of
image processing cells of retina and visual pathway, and
Visual perception, a function of visual cortex and related areas
of cerebral cortex.

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OPTHALMOLOGY – EYE ANATOMY, PHYSIOLOGY, BASIC EYE EXAM FOR 3RD YEAR – SY 2014-2015

PHYSIOLOGY OF VISION
rhodopsin or visual purple (rods)
When light strike rhodopsin, it
is split to cis retinal and opsin
pre-lumirhodopsin
after passing thru a series of
orange intermediate
lumirhodopsin
compounds like you
metarhodopsin
lumirodopsin metarhodopsin
etc…
retinene

vitamin A

vitamin esters

Rods and cones(terminal visual organ) receives waves of light

falling upon the retina and convert these vibrations into

nerve impulse

bipolar cells

optic nerve

optic tract

brain where the

sensation of sight is
produced

• Visual pathway: VISUAL ACUITY

• Light is refracted as it pass thru the cornea going to
the lens
• Light is again refracted by the lens focusing it on the
retina
• This double refraction of the light produce an inverted
image on the retina
• So the vision is generated by the photoreceptors of
you retina
• The information leaves the eye by way of the optic
nerve
• and there is a partial crossing of axons at the optic
chiasm.
After the chiasm, the axons are called the optic tract.
The optic tract wraps around the midbrain to get to the lateral VISUAL ACUITY TESTING
geniculate nucleus (LGN), where all the axons must synapse. • Fundamental element of the basic eye examination
From there, the LGN axons fan out through the deep white • Assess the function of the fovea centralis
matter of the brain as the optic radiations, which will • It should be done prior to any manipulation of the eye
ultimately travel to primary visual cortex, at the occipital area • Distance Visual Acuity (DVA) – for all patients
where the inverted image will be perceived by the brain as an including children
upright image • Near Visual Acuity (NVA) – for patients over 35 years
of age, in cases DVA is difficult to perform or not
possible (bedside)

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OPTHALMOLOGY – EYE ANATOMY, PHYSIOLOGY, BASIC EYE EXAM FOR 3RD YEAR – SY 2014-2015

Some charts are constructed such that there are equal number of letters in a row
like the chart designed by Bailey and modified by Lovie
DISTANCE VISION

Visual Acuity (VA) = distance of patient from the chart

distance at which normal eye can
read the given line

For example : VA = 20/50

indicates that the patient can see
at 20 feet what a person with
normal visual acuity can see at 50
feet

HOW TO TEST THE VISION?

DISTANCE VISION
(Distance Vision Chart)
Snellen Chart Tumbling E Chart Picture Chart LANDOLT BROKEN
RING – patient Alternative Notations For Recording Distance VA
describe location of
break in the ring English system Metric System Decimal LogMar
20/200 6/60 0.1 1.0
20/100 6/30 0.2 0.7
20/80 6/24 0.25 0.6
20/70 6/21 0.3
20/60 6/19 0.32 0.5
20/50 6/15 0.4 0.4
20/40 6/12 0.5 0.3
20/30 6/9 0.7 0,2
20/25 6/7.5 0.8 0.1
20/20 6/6 1.0 0

The standard distance of a patient from the chart • If the patient is unable to see the largest letter on
is 6 meters or 20 feet. the Snellen (<20/200), VA is measure using the
• The general steps are as follows: following methods:
1. Position the patient 20 ft. or 6 meters from a well 1. Reduce the distance between the patient and the
illuminated Snellen Chart. chart until he/she is able to read the 20/200 line.
2. Instruct patient to occlude one eye using his/her palm 2. If patient is unable to read the 20/200 line at 3 feet
or an opaque occluder. do Counting Fingers (CF)
3. Ask the patient to read the chart starting at the first 3. If patient is unable to count fingers, determine if patient
line proceeding until the smallest line that he/she can can distinguish presence or absence of Hand Movement
distinguish more than half of the figures (HM)
4. Record the visual acuity 4. If patient cannot detect HM – use penlight to determine
5. Instruct patient to occlude his/her other eye and if patient can correctly detect the direction of the light
repeat steps 3 and 4. source. Light Projection (LPj)
 Good LPj – 4 quadrants
The visual acuity is tested with the snellen chart  Fair LPj – 2-3 quadrants
located at 20 feet away from the patient because by  Poor LPj – 1 quadrant
mathematical computations which is beyond our scope of 5.If the patient is unable to correctly identify the direction
discussion is that at 20 feet distance parallel rays of light will of the light source but is able to detect the presence,
be focused at the retina. The measurement of visual acuity record the patient’s visual acuity as Light Perception
involves many factors not necessarily related to the ability to (LP).
see the test objects. This includes motivation, attention,
intelligence and physical conditions as well as the patience of
both the examiner and the subject. Each eye is measured
without lenses and with most recently prescribed lenses. So
one eye has to be occluded. , the visual acuity is measured by
asking the patient to read from the top to the bottom which is
the smallest letters in the chart.

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OPTHALMOLOGY – EYE ANATOMY, PHYSIOLOGY, BASIC EYE EXAM FOR 3RD YEAR – SY 2014-2015

• Near vision charts usually contain numbers or figures

Snellen’s index Common Practical test in varying sizes corresponding to particular point size
definition
or Jaeger notation
no light perception Can not see light • Standard near vision chart is held at a distance of 14
inches or 35cm under well lighted condition
Less than 3/200 Hand movement Can recognize form • If a patient normally wears glasses for reading , these
and motion at 1 m should be worn during testing.
Less than 10/200 Travel vision Can not read • In the absence of a standard near vision card, any
headlines printed material such as newspaper maybe used
Less than 20/200 Minimal reading Read headlines but instead.
not 14 point type

More than 20/200 Partially seeing Read 14 point type

but less than 20/70 with marked Abbreviations Used in Recording Visual Acuity
difficulty
ABBREVIATION FEATURES
• VA Visual acuity
OD (oculus dexter) Right eye

DISTANCE VISION OS
OU
(oculus sinister) Left eye
(oculus uterique) Both eyes
sc Without correction
• If the patient’s VA is <20/20 in either eye, cc With correction
pinhole visual acuity is performed to ph pinhole
determine if the vision is due to an NV Near Vision
uncorrected refractive error. DV Distance Vision

Occluder with Pinhole test GROSS EXAMINATION OF THE EYE

pinholes
Measurement of visual acuity with • Assess the position of the eyes in relation to other
the patient viewing the test facial structures
symbols through a small opening in • Symmetry between two eyes
an opaque shield • Inspect the lids, palpebral fissure and the
surrounding tissues
Normally, light entering the eye came from different • Take note of the presence of redness, masses or
direction. (peripheral/central light rays) abnormal pigmentation, discoloration on the eyelids
• In a normal eye (emme) light is brought to a focus in and periocular tissue
the retina • Eyelashes should be directed outward
• In an eye with a refractive error such as myopia, there
is an improper bending of light. Usually the peripheral It is recommended that one proceed from the more
light rays causes the blurring of vision. external towards the more internal eye structures.
• So when you apply pinhole, you only let the central
light rays to pass thru the central portion of the pupil. A systematic gross exam of the eye should be performed
So any refractive errors that is present in the lens and to ensure that all structures are evaluated.
cornea is not noticed as much.

HOW TO TEST THE VISION? EXTERNAL EXAMINATION OF THE EYES

(Near Vision Chart)

•
• The external examination of the eyes should be
Rosenbaum pocket vision chart conducted in a systematic manner .
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OPTHALMOLOGY – EYE ANATOMY, PHYSIOLOGY, BASIC EYE EXAM FOR 3RD YEAR – SY 2014-2015

• Good illumination is necessary. It is recommended

that one proceed from the more external towards the
more internal eye structures. EVERSION OF THE LOWER EYELID
• At first the examiner notes any abnormality in the
size and shape of the head as well as the position of
the eyes and their symmetry.
• The obliquity of the exposed portion between the
upper and lower eyelids called palpebral fissure is
readily observed
• Then the examination moves to the skin of face and
eyelids.
• The eyelashes should be outwardly directed
• Eye position should be examined from the front, side
and above by looking down over the patients brow
Inspection inside the lower eyelid is easier .The eyelid is drawn
while seated downward by the index finger applied to the orbital portion.
• With the aid of a flashlight the position of the eyelid
margin in relation to the eye is observed.
• A difference in the color of the irises of the 2 eyes
EXTERNAL EXAMINATION
suggests uveal inflammation, tumor or anomaly in the
sympathetic innervation of the dilator pupilllae.

EVERSION OF THE UPPER EYELID • The cornea is inspected for clarity as well as presence or
opacities or other abnormalities.
• The corneosleral limbus may be involved in arcus senilis
which is seen among elderly or people with lipid disturbances
• The anterior surface of the cornea is smooth and clear; in
cases of glaucoma, you can see that the cornea is steamy,
hazy…
• The anterior chamber filled with a normal aqueous humor is
acellular and transparent So having a clear cornea and
anterior chamber, the iris pattern is seen distinctly. The details
of the iris like the crypts and colarettes are visible

EXTERNAL EYE EXAMINATION

• Pupil Examination
– Assess the pupil size and
shape
The upper tarsal conjunctiva can only be inspected by – Assess the pupil reaction to
eversion of the upper eyelid. light
• Instruct the patient to look down , grasp the lashes of • Direct pupillary reaction
• Consensual pupillary
the upper eyelid between the thumb and index finger. reaction
• Place a cotton-tipped applicator at the palpebral – Assessment of the
sulcus with the other hand and fold back the upper reactions of the pupil to a
SWINGING FLASHLIGHT
eyelid on the cotton tipped applicator while the patient TEST
continuously look down.
• The tarsal conjunctiva is exposed . •There are 3 components in pupil examination. One is pupil size. In a dark room
instruct the patient to fixate on a distant object to prevent reaction to near vision.
• The meibomian glands perpendicular to the eyelid Shine just enough light to both eyes . Observe the size and shape of the pupils.
margin may be seen through the translucent tarsal •The normal size of the pupil range from 2-4 mm
•Asymmetry of both pupils by more than 2 mm is abnormal
conjunctiva

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OPTHALMOLOGY – EYE ANATOMY, PHYSIOLOGY, BASIC EYE EXAM FOR 3RD YEAR – SY 2014-2015

– refers to the pressure that is created within

OCULAR ALIGNMENT the closed environment of the eye
– Governed by a balance between the
production and aqueous humor and is
drainage.
– Vary from individual to individual and exhibits
normal fluctuations during the day
– Normal IOP 10-21mmhg

INTRAOCULAR PRESSURE
DETERMINATION
• IOP is measured by tonometry
Examination of eye movement begins by examining ocular alignment in the primary
position (straight gaze) • Methods commonly used for determining IOP levels
Hirschberg test – performed by instructing the patient to look straight and fixate at a are the following:
distant object while a light is shown towards both eyes ; if properly aligned the reflection
should be at the center of the pupil.
Taken from Self-instructional Materials in Ophthalmology 2nd Edition 1. Finger palpation – provides rough estimate of IOP
Findings are reported as soft, hypotonic or firm

2. Indentation tonometry – quantitative,

measures the amount of pressure required to
indent the cornea

The presence of misalignment will be observed as

appearance of the corneal reflection outside the center of
the pupil
Table show lists of common abnormalities in the alignment
of the eyes.

INTRAOCULAR PRESSURE
OCULAR MOTILITY TESTING DETERMINATION
3. Applanation Tonometry

Examine eye movement by instructing the patient to

follow your finger, or a small target through 6 cardinal
positions of gaze

Version – eye movement tested with both eyes open

Ductions – one eye at a time is tested
-Goldman applanation tonometer is considered the Gold
INTRAOCULAR PRESSURE DETERMINATION
Standard for IOP determination
• Intraocular pressure (IOP)
-Primary disadvantage is that it requires special equipment
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OPTHALMOLOGY – EYE ANATOMY, PHYSIOLOGY, BASIC EYE EXAM FOR 3RD YEAR – SY 2014-2015

-IOP measurements are based on the amount of pressure • Also a 90D hand held lens may be used and the
required to flatten a standard diameter (3.06mm) or area fundus and vitreous ispected as in indirect
(7.35mm2) of the cornea. ophthalmoscopy

FUNDUS EXAMINATION FUNDUS EXAMINATION

• 3 methods in viewing the ocular fundus: • There are 5 structures that should be observed in a
• Direct ophthalmoscopy systematic fundus examination:
• Indirect ophthalmoscopy 1. Optic Media
• Biomicroscopy/lens 2. Optic Disc
DIRECT FUNDUS EXAMINATION 3. Retinal Vasculature
4. Retinal Background
5. Macular Area

FUNDUS EXAMINATION

ISHIHARA COLOR TEST

• Normal color vision is a function of the macula and
optic nerve. ISHIHARA COLOR TEST is the most
common test for color vision.
• This is composed of series of polychromatic plates
designed Dr. Shinobu Ishihara of University of Tokyo,
Japan.
INDIRECT FUNDUS EXAMINATION • The series of plates provide a test to quickly and
accurately asses color vision deficiency,
• The plates are designed to be appreciated correctly in
a room adequately lit by daylight. The electric light in
FEATURES OF OPHTHALMOSCOPE the room should be adjusted to resemble the effect of
Direct natural daylight to avoid alteration in the appearance
• Upright Image of shades of color. The plates are held 75 cm from the
• Greater magnification(15 x) eyes of the subject and tilted such that the plane of
• Lesser field of view the paper is at right angle with the line of vision. The
• Handy numbers in the plates should be recognized without
more than 3 seconds delay.
Indirect • If the subject is unable to read numerals, there are
• Inverted Image plates with winding lines between the 2 x which are
• Lesser magnification (5 x) traced with a brush. Each tracing should be
• Wider field of view completed within 10 seconds
• Comfortable distance • The order of the plates could be varied if deliberate
deception is suspected
• Biomicroscopy The biomicroscope can be combined
with a 55D concave contact lens to neutralize the VISUAL FIELD
corneal refraction for study of the vitreous and the • Visual field is a function of the periphery of the retina.
retina. • It should be included in every ophthalmologic
examination because sometimes the disorder that
requires the examination may impair the patient’s
Page 11 of 13
eneganiron
OPTHALMOLOGY – EYE ANATOMY, PHYSIOLOGY, BASIC EYE EXAM FOR 3RD YEAR – SY 2014-2015

awareness that only the grossest response can be

obtained.
• Accurate measurement of the visual field requires an
SLIT LAMP EXAMINATION
attentive and responsive patient.
• Cofrontation test is a gross estimate of the visual field,
even when the results are normal, a defect may still
• It is a table-mounted binocular
be detected by more sensitive examinations.
microscope with special
• Measurement – detect targets that stimulate the retina
illumination source.
at varying distance from the fovea

CONFRONTATION TEST • A linear slit beam of light is

• Fingers projected onto the globe – optic
• Hat pin with a 3 or 5 mm white tip cross section of the eye.
• Children
• Colored object( top of an eyedropper bottle)
• Comparison of clarity

Confrontation test may also be done by substituting the fingers

with a hat pin with a 3 or 5 mm white tip or a colored object SLIT LAMP EXAMINATION
usually red top of an eyedropper bottle.
For children , the examiner may stand behind the child.

• Slit lamp alone, the

anterior half of the global
(anterior segment) can be
visualized.

• The procedure is done with examiner facing the

patient at a distance of 1 meter in an area of good
illumination.
• The patient is instructed to close one eye by holding
the eyelids close with in the fingers.
• The examiner closes the eye directly opposite the
patient’s closed eye. T
• The examiner’s own eye is the control .It is then
presumed that the examiner has a normal visual field.
• The patient is instructed to fix attention on the nose of
the examiner
• The hand of the examiner is placed midway from the EYE SYMPTOMS
patient with 1,2 or 3 fingers extended. • Eye symptoms can be classified into 3 general types:
• The patient states the number of fingers displayed – Abnormalities in vision
and recorded as normal if the patient and examiner – Abnormalities of ocular appearance
see the fingers at the same distance. The – Abnormalities of ocular sensation
temporal,nasal,superior and inferior fields are tested
in turn. • Symptoms should always be described according
to:
– Onset (gradual, rapid, asymptomatic)
– Duration (acute or chronic)

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OPTHALMOLOGY – EYE ANATOMY, PHYSIOLOGY, BASIC EYE EXAM FOR 3RD YEAR – SY 2014-2015

– Frequency (continuous, intermittent,

episodic) ABNORMALITIES OF OCULAR
– Degree (mild, moderate, severe ) SENSATION
– Location (focal or diffuse, unilateral or
bilateral)
• EYE IRRITATION
– Progression ( worsening of symptoms ) – Itching
– Dryness
ABNORMALITIES IN VISION
• “may buhangin”, “maaligasgas”, “may puwing”
• VISUAL LOSS
– “nanlalabo”, “maulap ang paningin”, “nawala – Tearing
ang paningin”, “hindi makakita “ or “nabulag” – Ocular Secretions
• VISUAL ABERRATIONS
• “nagmumuta”
– Glare, photophobia (“silaw or nasisilaw”)
References
• FLASHING/FLICKERING LIGHTS Ophthalmology Principles and Concepts 8 th Edition by
Frank Newell
– “may parang kidlat”, “biglang may Self-instructional Materials in Ophthalmology 2 nd
maliwanag”, “may kumikislap” Edition by Dr. Marissa N. Valbuena

• FLOATERS
– “may lumulutang sa harap ng mata”, “may
insekto na sumusunod sa paningin”
• OSCILOPSIA
– “gumagalaw o lumilikot ang paningin”
• DIPLOPIA OR DOUBLE VISION
– “nagdadalawa ang paningin”, “naduduling”,
“doble ang paningin”
RED EYE

One must differentiate

between redness of the lids
and periocular area from that
of the globe

Patient may complain

“namamaga ang mata”,
“namumula ang mata”

• EYE PAIN
– Must be characterized in terms of location
• Periocular – tenderness of the lid, tear sac, sinuses,
temporal artery
• Retrobulbar – orbital inflammation, orbital myositis,
optic neuritis
• Ocular – corneal abrasion,corneal foreign body,
glaucoma, corneal ulcer, endophthalmitis
• Non-specific – fatigue from ocular accomodation,
binocular fusion, referred discomfort from non-ocular
tension

Page 13 of 13
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 FUNDUSCOPY EXAM
(Ophthalmoscopy) • The patient ideally should be in a supine position
07 17 2018
Department of Ophthalmology – .
+ +

Ophthalmoscopy
DIRECT INDIRECT
15x magnified view of 3.5x magnification but wider
posterior pole view of peripheral retina
Monocular, 2D Binocular, 3D
Undilated pupil Dilated pupil
Portable, hand-held Light source from the head of
examiner, condensing lens in
the hand
Image is erect Image is inverted
NORMAL FUNDUS
Describe the following:
DIRECT OPHTHALMOSCOPY • Red orange reflex (ROR)
• Use the RIGHT eye and hold the ophthalmoscope with • Media (clear)
you RIGHT hand when examining the RIGHT eye • Optic Disc (yellow disc with distinct borders, CDR 0.3)
• Vascularization (vessels are well-distributed, AVR 2:3)
• Foveal reflex (good)

? Choroidal background
? Pathology

FUNDUS EXAMINATION
• Fundus can be examined using various methods
o Direct ophthalmoscopy
§ Every physician must gain
confidence in performing this exam
§ Generally used for screening
purposes
o Indirect ophthalmoscopy
INDIRECT OPHTHALMOSCOPY o Use of special lenses with the aid of slit lamp
biomicroscope
• Performed in examination of the peripheral retina • Best performed in a darkened room
• Location of retinal hole, tear, or lattice degenerative • Sufficient examination of the fundus can be done even
change is usually in the peripheral retina in a non-dilated pupil, provided that there are no
media opacities

Page 1 of 2
MD 2020
 o More thorough examination of the peripheral 10. Examine the retinal vessels by moving the beam
retina can be performed through a dilated slowly along the nasal retinal vessels and the
pupil temporal retinal vessels
• Before beginning the procedure:
o Ensure ophthalmoscope is working properly 11. Inspect the retinal background for the presence of
o Both you and the patient are positioned hemorrhages, exudates or any other abnormality
comfortably
12. Examine the macular area. Take note of the
1. Check the light source and select the large beam presence of the foveal reflex
aperture. Intensity of light from ophthalmoscope
should not be too much as this could lead to 13. Repeat the procedure with the opposite eye
excessive constriction of the patient’s pupil
Ø There are five structures that should be observed in a
2. Place your index finger on the lens selection dial and systematic fundus examination
adjust the lens setting to 0 diopter. Index finger is o Ocular media
placed on the lens selection dial to allow for
adjustment of the lens power during the conduct of o Optic disc
the examination o Retinal vasculature
o Retinal background
3. When examining the patient’s right eye, hold the o Macular area
ophthalmoscope with you right hand and use your
right eye to view the patient’s eye. Use the left hand
and left eye to examine the patient’s left eye
Tips (Dr. Ferdi)
4. The patient’s glasses should be removed. The 1. Always explain the procedure (what you’re
examiner may also opt to remove his glasses while about to do)
performing direct ophthalmoscopy. Contact lenses 2. Always make patient look at a distant
worn by the patient or examiner may be left in place object
3. Dark room is needed but since this wouldn’t
5. Instruct the patient to focus on a distant target. The be an option in the classroom just tell the
patient should also be instructed to maintain that proctor that the procedure is best
gaze throughout the examination performed in a darkened room
4. Always take note of the position: right eye
6. Begin to look at the patient’s eye thru the examiner right eye patient
instrument’s viewing aperture from about a distance 5. Note the reflex
of one to two feet. When you look straight down the 6. Adjust the dial of the ophthalmoscope so
patient’s line of sight at the pupil, the red-orange that it would have a small diameter (non-
reflex should be visible dilated pupil)
7. If macula is being examined, ask the patient
7. Slowly come closer to the patient at an angle of to look at the light source
about 15° temporal to the patient’s line of sight
keeping the pupil in view at all times. Turn the “Tapos sabihin niyo lang everytime kung ano gagawin
niyo
lens selection dial with you index finger to bring
the patient’s retina into focus Ex: "First I will explain the procedure, ma’am ganito
kasi sisilipin natin yung likod ng mata niyo etc para
8. You may place your free hand on the patient’s makita yung mga ugat etc
upper lid to keep the eye open, or on the
patient’s shoulder to keep yourself steady. Hold Tingin po kayo sa malayo, medyo may onting silaw
the ophthalmoscope comfortably against the arch lang etc”
of your brow
9. Move the beam until a retinal vessel comes into
view. If the image is not clear, turn the lens
selection dial up and down until it becomes clear.
Follow the retinal vessel until it converges to the
optic disc, which lies nasal to the center of the
retina. Take note of the disc color, its margins
and size of the optic disc cup

Page 2 of 2
MD 2020
(>’$‘)>'Orbit,'Lids,'and'Lacrimal'Apparatus' Exophthalmometry"
Lecturer:'Dr.'Santiago' ! Measures"anterior"projection"of"
*Copy"pasted"from"the"file"uploaded"by"Rex"Cu" cornea"relative"to"lateral"orbital"rim"
" and"quantifies"amt"of"proptosis"or"
CLASSIFICATION'OF'ORBITAL'DISEASES' enophthalmos"
' ! Measurements"between"the"two"
! INFLAMMATORY" eyes"are"usually"within"2'mm"of"
each"other"
• Infectious"–"Orbital"cellulitis"
! A"difference"of"3"mm"or"greater"is"an"
• NonIinfectious"
indication"for"further"investigation"
o Specific"–"ThyroidIrelated"orbitopathy"(because(
even"if"readings"fall"within"the"normal"range"
there(is(etiology(to(the(devt(of(the(disease(
! Types"of"exophthalmometer:"
(disturbance(in(the(immune(system(in(the(thyroid(
• Luedde"(louIday)"exophthalmometer"–"similar"with"your"
and(eom)"
o NonIspecific"–"Pseudotumor"(disease(because(it(is( ruler"with"mm"markings"(place"the"recessed"end"of"the"
idiopathic)" instrument"at"the"lateral"orbital"margin,"measure"the"
displacement"of"the"globe"by"reading"the"mm"marking;"
! NONIINFLAMMATORY"
repeat"test"on"the"other"eye)"
• Tumors"
• Hertel"exophthalmometer"–"measure"displacement"of"
• Congenital"
two"globes"simultaneously"
• Trauma"
"
"
Globe"Reposition"
! A"normal"position"of"the"
! Test"for"the"resiliency"of"the"globe"
globe"inside"the"orbital"
! It"is"normal"to"be"able"to"
cavity"is"marked"by"a"line"
retrodisplace"the"globe"by"applying"
drawn"from"the"superior"
you"thumb"over"the"eyeball"
to"the"inferior"orbital"
! In"the"absence"of"any"orbital"pathology,"you"can"easily"push"the"
margin."
globe"posteriorly"to"the"orbit"because"of"the"compressibility"of"
! This"line"is"theoretically"
the"orbital"structures"such"as"orbital"fat"
lies"tangential"to"the"most"
! In"the"presence"of"retroorbital/retrobulbar"tumors,"the"globe"is"
anterior"surface"of"the"
prevented"to"be"pushed"backward"into"the"orbit."
globe"which"is"your"cornea"
! (I)"resiliency"or"there"is"resistance"to"retropulsion"
! This"may"vary"within"10mm"anterior"or"posterior"to"this"line"
! Better"to"do"the"test"with"both"eyes"to"facilitate"comparison"of"
! Any"lesions"in"the"orbit"can"alter"the"position"of"the"globe"
the"2"orbits"
! Lesions"within"the"muscle"cone"produces"an"Axial"displacement"
'
of"the"globe""(eye"is"pushed"directly"forward)"
! Lesions"outside"the"muscle"cone"produces"a"non"axial" VISUAL'ABNORMALITIES'
displacement"(eye"is"pushed"in"opposite"direction)"ex"–"lacrimal" '
gland"tumor"pushes"the"globe"downward"and"inward"" I."VA"OS:"NLP""
" ! Visual"Acuity"Right"
! PROPTOSIS'(exopthalmos)$'hallmark"of"orbital"disease" Eye:"No"Light"
' Perception"
! Dx:"Retinoblastoma"
THYROID'DISEASE'
' ! Other"signs"of"orbital"disease"is"visual"disturbance"as"seen"in"
! The"most"common"cause"of"unilateral"or"bilateral"proptosis"in" this"case"
adults" ! Px"presents"with"leucocoria;"va"os"NLP"and"on"axial"ct"scan"
there"is"a"note"of"a"solid"intraocular"tumor"with"intratumoral"
! Female"to"Male"ratio:"5":"1"
calcifications"
! Mean"age:"49.2"years"(30I50)" "
! Smokers"2X"higher" II."Diplopia"
! 80%"clinically"hyperthyroid;"20%"clinically"euthyroid" ! Check"for"the"extraocular"muscles"when"evaluating"patient"with"
! Eye"signs"develop"within"18"months"or"concurrently" orbital"disease"
! ThyroidIrelated"eye"disease"signs:" "
• VON"GRAEFE’s"I"upper"eyelid"lag"on"downgaze" "
"
• GRIFFITH’s"I"lower"lid"lag"on"downgaze" "
• STELLWAG’s"I"incomplete"and"infrequent"blinking" "
• KOCHER’s"I"spasmodic"retraction"of"upper"lid"during" "
fixation" "
• ROSENBACH’s"I"tremor"of"gently"closed"lids" "
"
• GIFFOR’s"I"difficult"eversion"of"upper"lid"
"
• GROVE’s"I"resistance"to"downward"pull"of"upper"eyelid" "
"
"
1"|"C o p y " P a s t a " 2 0 1 4 " " " " . "
"
III."Afferent"Pupillary"Defect"(APD)" Advantages" Disadvantages"
! An"APD"indicates"injury"in" Metallic"FBs"eye/orbit" Localization"of"FB"
the"afferent"pathway,"found" Readily"available" """""""""Radiolucent"FB"
with"optic"nerve"injuries" CostIeffective" Often"misses(significant"
• contusion" ocular"and"orbital"injury"
• avulsion"and"transection" May"diagnose"orbital"wall"/" "
• retinal"injuries"such"as" skull""
commotio"retinae," "
retinal"detachment" CT'Scan'
• Major"vitreous" ! the"most"valuable"technique"for"delineating"the"shape,"location,"
hemorrhage" extent,"and"character"of"lesions"in"the"orbit"as"well"as"for"the"
! Lesion"affecting"the"optic" evaluation"of"fractures,"bone"destruction,"and"tissue"
nerve"can"produce"a"rapid" calcification"
afferent"pupillary"defect"(RAPD)"or"Ma" "
! Pupil"reaction"is"very"important"in"prognosticating"the"visual"
outcome"
"
ORBITAL'IMAGING'
'
The"comprehensive'physician'should:""
! Have"a"basic"understanding"of"the"relative"advantages"and"
disadvantages"of"each"imaging"modality"
! Know"which"study"should"be"ordered"in"different"clinical"
situations"
• XIray"
• Ultrasound"
• CT"scan""
• MRI" "
! Be"able"to"order"the"test"to"obtain"the"most"information"in"an" "
efficient"and"costIeffective"manner" MRI'
" ! has"an"advantage"in"soft"tissue"delineation,"contraindicated"in"
Ophthalmoscopy' patients"who"have"ferromagnetic"metallic"foreign"bodies"in"the"
! Check"the"fundus"as"well." orbit"or"periorbital"soft"tissue"
! Traumatic"injury"to"the"globe"may"present"with"edema,"macular" ! NEVER'a'primary"imaging"study"for"trauma"contraindicated"
hole,"choroidal"rupture"or"sub/intra"retinal"hge"in"cases"of"SAH" with"metallic"foreign"body"
or"intracerebreal"hge"2"to"trauma" "
"
Normal:""
"
"
"
"

"
"
! T1"Weighted"Sequences"
" • "Provide"the"best"
anatomical"details"of"the"
Radiography'
! Water’s"View"Xray" orbit"because"they"
display"superior"contrast"
• Most"common"
resolution"between"
• Visualizes"maxilla,"maxillary"sinus,"orbital"floor"and"rim,"
normal"structures""
zygomatic"bone,"nasal"bone,"mandible"fractures."" • Yields"maximum"energy"
• Submentovertex"I"visualization"of"the"zygomatic"arches" release"per"unit"time"I>"
and"any"impingement"of"these"bones"upon"the"coronoid" higher"resonance"signal"I>"BRIGHTER"IMAGE"
process"of"the"mandible"
! Frontal"(Caldwell)"and"lateral"view"sometimes"helpful"for" "
visualization"of"frontal"bone,"zygomaticofrontal"suture,"frontal"
"
sinus,"medial"orbital"rim,"ethmoid"
"
2"|"C o p y " P a s t a " 2 0 1 4 " " " " . "
"
! T2"Weighted"Sequences" MUST"KNOW:"
• Not"ideal"for"imaging"
normal"anatomy;"" Horizontal"Entrance"Width" 40"mm"
• Useful"in"revealing"
pathologic"conditions"" Vertical"Entrance"Height" 35"mm"
• Easily"recognized"by"a"
bright"vitreous"signal" Volume" 30'cm3"

" Orbital"Depth"(measured"from" 45"I"55"mm"

the"rim"to"the"optic"strut)"
"
Globe' 7.5'cm3'
" "
"
ORBITAL'BONES'AND'WALLS'
"
Bones:"
" ! Frontal"
! Zygomatic"
" ! Maxillary"
! Sphenoid"
"
! Lacrimal"
" ! Ethmoid"
! Palatine"
ORBIT'DIMENSIONS'
"
! Lateral"walls" Walls:"
• perpendicular;"""""""
• length"="40"to"45" "
mm"long"
! Medial"walls"" "
• parallel,"25"mm"
apart;"" "
• length"="45"to"50"
"
mm"long"
! PearIshaped,"tapering"
"
posteriorly"
! Widest"dimension":"10"mm"
"
behind"the"rim"
! Orbit"is"describe"as"4"sided"
bony"cavity"located"on"both" ! The"orbital"walls"are"composed"of"7"Bones:"Frontal,"Sphenoid,"
sides"of"the"nose" Zygomatic,"Palatine,"Maxillary,"Lacrimal"and"Ethmoid"
! Serves"as"a"socket"for"the" ! Roof:"frontal"and"lesser"wing"of"sphenoid"
eyeball"and"a"passage"for" • Superior"orbital"fissure"lies"between"the"body"and"the"
blood"vessels"and"nerves" greater"and"lesser"wings"of"sphenoid"bone"
which"supply"the"eyeball" • SOV,"lacrimal,"
and"the"periocular"adnexa" frontal"and"
! Shaped"like"a"pyramid"whose"orbital"margin"serves"as"a"base" trochlear"
and"optic"foramen"as"the"apex."
nerves"pass"
! The"globe"which"occupies"1/5"of"the"orbital"volume"is"
connected"to"the"orbital"apex"by"the"optic"nerve"" through"the"
! Medial"wall"of"the"orbit"is"parallel"to"one"another"and"is" lateral"portion"
separated"by"the"ethmoid"sinuses" of"the"fissure"
! Lateral"wall"is"directed"laterally"and"outwards,"subtending"an" that"lies"
angle"of"45"deg"from"the"medial"walls" outside"the"
" annulus"of"zinn"
" • Sup"and"inf"divisons"of"CN3,"abducens"and"nasociliary"
nerves"pass"thru"the"medial"portion"of"the"fissure"within"
" the"annulus"of"zinn"

3"|"C o p y " P a s t a " 2 0 1 4 " " " " . "

"
! Lateral:"zygomatic"bone"and"greater"wing"of"the"sphenoid;" APERTURES'AND'NOTCHES'
strongest"and"thickest"bone"
! Medial:"ethmoid,"lacrimal,"maxillary"and"sphenoid"bones" ! Supraorbital"notch"or"foramen"
• located"
• Supraorbital"neurovascular"""bundle"
adjacent"to"the"
ethmoid"and" • The"supraorbital"branch"of"the"frontal"nerve"(supraorbital"
sphenoid" nerve)"exits"at"the"supraorbital"notch"in"company"with"the"
sinuses"and" supraorbital"artery"
nasal"cavity"" ! Zygomatic"foramina"
• medial"wall"of" ! Infraorbital"foramen"
the"optic"canal" • infraorbital"groove""canal"foramen"
forms"the"
lateral"wall"of" • infraorbital"neurovascular"bundle"(V2)"
the"sphenoid" ! Nasolacrimal"canal"
sinus"" • In"the"extreme"anteromedial"wall"of"the"maxillary"sinus"
• The"thinnest"walls"of"the"orbit"are"the"lamina"papyracea," • Separated"from"both"the"sinus"and"the"nasal"cavity"by"a"thin"
which"covers"the"ethmoid"sinuses"along"the"medial"wall," laminae"of"bone"
and"the"maxillary"bone,"particularly"in"its"posteromedial"
• Lacrimal"sac"fossa"to"inferior"meatus"
portion."These"are"the"bones"most"frequently"fractured"as"a"
! Ethmoidal"foramina"
result"of"indirect,"or"blowout,"fractures""
• Infections"of"the"ethmoid"sinuses"may"extend"through"the" ! Superior"orbital"fissure"
lamina"papyracea"to"cause"orbital"cellulitis"and"proptosis."" • The"central"portion"of"the"SOF"is"divided"by"the"Annulus"of"
! Floor:"maxillary,"palatine"and"zygomatic" Zinn"
• forms"the"roof"of"the"maxillary"sinus;"does"not"extend"to" o also"known"as"the"annular"tendon"or"common"
the"orbital"apex"but"instead"ends"at"the"pterygopalatine" tendinous"ring"
fossa;""
o "fibrous"tissue"surrounding"theoptic"nerve"at"its"
• shortest"of"the"orbital"walls""
entrance"at"the"apex"of"the"orbit"
• important"landmarks:"the"infraorbital"groove"and"
infraorbital"canal,"which"transmit"the"infraorbital"artery"and" o "origin"for"four"of"the"seven"extraocular"muscles,"
the"maxillary"division"of"the"trigeminal"nerve"" omitting"the"inferior"oblique"muscle"
• The"lateral"wall"and"the"floor"of"the"orbit"are"separated" o It"can"be"used"to"divide"the"regions"of"the"superior"
posteriorly"by"the"inferior"orbital"fissure"which"transmits" orbital"fissure""
the"zygomatic"branch"of"the"maxillary"nerve,"and"the" ! Inferior"orbital"fissure"
ascending"branches"from"the"pterygopalatine"ganglion."" • Zygomatic"
• The"infraorbital"vessels"are"found"in"the"inferior"orbital"
• "Infraorbital"
fissure,"and"travel"down"the"infraorbital"groove"into"the"
infraorbital"canal"and"exit"through"the"infraorbital"foramen." • "IOV"
Inferior"division"of"opthalmic"vein"passes"through"the" ! Optic"canal"
inferior"orbital"fissure" • Optic"nerve,"ophthalmic"artery,"sympathetic"nerves"
" • Optic"foramen""
Indirect'or'“Blowout”'Fractures'
o Orbital"end"of"canal""
! 1I2"walls"(floor,"
o Adult"size"by"3"yrs"of"age;""<"6.5mm"
medial"wall)"
• Optic"strut""
! Orbital"Rim"
o Separates"from"SOF"
uninvolved"

Complex'Fractures' ORBITAL'PENETRATING'INJURIES'
! >1"wall"
! Orbital"rim" ! Considerations:"
involved" • Injury"to"adjacent"structures:"eyeball,"brain,"sinus"
! ZygomaticoI • Foreign"body"retention"
maxillary"complex"or"“tripod”"fracture" ! Orbital"Foreign"Body:"
! NasoIorbitalIethmoidal"(NOE)"fracture"
• Size"
! Le"Fort"(I),"II"&"III"midfacial"fractures"
• Location"
PERIORBITAL'STRUCTURES' • Velocity""
• Composition"
! Nasal"cavity"
! Paranasal"Sinuses" "
! Fossae"
! Cavernous"Sinus"

4"|"C o p y " P a s t a " 2 0 1 4 " " " " . "

"
DEVELOPMENTAL'ANOMALIES' 2. Neurofibromatosis"
• Optic"Nerve"Glioma"
I.'Crouzon’s'Disease' • In"children"before"age"10,"fusiform"enlargement"of"
! Also"called"Craniofacial"Dysostosis"" your"optic"nerve,"kinking"or"sI"shaped"appearance"
! Premature"synostosis"(fusion)"of"the"coronal,sagittal,"and" ! Plexiform"Neurofibroma"
occasionally"lambdoidal"sutures"beginning"the"first"year"of"life"
• Characteristic"in"NF;"can"distort"the"eyelids"
and"completed"by"2I3"years"of"age"
! Often"associated"with"widely"spaced"orbits"or"what"you"called" producing"an"s"shaped"appearnce"
hypertelorism" ! Neurilemmoma"(Schwannoma)"
! Because"of"the"premature" • Benign"peripheral"nerve"tumor"characterized"by"
closure"of"sutures,"orbits" pure"proliferation"of"Schwann"cells.""
become"shallow"making" • Young"to"middleIaged"adults""
the"globe"to"protrude" • Found"in"1.5%"of"patients"with"neurofibromatosis"
! Incidence:"1/25,000" ! Malignant"Peripheral"Nerve"Sheath"Tumor"
! Autosomal"dominant" • very"rare"tumor"in"the"orbit"(0"to"0.2%)""
(chromosome"10q25I26)"" • Usually"arises"de"novo"in"the"orbit,"although"it"may"
! Clinical"features:"" also"arise"from"a"neurofibroma"or"schwannoma"
• Acrocephaly"(coneIshaped"head)""
• Brachycephaly"(shortened"AIP"diameter)"" C."Mesenchymal"
• Palpable"ridging"" 1. Bone"
• Flat"occiput"" 2. Cartilage"
• Prominent"forehead" 3. Muscle"
• +/I"Frontal"bossing" ! Rhabdomyosarcoma"
• Childhood"cancer"with"an"estimated"250I350"new"
II.'Orbital'Wall'Defects' cases"per"year"""
! Cephalocele"I"herniation"of"maldeveloped"tissues"of"the"central" • The"head"and"neck"region"and"in"particular,"the"
nervous"system"(CNS)")"into"the"orbital"cavity" orbit,"represent"a"major"anatomic"site"for"RMS."""
! Meningocele"I"meninges""
• Orbital"RMS"is"the"most"common"primary"orbital"
! Encephalocele"–"brain"parenchyma"
malignancy"in"children"with"approximately"35"new"
! Meningoencephalocele"–"combination"of"the"two" cases"per"year"
4. Vascular"
III.'Developmental'Tumors'
5. Fat"
A."Choristomas"–"normal"tissue"in"abnormal"location"
! Lipoma"
1. Dermoid"Cyst"
• "benign"tumor"composed"of"adipose"(body"fat)"
! contain"one"or"more"epidermal"appendages"such"as"hair"
• Associated"with"a"number"of"congenital"
follicles,"sweat"glands,"and"sebaceous"glands"
developmental"disorders"including"Goldenhar"
2. Epidermoid"Cyst"
syndrome,"Treacher–Collins"syndrome,"
! lined"by"squamous"epithelium"but"does"not"contain"any"
hemifacial"microsomia,"and"linear"nevus"
other"tissue"elements"of"skin"in"its"surrounding"wall"
sebaceous"syndrome."
3. Teratoma"
! a"germ"cell"tumor"that"contains"tissues"derived"from"the" • "Unless"it"reaches"a"very"large"size,"enough"to"
endoderm,"ectoderm,"and"mesoderm"i.e."may"contain" distort"the"eyelid"anatomy,"or"unless"they"
skin,"bowel,"lung,"brain,"thyroid,"cartilage,"and"bone" contain"hairs"on"their"surface"that"cause"
tissues"" persistent"foreign"body"sensation,"they"should"be"
**Majority"are"benign"with"occasional"malignant"transformation" observed"and"managed"conservatively"
" ! Liposarcoma"
B."HamartomasI"normal"tissue"in"normal"location" 6. Connective"Tissue"
1. Hemangioma" "
! Capillary" IV.'Secondary'Orbital'Neoplasms'
• the"most"common"vascular"orbital"tumor"in"children' A. Direct'Extension"
1. Eyelid"(SqCCA,"BCCA)"
(0.7"to"2.2%)"
2. Eye"(Malignant"Melanoma,"Retinoblastoma)"
• apparent"at"birth"or"within"the"first"8"weeks"of"life." 3. Intracranial"Cavity"(Meningioma)"
• usually"enlarges"for"several"months"and"then"slowly" 4. Nasal"Accessory"Sinus"(Mucocele,"Osteoma)""
regresses"without"treatment." B. Metastatic"
• Approximately"70%"regress"completely"by"7"years"of" 1. Neuroblastoma"
age" 2. Granulocytic"Leukemia"
3. Lymphatic"Leukemia"
! Cavernous"
4. Carcinoma:"breast,"lung,"prostate"
• Located"within"the"muscle"cone"producing"axial" "
proptosis" "
• most"common"benign"intraorbital"tumor"in"adults" "
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C. Inflammatory" What"are"the"2"muscles"responsible"for"eyelid"movement?""
1. Pseudotumor" • The"orbicularis"oculi"closes"the"eyelids"and"is"innervated"by"
! Clinical"Characteristics:" cranial"nerve"7.""
• "Abrupt"onset"" • Patients"with"a"facial"nerve"paralyses,"such"as"with"Bell’s"
• "Unilateral"I"The"left"orbit"is"affected"twice"as"often" Palsy,"can’t"close"their"eye"and"their"eyelids"may"need"to"
as"the"right,"but"bilateral"orbital"involvement,"either" be"patched"(or"sutured"closed)"to"protect"the"cornea"from"
simultaneous"or"separated"by"variable"intervals," exposure.""
occurs"in"almost"half"of"the"cases" • The"levator"palpebrae"opens"the"eye"and"is"innervated"by"
• "NO"sex"predeliction" CN3.""Oculomotor"nerve"(CN3)"palsy"is"a"major"cause"of"
• "Rapid"development" ptosis"
• "Blurring"of"vision"–"6/12"or"better"in"75%" "
• "Optic"nerve"head"
edema"is"noted"in" ** The"retractive"and"protractive"forces"
one"third"of"cases."" constitute"the"external"forces"in"the"lid"
• "Fever,"malaise," "
"
anorexia,"and" Chalazion'
nausea."" ! Lipogranulomatous"lesion"
• May"follow"an" ! Gradually"enlarging"painless"nodule"
upper"respiratory" ! Clinical"Manifestation:"
tract"infection" • Any"age"with"a"gradually"enlarging"painless"nodule"
! Clinical"Presentation:" • Very"occasionally"a"large"upper"lid"chalazion"may"press"on"
• Proptosis" the"cornea,"induce"astigmatism"and"cause"blurred"vision."
• Eyelid"edema" ! Treatment"may"not"be"required"
• Pain" ! Persistent"lesions"may"be"treated"as"follows:"
• Chemosis,"and"conjunctival"vascular"engorgement" • Surgery"IThe"eyelid"is"everted"with"a"special"clamp,"the"
2. Cellulitis,"Abcess"
cyst"is"incised"vertically"and"its"contents"curetted"through"
3. Periostitis"
" the"tarsal"plate"
EXTERNAL'EYE' • Steroid"injectionI"into"the"lesion"is"preferable"if"close"to"
" the"lacrimal"punctum"because"of"the"risk"of"surgical"
" damage"
! The"upper" • Systemic"TetracyclineI"may"be"required"as"prophylaxis"in"
eyelid"margin" patients"with"recurrent"chalazia,"particularly"if"associated"
lies"at"the" with"acne"rosacea"
superior" '

corneal"limbus" Hordeolum/Stye'
in"children" ! Acute"infection"of"meibomian"gland"(internal"stye"or"acute"
and"1.5"to"2" chalazion)"or"Zeis’"or"Moll’s"gland"(external"or"common"stye)"
mm"below"it" ! may"become"chalazia"(chronic)."
in"the"adult." ! Don’t"confuse"a"chalazion"with"a"stye"
! The"lower"eyelid"margin"lies"at"the"inferior"corneal"limbus" • A"stye"is"a"pimpleIlike"infection"of"a"sebaceous"gland"or"
! Seven"structural"layers"of"the"Eyelid:"
eyelash"follicle,"and"is"superficial"to"the"tarsal"plate.""
• Skin"and"
subcutaneous" • Styes"are"painful,"while"deeper"chalazions"are"not.""
tissue" ! Posterior"to"the"lash"line"and"anterior"to"the"tarsus"on"the"
• Muscle"of" eyelid"margin"is"the"gray"line"referred"to"as"the"muscle"of"Riolan"
protraction" and"represents"the"pretarsal"orbicularis"muscle"on"the"eyelid"
• Orbital"septum" margin"
• Orbital"fat"
Trichiasis'
• Muscles"of"
! Ingrowth"or"introversion"of"eyelashes"
retraction"
! Primary"trichiasis""
• Tarsus"
• Managed"conservatively:"Epilation,"Soft"contact"lenses,"
• Conjuctiva"
Electrolysis"(valuable"if"only"a"few"lashes"are"affected)"
"
• A"new"lash"will"regrow"in"6"weeks"
Eyelid"Skin"
! Thinnest"of"the"body;"no"subcutaneous"fat"layer" • If"more"than"a"few"lashes"are"involved,"a"more"complex"
surgical"approach"is"recommended""
! Subjected"to"constant"movement"with"each"blink""
! Secondary"trichiasis""
! Very"minimal"dermal"tissue" • If"the"trichiasis"is"secondary"to"a"primary"lid"abnormality,"
surgical"correction"of"the"lid"position"resolves"the"
" trichiasis""

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Congenital'Districhiasis' ! The"orbital"portion"is"thicker"and"of"a"reddish"color;"its"fibers"
! Rare"familial"condition"in"which"an"accessory"row"of"lashes"is" form"a"complete"ellipse"without"interruption"at"the"lateral"
present"in"or"near"the"orifices"of"the"Meibomian"glands" palpebral"commissure;"the"upper"fibers"of"this"portion"blend"
" with"the"Frontalis"and"Corrugator."
! The"lacrimal"part"(tensor"tarsi)"is"a"small,"thin"muscle,"about"
" 6"mm"in"breadth"and"12"mm"in"length,"situated"behind"the"
medial"palpebral"ligament"and"lacrimal"sac."It"arises"from"the"
" posterior"crest"and"adjacent"part"of"the"orbital"surface"of"
the"lacrimal"bone,"and"passing"behind"the"lacrimal"sac,"divides"
" into"two"slips,"upper"and"lower,"which"are"inserted"into"the"
superior"and"inferior"tarsi"medial"to"the"puncta"lacrimalia;"
" occasionally"it"is"very"indistinct"

Entropion' ORBITAL'SEPTUM'
! Eyelid"margin"turns"inward"against"the"globe"
! Causes:"
'
! Anteriormost"septal"
• Congenital"
sheet"of"the"orbital"
• Spastic"
fascial"complex"
• Involutional"
! Membranous"sheet"that"
• Cicatricial"
acts"as"the"anterior"
" boundary"of"the"orbit.""
! Extends"from"the"orbital"
Ectropion" rims"to"the"eyelids."
! Malposition"of"the"eyelid"in" ! It"forms"the"fibrous"portion"of"the"eyelids"
which"the"upper"or"lower"
! Important"landmark"in"distinguishing"between"orbital"
eyelid"falls,"or"is"pulled"away"
from"its"normal"apposition"to" cellulitis"(inside"the"septum)"and"periorbital"cellulitis/preseptal"
the"globe" (outside"the"septum)"
! Classification:"
• Flaccid"I"excess" Cellulitis'
relaxation"of"eyelid"tissues" " Preseptal"Cellulitis" Orbital"Cellulitis"
• Cicatricial"I"deficiency"of"tissue"in"the"anterior"lamellae" Vision" Normal" Decrease"
• Mechanical" Pupillary"Rxn" Normal" AbN,"+APD"
Proptosis" I" +"
SOFT'TISSUES' Orbital"Pain" I" +"
' Pain"on"Motion" I" +"
! Periorbita" Motility" Normal" Decreased"
! Orbital"Fat" Chemosis" Rare" Common"
! Optic"Nerve" Corneal"Sensation" Normal" May"Decrease"
! Other"Nerves" Opthalmoscopy" Normal" Venous"Cong’n;"Disc"
! Extraocular"Muscles" Edema"
'

! Annulus"of"Zinn" TARSAL'PLATES'
! Vascular"System" "
! Lacrimal"Gland" ! Dense"fibrous"tissue"approx."1I"1.5"
"
mm"thick"
ORBICULARIS'OCULI' ! Give"structural"integrity"to"the"
! Responsible"for"the"closure"of"your"lid"
eyelids"
! Parts:"
! Horizontal"length:"25"I"28"mm"
• OrbitalI"voluntary"
! Central"vertical"height:"Upper:"8I12"mm;"Lower:"3.5"–"4"mm"
closure"of"lids"
! Medially"and"laterally"connected"to"the"bony"orbital"margins"by"
• Palpebral"–"involuntary" ligamentous"fibrous"tissue"
(blinking)" ! Inner"margin"of"the"tarsus"are"modified"sebaceous"glands"
! The"palpebral"portion"of"the" known"as"tarsal"glands"(or"Meibonian"glands),"aligned"vertically"
muscle"is"thin"and"pale;"it" within"the"tarsi:"30"to"40"glands"in"the"upper"lid,"and"20"to"30"in"
arises"from"the"bifurcation"of" the"lower"lid,"which"secrete"a"lipidIrich"product"which"helps"
the"medial"palpebral"ligament,"forms"a"series"of"concentric" keep"the"lacrimal"secretions"or"tears"from"evaporating"too"
curves,"and"is"inserted"into"the"lateral"palpebral"raphe""at"the" quickly,"thus"keeping"the"eye"moist"
outer"canthus"(corner)"of"eye"
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Levator"Muscle" ! Orbital"lobe""
! Upper"eyelid"retractor" • 65%"I75%"of"the"gland,"20mm"long"x"5mm"thick"x"12mm"
! Originates"in"the"apex"of"the" wide"
orbit"from"the"periorbita"of"the" • located"in"tha"lacrimal"fossa"in"the"anterior"upper"
lesser"wing"of"the"sphenoid." temporal"segment"of"the"orbit"
! The"superior"division"of"the" ! Palpebral"lobe""
oculomotor"nerve"innervates" • 25%I35%"of"the"gland "
the"levator"muscle." • portion"located"just"above"the"the"temporal"segment"
! The"aponeurosis"lies"behind"the"orbital"septum"and"fat,"loosely" of"the"superior"conjunctival"fornix"
connected"to"the"orbicularis"muscle"anteriorly"except"for"the" ! Inflammation"of"the"lacrimal"glands"is"called"dacryoadenitis"
slips"of"tissue"that"form"the"eyelid"crease."" ! Blood"supply:"lacrimal"artery"
! Disinsertion,"dehiscence,"or"rarefaction"of"the"aponeurosis"may" ! Nerve"supply:"lacrimal"nerve,"great"superficial"petrosal"nerve,"
result"to"ptosis." and"sympathetic"nerves"
! The"levator"palpebrae"superioris"originates"on"the"lesser"wing"
of"the"sphenoid"bone,"just"above"the"optic"foramen."It" THE'LACRIMAL'SYSTEM'
broadens"and"becomes"the"levator"aponeurosis."This"portion"
inserts"on"the"skin"of"the"upper"eyelid,"as"well"as"the" ! The"path"for"tears"to"travel"from"the"eye"into"the"nose"begins"at"
superior"tarsal"plate."" the"punctum"and"continues"into"the"horizontal"canaliculus"
! The"superior"tarsal"muscle,"a"smooth"muscle,"is"attached"to"the" towards"the"nose"
levator"palpebrae"superioris,"and"inserts"on"the"superior"tarsal" ! Most"of"the"tear"flow"is"actively"pumped"from"the"tear"lake"by"
the"orbicularis"muscle"
plate"as"well"
! Evaporation"accounts"for"approximately"10%"of"tear"elimination"
in"the"young,"and"up"to"20%"or"more"in"older"adults"
Muller’s"Muscle"
! The"lacrimal"puncta"conduct"the"tear"fluid"from"the"tear"
! Originates"posterior"to"the"
meniscus"and"lacrimal"lake"into"the"ampulla"and"canaliculi"
levator"aponeurosis" ! This"is"affected"by"a"lacrimal"pump"mechanism"that"actively"
! 10I12"mm"in"height."" pumps"tear"into"the"sac"with"each"blink."
! Provides"approx."2"mm"of" ! Tears"secreted"by"the"main"and"accessory"lacrimal"glands"pass"
elevation"of"the"upper" across"the"ocular"surface"
eyelid"" • "Tears"flow"along"the"upper"and"lower"marginal"strips"
! Inserts"on"the"superior" (and"enter"the"upper"and"lower"canaliculi"by"capillarity"
tarsal"border"" and"also"possibly"by"suction"
• With"each"blink,"the"pretarsal"orbicularis"oculi"
Preaponeurotic"Fat"Pockets" compresses"the"ampullae,"Simultaneously,"the"lacrimal"
! Upper"eyelid" part"of"the"orbicularis"oculi,"contracts"and"compresses"the"
preaponeurotic"fat"is" sac,"thereby"creating"a"positive"pressure"which"forces"the"
found"immediately" tears"down"the"nasolacrimal"duct"and"into"the"nose"
posterior"to"the"orbital" • When"the"eyes"open"the"muscles"relax,"the"canaliculi"and"
septum"and"anterior"to" sac"expand"creating"a"negative"pressure"which,"assisted"
the"levator"aponeurosis."" by"capillarity,"draws"the"tears"from"the"eye"into"the"
! 2"fat"pockets"at"the" empty"sac"
'
upper"lid,"3"fat"pockets" 2"Components"of"the"lacrimal"apparatus:"
in"the"lower"lid" 1."Secretory"system"I"structures"that"contribute"to"the"formation"of"
! These"fat"pockets"are" the"middle"(aqueous)"layer"
surgically"important"landmarks"because"they"help"identify"a" 2."Excretory"systemI"structures"that"form"the"conduit"by"which"the"
plane"immediately"ant"to"the"major"eyelid"retractors" tears"pass"from"the"conjunctival"fornices"into"the"nasal"cavity"
! In"the"upper"eyelid"these"fat"lies"just"infron"of"the"levator"
apoeurosis"thus"it"is"impt"during"eyelid"surgery"or"in"cases"of" Hyperlacrimation'VS.'Epiphora'
trauma"where"the"other"normal"anatomic"relationships"may"be" ! Hyperlacrimation"excessive"production"of"tears"by"the"lacrimal"
distorted" gland"
" ! Epiphora"sec"to"irritation,"infection,"obruction"on"the"drainage"
THE'LACRIMAL'GLAND' "
" Findings"suggesting"obstruction"of"the"Lacrimal"system:"
! Within"lacrimal"fossa"in"superolateral"orbit" ! Epiphora"
! Secrete"the"aqueous"layer"of"the"tear"film."" ! Unilateral"symptoms"
! Orbital"and"palpebral"lobes"–"divided"by"lateral"horn"of"levator" ! History"of"dacryocyctitis"
aponeurosis" ! Onset"after"the"following:"Conjunctivitis,"Facial"fracture,"Nasal"
surgery"
"
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ORBITAL'SURGERY' Exenteration'
! Removal"of"the"globe"and"the"soft"tissues"of"the"orbit."
Enucleation'and'Evisceration' Indications"include"the"following:""
• Orbital"malignancies"that"may"be"primary"or"where"
' tumours"have"invaded"the"orbit"from"the"eyelids,"
conjunctiva,"globe"and"bony"surrounds"and"where"other"
' forms"of"treatment"are"unlikely"to"be"effective.""
o Anteriorly"sited"tumours"may"allow"relative"sparing"of"
'
tissue"at"the"posterior"orbit,"and"posterior"tumours"
' may"allow"sparing"of"eyelid"skin"which"helps"in"lining"
the"new"socket""
' o Prostheses"following"exenteration"can"be"temporarily"
stuck"onto"the"surrounding"skin,"mounted"on"glasses,"
' or"secured"with"osseoIintegrated"magnets"mounted"
on"the"orbital"rim"bones."The"socket"may"be"lined"
'
with"skin"or"a"splitIskin"graft"or"left"to"heal"by"
secondary"intention."
'
• NonImalignant"disease"such"as"orbital"mucormycosis"is"a"
' rare"indication"

' ORBITAL'NERVES'

' Sensory"Nerves:"
! Trigeminal"V1I"grontal,"lacrimal,"nasociliary"
! After"enucleation/evisceration"we"replace"the"loss"orbital" ! Trigeminal"V2I"infraorbital,"zygomatic"
volume"with"orbital"implants" ! The"sensory"component"of"the"trigeminal"nerve"carries"fibers"
! Orbital"implants"comes"from"different"types"and"sizes." for"pain,"touch,"temperature"and"proprioception"from"the"eye,"
! Most"common"are"PMMA,"silicone"implants" face"and"scalp"
"

! Others"utilize"porous"implants"(promotes"fibrovascular" Trigeminal"Nerve"
proliferation)"it"becomes"a"part"of"your"eye"after"some"time" ! Consists"of"a"small"motor"component"and"a"larger"sensory"
component"
" ! Three"main"divisions:"ophthalmic,"maxillary"and"mandibular"
! Ophthalmic"division"–"major"sensory"input"from"the"eyelids"and"
" orbit"
! Maxillary"division"–"contributes"a"small"component"from"the"
" lower"lid"
! The"motor"fibers"supply"the"masseter,"temporalis,"internal"
" pterygoid"muscles;"tensor"tympani;"tensor"veli"palatini;"
omohyoid;"and"the"anterior"belly"of"the"digastric"muscle"
"
Motor"Nerves:"
! IIII"inferior"(Inferior"Rectus,"Medial"Rectus,"Internal"Oblique),"
"
superior"(Superior"Rectus,"Levator"Palpebra)"
! VI"–"Lateral"Rectus"
" ! IV"–"Superior"Oblique""

" Ciliary"Ganglia"
! Ganglion"is"small,"irregular,"measuring"2mm"horizontally"by"1"
" mm"vertically"
! Postganglionic"fibers"pass"from"the"ciliary"ganglion"into"4"to"6"
" short"posterior"ciliary"nerves"
! 95%"to"97%"innervate"the"ciliary"muscle,"3%"to"5%"destined"for"
" the"pupillary"sphincter"muscle"of"the"iris"
! Lies"about"10"mm"anterior"to"the"SOF"and"7"mm"anterior"to"the"
" annulus"of"Zinn"
! In"retrobulbar"anesthesia,"anesthetic"agent"must"be"placed"in"
" the"vicinity"of"the"ciliary"ganglion"and"the"motor"nerves"to"the"
EOMs"to"achieve"both"sensory"and"motor"blockade"

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"
Oculomotor"Nerve"(CN"III)" ! In"the"adult,"the"vascular"supply"to"the"orbit"derives"primarily"
! Carries"somatic"motor"fibers"to"medial,"superior"and"inferior" from"the"internal"carotid"artery"
rectus"muscles;"inferior"oblique"muscle,"and"levator"palpebrae" ! The"ophthalmic"artery"carries"the"major"blood"supply"to"the"
superioris"muscle" orbit"in"96%"of"individuals."In"about"3%,"the"middle"meningeal"
! Carries"parasympathetic"fibers"to"intrinsic"muscles"of"the"eye" artery"shares"equally"through"an"enlarged"accessory"ophthalmic"
and"sensory"neurons"from"proprioceptive"receptors"in"EOMs"it" (“recurrent"meningeal”)"branch."In"1%"of"individuals,"the"
innervates" middle"meningeal"artery"is"the"only"source"of"arterial"blood"to"
! Within"the"main"nerve"trunk,"puppilomotor"fibers"maintain"a" the"orbit"
superomedial"position"I>"lesions"located"in"the"cavernous"sinus" ! The"order"of"branching"along"the"arterial"tree"varies"
rd
result"in"partial"3 "nerve"palsies"with"sparing"of"pupillary" considerably"
function"
rd
! Complete"dysfunction"of"the"3 "nerve"results"in"a"downward" Venous"System"of"the"Orbit"
outward"deviation"of"the"globe"with"ipsilateral"upper"lid"ptosis" ! The"orbital"venous"system"is"composed"of"two"major"vessels:"
the"superior"and"inferior"ophthalmic"veins"
Trochlear"Nerve"(CN"IV)" ! Unlike"the"arterial"system"in"the"orbit,"the"veins"maintain"an"
! Innervate"the"contralateral"superior"oblique"muscle" intimate"relationship"with"the"orbital"fascial"systems"I>"more"
! Has"a"long"intracranial"course."Part"of"its"orbital"extent"lies" vulnerable"to"compression"by"enlarging"adjacent"muscles"or"
adjacent"to"the"bony"wall,"thus,"it"is"predisposed"to"injury"from" masses"
blunt"head"trauma" ! The"orbital"veins"do"NOT"contain"valves,"and"blood"flow"within"
them"depends"largely"on"local"pressure"gradients"
Abducens"Nerve"(CN"VI)" ! The"major"drainage"is"backward"to"the"cavernous"sinus,"
! It"is"the"last"of"the"motor"nerves"to"appear"in"embryogenesis:" secondary"flow"is"into"the"pterygoid"plexus"and"in"some"may"
first"seen"in"8Iweek"stage"of"development" drain"forward"to"the"fascial"system"
! Failure"to"develop"may"result"in"aberrant"innervation"of"the" ! The"orbital"veins"do"not"follow"a"course"parallel"to"the"arteries,"
lateral"rectus"muscle"by"the"oculomotor"nerve"(Duane’s" as"do"the"veins"in"other"parts"of"the"body."Exceptions:"lacrimal"
syndrome)" and"ethmoidal"veins"
! Unlike"the"oculomotor"and"trochlear"nerves,"it"does"not"lie"
within"the"lateral"wall"of"the"cavernous"sinus"but"runs"within" Lymphatic"System"
the"body"of"the"sinus"I>"the"first"nerve"affected"by"an" ! The"primary"function"of"lymphatic"vessels"is"to"return"to"the"
intracavernous"carotid"aneurysm" vascular"compartment"large"protein"molecules"and"excess"fluid"
extravasated"into"tissues"from"the"blood"
Other"Nerves" ! Two"divisions:"
! Parasympathetic" • Superficial"system"I"drains"the"skin"and"orbicularis"oculi"
• "Accommodation,"" muscle""
• Pupil"constriction,"" • Deep"system"I"drains"the"tarsi"and"the"conjunctiva"
• Lacrimal"stimulation;"" ! Preauricular"Nodes"
• Drainage"from"the"lateral"2/3"of"the"upper"lid,"the"lateral"
• Complicated"course"
1/3"of"the"lower"lid,"and"the"lateral"half"of"the"conjunctiva"
! Sympathetic" ! Submandibular"Nodes"
• Pupil"dilation" • The"medial"1/3"of"the"upper"eyelid,"the"medial"2/3"of"the"
• Vasoconstriction" lower"eyelid"and"the"medial"half"of"the"conjunctiva"
• Muller’s"muscle" ! Anterior"and"Cervical"Nodes"
• Hydrosis""
"
• Follows"arterial"supply"
"
"

"

"

"

"

"

"

"

Arterial"Supply"to"the"Orbit"
10"|"C o p y " P a s t a " 2 0 1 4 " " " " . "
"
 FEU NRMF Institute of Medicine
Ophthalmology – ORBIT APERTURES / NOTCHES
Ruperto V. Roasa, MD
SUPRAORBITAL NOTCH OR FORAMEN
→ Supraorbital neurovascular bundle
ORBIT ANATOMY → The supraorbital branch of the frontal nerve
→ A pear shaped cavity, tapering posteriorly (supraorbital nerve) exits at the supraorbital notch in
→ With a stalk – optic canal company with the supraorbital artery
→ Intraorbital portion of the optic nerve -25mm
→ Globe to the optic canal – 18mm ZYGOMATIC FORAMINA
→ Zygomaticotemporal (to temporal fossa)
ORBITAL BONES → Zygomaticofacial (to cheek)
• Frontal
• Zygomatic INFRAORBITAL FORAMEN
• Maxillary → Infraorbital groove à canal à foramen
• Sphenoid → Infraorbital Neurovascular Bundle (V2)
• Lacrimal → Zygomatic Branch of Maxillary Division of CN V
• Ethmoid → Infraorbital Nerve & Vein
• alatine → Inferior Orbital Vein

ADULT ORBITAL DIMENSIONS NASOLACRIMAL CANAL

→ In the extreme anteromedial wall of the maxillary
Horizontal Entrance Width 40 mm sinus
Vertical Entrance Height 35 mm → Separatedfromboth the sinus and the nasal cavity by
3
Volume 30 cm a thin laminae of bone
Orbital Depth 45 – 55 mm → Lacrimal sac fossa to inferior meatus
(measured from rim to the optic
strut) ETHMOIDAL FORAMINA
3
Globe 7.5 cm → Anterior ethmoidal foramen – branch of Nasocialiary
Nerve
ORBITAL DIMENSIONS → Posterior Ethmoidal Foramen

SUPERIOR ORBITAL FISSURE

• Lateral walls - perpendicular; length = 40 to 45 mm long

• Medial walls - parallel, 25 mm apart; length = 45 to 50 mm
long
→ Outside of Annulus of Zinn:
ORBITAL WALLS o CN IV
o Lacrimal
SUPERIOR WALL LATERAL WALL o Frontal
Frontal Zygomatic o SOV
Lesser Wing of the Greater Wing of the → ANNULUS OF ZINN:
Sphenoid Sphenoid o Occulomotor Forame
INFERIOR WALL MEDIAL WALL o CN III (sup/inf)
o CN VI
Maxillary Maxillary
o Nasocialiary
Zygomatic Lacrimal
Palatine Ethmoid
Sphenoid INFERIOR ORBITAL FISSURE

AMDGS PAGE 1 OF 1
OPTIC CANAL PREAPONEUROTIC FAT POCKETS
→ Optic Nerve, Ophthalmic Artery, Sympathetic Nerves
→ Optic Foramen
o Orbital End of Canal
o Adult Size by 3 yrs of age; <6.5 mm
→ Optic Strut
o Separates from SOF

OPTIC NERVE
→ Neural fibers from the optic nerve arise from primitive
neuroblasts that become the ganglion cells in the retina
and grow toward the brain
→ The retina differentiates from the wall of the forebrain ->
the optic nerve is NOT a true peripheral nerve but an
evaginated fiber tract from the diencephalon
→ These fibers are customarily classified as a special
somatic sensory cranial nerve
→ In the adult, about 50 mm in length from the optic disc LACRIMAL GLAND
to the optic chiasm → Within lacrimal fossa in superolateral orbit
→ Each nerve contains approximately 0.7 to 1.4 million → Orbital and Palpebral lobes – divided by lateral horn of
axons, with a mean axon diameter of 0.85 um levator aponeurosis
→ Ducts from both lobes pass through the palpebral lobe
INTRAOCULAR INTRACANALICULAR TRIGEMINAL NERVE
Within the posterior sclera: 5 – 6 mm in length → Consists of a small motor component and a larger
lamina cribrosa sensory component
1 mm in length
→ Three main divisions: ophthalmic, maxillary and
mandibular
INTRAORBITAL INTRACRANIAL
Immediately behind the From the intracranial → Ophthalmic division – major sensory input from the
sclera opening of the optic canal to eyelids and orbit
Become myelinated by the optic chiasm → Maxillary division – contributes a small component
oligodendrocytes & from the lower lid
10 mm long (3 – 16 mm)
surrounded by pia, arachnoid → The motor fibers supply the masseter, temporalis,
and dura matter -> internal pterygoid muscles; tensor tympani; tensor veli
enlargement to 3 – 4 mm in palatini; omohyoid; and the anterior belly of the
diameter as it exits the globe digastric muscle
25 - 30 mm length:
redundancy for ocular SENSORY NERVES
motility V1 V2
Frontal Infraorbital
Lacrimal Zygomatic
SOFT TISSUES Nasocialiary

PERIORBITA MOTOR NERVES

→ Fuses to dura of optic nerve, orbital septum, CN III CN IV CN VI
periosteum Inferior: IR, MR, IO Superior Lateral
→ Tightly adherent: arcus, sutures, fissures, foramina, Superior: SR, Levator Oblique Rectus
canals
→ Arcus Marginalis – fusion of periorbita, orbital septum, CILIARY GANGLIA
periosteum → Ganglion is small, irregular, measuring 2mm
horizontally by 1 mm vertically
ORBITAL SEPTUM → Postganglionic fibers pass from the ciliary ganglion into
4 to 6 short posterior ciliary nerves
→ 95% to 97% innervate the ciliary muscle, 3% to 5%
destined for the pupillary sphincter muscle of the iris
→ Lies about 10 mm anterior to the SOF and 7 mm
anterior to the annulus of Zinn
→ In retrobulbar anesthesia, anesthetic agent must be
placed in the vicinity of the ciliary ganglion and the
motor nerves to the EOMs to achieve both sensory and
motor blockade

AMDGS PAGE 2 OF 2
OCULOMOTOR NERVE (CN III) In general:
→ Carries somatic motor fibers to medial, superior and o All oblique muscles are abductors
inferior rectus muscles; inferior oblique muscle, and o All vertical recti muscles are adductors
levator palpebrae superioris muscle o All superior muscles are intorters
→ Carries parasympathetic fibers to intrinsic muscles of o All inferior muscles are extorters
the eye and sensory neurons from proprioceptive
receptors in EOMs it innervates ARTERIAL SUPPLY TO THE ORBIT
→ Within the main nerve trunk, puppilomotor fibers
maintain a superomedial position -> lesions located in • In the adult, the vascular supply to the orbit derives primarily
rd
the cavernous sinus result in partial 3 nerve palsies from the internal carotid artery
with sparing of pupillary function • The ophthalmic artery carries the major blood supply to
rd
→ Complete dysfunction of the 3 nerve results in a the orbit in 96% of individuals. In about 3%, the middle
downward outward deviation of the globe with meningeal artery shares equally through an enlarged
ipsilateral upper lid ptosis accessory ophthalmic (“recurrent meningeal”) branch. In 1%
of individuals, the middle meningeal artery is the only
source of arterial blood to the orbit
TROCHLEAR NERVE (CN IV)
→ Innervate the contralateral superior oblique muscle • The order of branching along the arterial tree varies
considerably
→ Has a long intracranial course. Part of its orbital extent
• Ophthalmic Artery supplying branches to:
lies adjacent to the bony wall, thus, it is predisposed to
o Muscular arteries, central retinal arteries,
injury from blunt head trauma
ciliary arteries
o Anastomosing with branches of External
ABDUCENS NERVE (CN VI) Carotid Artery
→ It is the last of the motor nerves to appear in
embryogenesis: first seen in 8-week stage of
development
→ Failure to develop may result in aberrant innervation of
the lateral rectus muscle by the oculomotor nerve
(Duane’s syndrome)
→ Unlike the oculomotor and trochlear nerves, it does not
lie within the lateral wall of the cavernous sinus but runs
within the body of the sinus -> the first nerve affected
by an intracavernous carotid aneurysm

OTHER NERVES
→ Parasympathetic
o Acommodation, pupil constriction, lacrimal VENOUS SYSTEM OF THE ORBIT
stimulation; complicated course
→ Sympathetic • The orbital venous system is composed of two major
o Pupil dilation, vasoconstriction, Muller’s m, vessels: the superior and inferior ophthalmic veins
hydrosis; follows arterial supply • Unlike the arterial system in the orbit, the veins maintain an
→ FACIAL NERVE intimate relationship with the orbital fascial systems -> more
o Not an orbital nerve vulnerable to compression by enlarging adjacent muscles
o Supply motor fibers to eyelid protractors or masses
temporal and zygomatic branches • The orbital veins do NOT contain valves, and blood flow
o Parasympathetic fibers to the lacrimal gland within them depends largely on local pressure gradients.
o Hemifacial spasm results from a vascular • The major drainage is backward to the cavernous sinus,
cross- compression of the facial nerve root secondary flow is into the pterygoid plexus and in some may
drain forward to the fascial system
EXTRAOCULAR MUSCLES • The orbital veins do not follow a course parallel to the
arteries, as do the veins in other parts of the body.
EOM 1 2 3 Exceptions: lacrimal and ethmoidal veins
Medial Adducts • VENOUS DRAINAGE
Rectus o Superior Ophthalmic Vein to Cavernous Sinus
Lateral Abducts o Inferior Ophthalmic Vein to Pterygoid Plexus
Rectus
Superior Elevates Adducts Intorts
Rectus
Inferior Depresses Adducts Extorts
Rectus
Superior Depresses Abducts Intorts
Oblique
Inferior Elevates Abducts Extorts
Oblique

AMDGS PAGE 3 OF 3
 LYMPHATIC SYSTEM ULTRASOUND
• The primary function of lymphatic vessels is to return to the
vascular compartment large protein molecules and excess ADVANTAGES DISADVANTAGES
fluid extravasated into tissues from the blood. Posterior segment pathology May miss deep orbital FBs
• TWO DIVISIONS: with media haze (next to orbital wall)
o Superficial system – drains the skin and Can detect and localize FB Contraindicated in
orbicularis oculi muscle in anterior orbit suspected open globes
o Deep system – drains the tarsi and the Can determine lens position Muscles poorly defined
conjunctiva Posterior optic nerve
• PREAURICULAR NODES – Drainage from the lateral 2/3 poorly visualized
of the upper lid, the lateral 1/3 of the lower lid, and the lateral May miss scleral ruptures
half of the conjunctiva (25%)
• SUBMANDIBULAR NODES – The medial 1/3 of the upper
eyelid, the medial 2/3 of the lower eyelid and the medial half CT SCAN
of the conjunctiva
• ANTERIOR & DEEP CERVICAL NODES

CLINICAL EVALUATION
• Direction of proptosis – clues to pathology
o Lesions within the muscle cone cause an axial
proptosis
o Lesions outside the muscle cone cause eccentric
proptosis

• Severity of proptosis - measured by Hertel

Exophthalmometer
o Distance – lateral orbital rim and apex of the cornea <
20mm ADVANTAGES DISADVANTAGES
• Impaired ocular Motility – evaluated Forced Duction Tests Exact determination of Thick slices may miss small
§ Restrictive myopathy orbital fracture/s FB
§ Third nerve palsy Good soft tissue delineation Multiple FBs – artifacts may
§ Tethering of an extraocular muscle Deep orbit / intracranial / be misleading
§ Splinting of the optic nerve PNS visualization Dental filling interference
Readily detects air in globe / Wooden FBs missed
FORCED DUCTION TESTS orbit Frequently
POSITIVE NEGATIVE Exposure to radiation*
Most radiolucent FBs
Difficulty or inability to move No resistance encountered diagnosed (except wood)
the globe with the forceps Localization of FB – globe,
indicates a restrictive orbit, intracranial
problem
Contrast – vascular lesions
• Impaired Visual Acuity
o Choroidal folds at the macula
MRI
o Optic nerve compression
o Exposure keratopathy
ADVANTAGES DISADVANTAGES
SPECIAL INVESTIGATIONS Excellent soft tissue Poor visualizationof bone /
delineation bone marrow
PLAIN RADIOGRAPHS Blood in eye / brain Longer scanning time
diagnosed easily Metallic FB
Vegetable FBs diagnosed
Optic nerve/optic canal
anatomy better visualized

DYSTHYROID OPHTHALMOPATHY
• Organ specific auto immune disorder
th th
• Common in 4 and 5 decade of life
• F > M, 8:1 ratio
• Pathogenesis Hypertrophy of extraocular muscles à
ADVANTAGES DISADVANTAGES
Cellular infiltration of interstitial tissues à Proliferation of
Metallic FBs eye/orbit Localization of FB orbital fat, connective tissue
Readily available Radiolucent FB
Cost effective Often misses significant
May diagnose orbital wall / ocular and orbital injury
skull fracture/s

AMDGS PAGE 4 OF 4
5 MAIN CLINICAL MANIFESTATION KEY FEATURES to distinguish:
1. Eyelid retraction PRESEPTAL vs ORBITAL CELLULITIS
2. Soft tissue involvement • Pain with eye movement: more common in orbital
3. Proptosis cellulitis, can also occur in preseptal cellulitis.
4. Optic neuropathy • Chemosis (conjunctival swelling): far more common in
orbital cellulitis but has been observed in severe
5. Restrictive myopathy
preseptal cellulitis.
• Orbital cellulitis, (no tpreseptal cellulitis) causes:
GRAVES DISEASE: THYROID OPHTHALMOPATHY
o Proptosis
o Globe displacement
o Limitation of eye movements
o Double vision
o Vision loss (indicates orbital apex
involvement)

BLOWOUT FRACTURE
→ Cause by a sudden increase in the orbital pressure 2ndary
to blunt trauma
• Swelling of muscle bellies; Sparing of tendons
• Intraconal changes possible → Clinical features:
• Hyper or euthyroid o Periocular signs
§ ecchymosis, oedema, subcutaneous emphyma
ORBITAL INFECTIONS o Enophthalmos
PRESEPTAL CELLULITIS o Infrorbital nerve anesthesia
o Diplopia
→ Affects children
→ Secondary to lid infection, skin laceration or insect bite
PEDIATRIC ORBITAL TUMORS
→ Infection does not penetrate the orbital septum
→ Differs substantially from adult types
→ Signs & Symptoms:
→ More often congenital lesions and infectious
o Periorbital swelling and tenderness
o No proptosis → Most common – cystic lesions (dermoids)
nd
o Ocular motility, VA and pupillary reactions – normal → 2 most common – vascular lesions
→ Treatment: Oral Antibiotics → Most common malignancy – rhabdomyosarcoma

ORBITAL CELLULITIS CYSTIC LESIONS

→ Infections of the soft tissue behind the orbital septum DERMOID CYST
→ Less common but more serious
→ Most common causative organism:
o Streptococcus pneumonaie/pyogenes
o Staphylococcus aureus
o Haemophilus influenzae <5 y/o
→ Causes
o Sinus related
o Infection from adjacent structures ie. dacryocystitis,
mid-facial or dental infection
o Post-traumatic – Post-surgical
→ Treatment → Mostcommon
o Children < 5 y/o ampicillin and penicillinase-resistant → Preschoolchild
penicillin combination → Superotemporalmass
rd th
o Adult – 3 & 4 eneration cephalosporins and
→ Mobileandnontender
metronidazole
→ Well circumscribed on CT with
PRESEPTAL vs ORBITAL CELLULITIS rare bony remodeling
Both can present with fever, redness and swelling of eye → Deeper lesionsusually show
and surrounding structures
bony abnormality
Both are most common in children
1-3% of cases of sinusitis will lead to orbital cellulitis → May present with proptosis
Preseptal cellulitis associated with infection of local and visual s/s
structures, trauma, insect/animal bites or foreign bodies → Surgical excision at around 1
PRESEPTAL ORBITAL year of age
Less commonly associated Serious morbidity & mortality
with sinus infections possible
Rarely leads to serious – 1-2% mortality – 3-11% TERATOMA
complications vision loss → Rare congenital germ-cell tumors
Treatment as outpatient in Much less common → Ectodermal, mesodermal and endodermal elements
most cases 73-94% of cases caused by → Present at birth,usually with significant morbidity
coexisting sinus infection → Massiveproptosiswith large intraconal masses

AMDGS PAGE 5 OF 5
 VASCULOGENIC LESIONS RHABDOMYOSARCOMA
CAPILLARY HEMANGIOMA

→ 1/3 diagnosed at birth

→ 90% visible by 6 months
→ Most common presenting as superficial tumor that develops
“strawberry” appearance
→ Enlarge with Valsalva
→ CT/MRI: diffusely infiltrating non- encapsulated mass
→ Usual course
o Normal at birth – noticed at one month – enlarge till 1 → Most common malignant tumor in children
to 2 years of age – spontaneous involution by age 4 to →
st
Presents within 1 decade
8 yr
→ Rapid unilateral proptosis and globe displacement
→ Cosmetic sequelae minimal
→ CT scan shows irregular margins and often bony
→ Visual complications: Amblyopia or Astigmatism
destruction
→ Major complications: Superinfection, Ulceration
→ Excisional biopsy ASAP for diagnosis if suspected
→ OUTCOME:
→ Take as much tumor as possible on biopsy
→ Disseminated or gross residual disease after biopsy carries
35% 5-year survival rate
→ Chemotherapy and XRT after biopsy (90% 5-yr for localized
disease)

OPTIC NERVE GLIOMA

→ TREATMENT:
o Indications include any complication
o Medical therapy – steroids (systemic, intralesional)
o Radiation therapy
o Surgical resection for unresponsive or well-
encapsulated lesions

LYMPHANGIOMA

→ 3rd most common in children; Mean Age: 8 years old

→ May occur randomly although often associated with NF
type I (up to 50%)
→ Proptosis and visual symptoms
→ Headache and pain with intracranial extension
→ Diagnosis clinically and radiographically
→ Benign congenital vascular malformations
→ May involve conjunctiva, eyelids or deep orbit
→ Usually identified prior to teenage years
→ Usually slow enlargement and increasing proptosis
→ Sudden proptosis from hemorrhage into cyst
→ No enlargement with Valsalva
→ CT/MRI shows multi-compartmental nature
→ TREATMENT for significant proptosis, corneal exposure or
optic nerve compression → CT/MRIshowsfusiform enlargement of optic nerve
o Debulking and cyst drainage usually → MRI for intracranial extension
o Complete removal often not possible → Significant mortality once into chiasm
→ Must be excised while confined to nerve, esp. if blind or
proptotic

AMDGS PAGE 6 OF 6
 METASTATIC TUMOR ORBITAL PSEUDOTUMOR
NEUROBLASTOMA

→ Idiopathic orbital inflammation

→ 1905 by Birch-Hirschfiel first described
→ Excludes systemic diseases (sarcoid, thyroid, autoimmune
and Wegener’s)
→ Most frequent in kids nd th
→ 2 to 7 decade
→ Neuroblastoma accounts for 10% of all childhood
→ Multifocal involvement of any orbital structure
malignancies
→ Proptosis – acute onset of a few days
→ Primary: usually adrenal
→ Eyelid swelling, chemosis and diplopia also common
→ Bilateral metastasis with eyelid ecchymoses and proptosis
common → Visual loss with optic nerve involvement
→ Survival rate–15% → CT findings – hazy enlargement of affected structures
→ Treatment – Steroids, immunosuppresive meds, radiation
therapy when steroids adverse
ADULT ORBITAL TUMORS → Involvement of Muscle & Tendon
→ Vary significantly from children
→ Most common LACRIMAL GLAND TUMORS
o Carcinoma → Enlargement of lacrimal fossa with displacement of globe
o Pseudotumor and no inflammatory signs
o Lacrimal gland tumors → 50% epithelial, 50% lymphoproliferative
o Lymphomas → CT scan – lymphoid show smooth
o Cysts, meningiomas, vascular tumors → enlargement of gland, epithelial are irregular
→ Primary epithelial neoplasms of lacrimal gland are rare
PARANASAL SINUS MASSES
→ Masses of the paranasal sinus potentially can spread to PLEOMORPHIC ADENOMA
involve the orbit
→ Most common: mucocele
→ Neoplasms of this area are uncommon, but frequently
involve orbit
→ Benign tumors push periorbita, malignant invade

MUCOCELES

→ Obstruction of ostium in a sinus

→ Enlarging fluid filled sinus
→ Erodesthroughbonyorbit wall → Benign mixed tumor
→ Most arise from frontal and ethmoid → Most common of these
→ CT – homogenous mass → 20 to 50 years
→ Painless proptosis with inferior/medial globe displacement
NEOPLASMS OF PARANASAL SINUS → Many months or years
→ Uncommon; Most common – SCCa → Excisional biopsy (total)
→ Orbital invasion in 2/3 of patients with SCCa
→ Glandular malignancies from minor salivary glands or
respiratory epithelium
→ Orbital extensive gives poor prognosis
→ Biopsy to Dx; radical resection to treat

AMDGS PAGE 7 OF 7
 ADENOID CYSTIC CARCINOMA SCHWANNOMAS

→ Most common malignant of these → Neurilemoma – benign, non-invasive peripheral nerve

→ Progressive onset of symptoms tumor, from any nerve in orbit
→ Rare, ages 20 to 70 years
→ Pain and numbness
→ CT/MR show well circumscribed ovoid mass
→ CT with bony destruction and infiltration
→ Most commonly intraconal, may be extraconal (trochlear,
→ 50%mortality, requires aggressive surgical Tx supraorbital nerves)
LYMPHOID TUMORS CAVERNOUS HEMANGIOMAS

→ Encapsulated venous malformation

→ Incidence between 4 to 13 % of all orbital tumors → Most common vascular lesion of adults
→ Primary or secondary to systemic disease
→ Peak incidence – middle age (40 years); Women > Men
→ Most patients who present with localized orbital disease will → Slowly progressive painless proptosis over several years
develop systemic lymphoma
→ Do not enlarge with Valsalva, but grow slowly
→ Presents between age 50 and 70
→ CT/MRI reveals well- defined mass, oval
→ Anterior, “salmon patch” mass causing progressive → Homogeneous with increased density – CT
painless proptosis
→ MRI – isointense to muscle
→ Generous biopsy needed to make diagnosis
→ Treatment–surgical excision, recur rarely
→ Systemic workup necessary
→ Localized orbital lymphoma – XRT
METASTATIC TUMORS
→ Systemic lymphoma – XRT + chemotherapy
BREAST
→ Consultation of oncologist should be obtained
→ 8% of all orbital tumors
ORBITAL MENINGIOMAS → Most common in women – breast (& overall)
→ Most common in men – prostate & lung
→ Symptoms – proptosis, diplopia, pain, vision loss
th
→ Presents in 7 decade
→ Prognosis is very poor (avg. survival 10 months)
→ XRT usual; Chemo and Hormonal occasional

th th
→ 4 to 7 decade of life, rare in children
→ Most (70%) invade from cranium
→ Primary orbital meningiomas may arise from optic nerve
→ Proptosis, visual disturbances, headache and diplopia
→ CT/MRI fusiform enlargement of optic nerve Noted from Dr. Roasa’s PPT lecture only. No proofreading done. Use at your own risk!

AMDGS PAGE 8 OF 8
OPTHALMOLOGY – OPTIC NERVE
FEU-NRMF Institute of Medicine
3B-Medicine 2017
Lecturer: Dr. Fermin/ Dr. Rivadillo
Note: This is based on doc Fermin’s ppt & lecture, those in pink text are the Optic Disc
ones highlighted by doc fermin (she will give 15points sa prelims) & the
ones in gray text are additional notes from doc rivadillo na wala sa ppt. - major ophthalmic landmark
Parang laging nababanggit ni doc kung unilateral/bilateral, take note . - surface of the intraocular portion of the optic nerve
THE FUNDUS: Window into the brain - axons of retinal ganglion cells right angle turn to enter the
posterior sclera canal

Physiologic cup:
- white depression in the central portion of the disc
wherein central retinal artery & optic nerve passes
through
- size varies: concentric w/ post sclera canal
- edges are lined by astrocytes
NORMAL OPTIC DISC:
Color: yellow orange  Neural rim: surrounding the optic cup; axons,
CDR: 0.3 – 0.5 astrocytes & capillaries giving a pink appearance
AV ratio: 2:3
Cup Disk Ratio (CDR): ratio of the horizontal width of
Border of disc/Margin: well
demarcated
the disk to the cup (Normal value: 0.3 -0.5)

OPTIC NERVE ANATOMY Blood supply

- Central retinal artery: surface of the optic disc
Sheaths covering the optic nerve: (prelaminar)
 Pia mater: contains - Posterior ciliary arterioles: remainder of intraocular
the blood vessesls; portion of the optic nerve (laminar)
divide via collagen
septa EVALUATION OF PATIENTS WITH OPTIC NERVE
 Dura (outer sheath): DISEASES
arachnoid matter; 1. History taking
continous w/ sclera - Most common complaint: Blurring of vision; take note
 Meningeal covering: of there is headache
12mm posterior to 2. Ocular Examination
the globe A. Visual Acuity
*Myelination begins at B. Pupillary Testing - Assessed by:
the lamina cribrosa  Size & shape (normal: 2-4mm)
 Reaction to light
4 Divisions: (memorize lengths)  Reaction to swinging light (RAPD or Marcus-Gunn
1. Intraocular (1-2mm witdth, 1mm length) Pupil – one abnormality detected)
- also known as optic nerve head C. Opthalmoscopy
- major ophthalmic landmark 3. Ancillary Tests
2. Intraorbital (3-4mm width, 20-30mm length) A. Visual field test (most important): confrontation
- S-shaped: permit the rotation of the eye so nerve does test
not have to stretch B. Others: Color blindess, Visual evoke response, CT
- Longest part scan, MRI
3. Intracanalicular (5 (6)mm long)
- fixed to optic canal d/t dura matter
- 2 structures that accompany: ophthalmic artery OPTIC NERVE DISEASES
&posterior ganglionic fiber
- Passes a narrow space so most commonly injured Optic Neuritis Giant Cell Arteritis
4. Intracranial – 10mm long (varies,range: 5-16mm) Papilledema Toxic Optic Neuropathy
- short bridge between optic foramen going up the Optic Atrophy Optic Nerve Tumor
contralateral chiasm Optic Neuropathy Developmental Anomalies
- vulnerable to lesions d/t variable length

1 Specially made for bigote boy 

OPTHALMOLOGY – OPTIC NERVE
FEU-NRMF Institute of Medicine
3B-Medicine 2017
Lecturer: Dr. Fermin/ Dr. Rivadillo

DEVELOPMENTAL ANOMALIES - There is diminished vision, pendular nystagmus & (+)

esotropia
- Unilateral in 20%& bilateral in 80%
- Image: unclear development of small disc, “double
ring sign”

OPTIC NEURITIS
- Inflammation of the optic nerve that may occur
anywhere in its course from the optic disc to optic
chiasm
- Causes: Infection (common in Phils), demyelinating
dse (MS), autoimmune disorders
- Optic neuritis subacute loss of vision associated with
Myelinated/Medullated Nerve Fibers retrobulbar pain that worsens w/ ocular mov’t
- Feathery white glistening discoloration at superior usually affects young women (15-45 yo)
margin - Symptoms are unilateral except in children
- Optic disc still w/ distinct border - Exam shows ↓ VA, ↓ color vision, RAPD, ↓
- Vision not affected brightness sensitivity & VF defects
- Can be mistaken for Chorioretinitis Signs & Symptoms:
myelinated nerve fibers usually doesn’t have pigmentation
 Severe loss of vision in one eye (unilateral)
& visual affectation unlike chorioretinitis
Normal myelination  scotoma
 Starts at lateral geniculate body at 5 mos gestational age  markedly reduced color vision
 6-7 mos in optic chiasm  afferent papillary defect
 8 mos becomes intraorbital  orbital pain on eye mov’t d/t inflammation
 At birth, it stops at the lamina cribrosa
 reduced perception of light intensity
Coloboma  Other focal neurologic symptoms: weakness,
- Incomplete closure of fetal fissures resulting to bowl numbness, tingling in extremities
shaped excavation  History of adjacent flu-like viral syndrome in
- Almost always accompanies Coloboma of choroid/iris children
- Mainly unilateral but bilateral colobomas can occur
*usually regresses spontaneously but can administer IV
- Image: pale yellow reflex, vessels come out of space,
methylprednisone 250mg q6h for 3 days to shorten course of
border is indistinct dse
Pits: communicate w/ space that results to fluid Classifications:
accumulation in retinal space  central serous
choroidal artery (image: hyperaemic)
Drusen
- Laminated, calcareous, acellular accretions
- Differentiated from papilledema by its lack of dilated
veins
- There are visual field defects but rarely reduces visual
acuity
1. Retrobulbar neuritis (2/3 of cases)
- Image: “scalloped border”, presence of pale yellow
 Optic disc is normal
calcific deposits around disc
 Demyelination: most common
Hypoplasia  Sinus related (ethmoiditis)
- Very small optic nerve d/t low number of ganglion  Lyme Disease
cells & its axons but no reduction in supporting  Dx by MRI
tissues
- Optic disc appear very small
2 Specially made for bigote boy 
OPTHALMOLOGY – OPTIC NERVE
FEU-NRMF Institute of Medicine
3B-Medicine 2017
Lecturer: Dr. Fermin/ Dr. Rivadillo

2. Papillitis or Anterior Optic Neuritis (1/3 of cases) Stages of Papilledema:

 Optic disc is swollen & hyperemic
 Intraocular portion of the nerve is affected
 Demylination is uncommon
 Viral infections & immunization in children
(bilateral)
 Syphillis 1. Early
- Visual symptoms are absent, visual acuity normal
3. Neuroretinitis
- (+) impingement, (-) inflammation of nerve
 optic disc & adjacent temporal retina are
- Optic discs show hyperaemia & mild elevation
inflamed & edematous
- Disc margins (nasal, superior, inferior & temporal)
 papillitis & macular star
indistinct, swelling of parapapillary RNFL develops
 Cat-scratch fever (if w/ pets,common in children),
- Loss of previous spontaneous venous pulsations
Lyme disease, Syphillis
- Enlargement of blind spot
PAPILLEDEMA 2. Fully Developed (Established)
- Transient visual obscurations
- Passive swelling of the optic nerve that occurs
- Unilateral/bilateral
secondary due to ↑ pressure in the subarachnoid
- Visual acuity is normal or reduced
space of brain & optic nerves
- Optic discs: severe hyperaemia & moderate
- almost always bilateral & vision is often normal
elevation w/ indistinct margins
- Dx: CT scan, MRI
- Optic cup & small vessels on the discs are obscured
Signs & Symptoms: - Venous engorgement, parapapillary flame shaped
 s/sx of ↑ICP - headache (early morning), nausea haemorrhages, cotton wool spots & exudates
&vomiting
3. Chronic (Long standing/ Vintage)
 double vision (only 1 eye is affected; CN6 is impinged at
- Visual acuity is variable & visual fields begin to
petrous apex so abduction is limited)
constrict
 ↓ visual acuity, visual field defects
- Optic discs are markedly elevated w/ a
“champagne cork” appearance
Features of True Papilledema:
- Cotton wool spots & haemorrhages are absent
 Elevated nerve head
- Optociliary shunts & drusen like crystalline
 Narrowing of cup with relative preservation of cup
deposits (corpora amylacea) may be present on
depth
disc surface
 Edema of nerve fiber layer obscuring underlying disc
margin 4. Atrophic
 Retinal (Paton’s lines)/ choroidal fold - Visual acuity is severely impaired
 Hyperaemia - Optic discs are dirty grey in color, slightly elevated
 Venous congestion w/ few crossing blood vessels & indistinct margins
 Peripapillary hemorrhage (most commonly flame) - 4-6 weeks (ave: 5 weeks)
 Cotton wool spots Causes: (what needs to be treated to relieve
 Hard exudates papilledema)
 Space occupying lesion
Causes of Pseudopapilledema  Idiopathic intracranial hypertension
 Oblique insertion of th ONH  Developmental disorder
 Small (headed up) ONH: hyperopia  Vascular hypertension
 Myelinated nerve fibers  Cranial trauma
 Buried disc druse: swelling of the ONH from  Toxicity
infiltration by hyaline bodies, which can be assoc. w/  Metabolic disorders
VF defects or APD  Hematologic disorders
 Remnants of the hyaloids canal  Occlusive disease

3 Specially made for bigote boy 

OPTHALMOLOGY – OPTIC NERVE
FEU-NRMF Institute of Medicine
3B-Medicine 2017
Lecturer: Dr. Fermin/ Dr. Rivadillo
MEMORIZE TABLE GIANT CELL ARTERITIS
- Chronic, disseminated, inflammatory disease of
segment of large & medium sized arteries
- Autoimmune hypersensitivity to elastic tissue of
Early: w/ blurring arteries
Early: no blurring
Clinical Manifestations:
- Severe headache
- Sudden loss of vision
- Inflammation of the central retinal artery or short
posterior ciliary artery that
supply the optic disk
Diagnosis:
- ESR (erythrocyte
sedimentation rate)
- Temporal artery biopsy
OPTIC NEUROPATHY
- Serum alkaline phosphate
- Causes: Ischemia, toxins, vascular BP abnormality, - C reactive protein
compression w/in the orbit
Treatment: steroids to recover vision
Classification:
I. Anterior (optic disk edematous) TOXIC OPTIC NEUROPATHY
A. Ischemic: Arteritic (seen in pt w/ temporal/giant
- Characteristic finding: scotoma that includes both
cell arteritis)
blind spot & the fovea
B. Occlusive: Non-arteritic (more common, seen in
- Cecocentral scotoma
HTN, dyslipidemia & DM pt)
- Slow, bilateral, symmetrical, progressive blurring of
C. Idiopathic: Compressive, Ocular hypotony, Toxic,
vision/visual loss
Primary tumor of optic disk
- Papillomacular retinal nerve fiber atrophy
II. Posterior (w/o optic disk edema) - Temporal disc pallor
A. Idiopathic: Compressive, Toxic, Infiltrative, - Can be caused by:
Hereditary  Excess alcohol
B. Ischemic: Arteritic  Diet + anemia
D. Occlusive: Non-arteritic  Elderly, HTN, DM
ANTERIOR ISCHEMIC OPTIC NEUROPATHY
- interruption of the blood flow in the short posterior
ciliary arteries that supply the optic disc
- sudden, painless, non progressive visual field vision
- non-inflammatory condition
- pale & swollen optic disc
- peripapillary flame shaped hemorrhage
- afferent papillary defect
- severe loss of vision
- altitude visual field defects
POSTERIOR ISCHEMIC OPTIC NEUROPATHY
- uncommon type
- diagnosis depend on exclusion
- altitude visual field defects
- ↓ visual acuity

4 Specially made for bigote boy 

OPTHALMOLOGY – OPTIC NERVE
FEU-NRMF Institute of Medicine
3B-Medicine 2017
Lecturer: Dr. Fermin/ Dr. Rivadillo

OPTIC ATROPHY 2. JUVENILE GLIOMA

- Loss of axons which reorients the astrocytes within - Occurs in the 1st decades of life
the optic disc giving it a very pale, white color optic - Benign, common
nerve - Astrocytic hamartomas
- Loss of central or peripheral vision - 50% occurs in orbital portion of the optic nerve
- Sign of chronicity: 4-6 weeks - Proptosis, loss of vision or strabismus
- Primary: no ophthalmologic signs of preceding - 15% occurs in patient w/ Neurofibromitosis
edema or inflammation
*most common cause: untreated open angle galucoma - MRI/CT: fusiform
- Secondary: (+) preceding papillitis or papilledema enlargement of optic
*disc margins are blurred nerve, w/c may have a
kinked appearance

3. ADULT GLIOMA
- malignant
- Rapidly progressive malignant astrocytoma
- Glioblastoma
- Occus in middle aged adults

4. OPTIC NERVE SHEATH MENINGIOMA

- Occurs in middle-aged adults, more often in
women (5:1)
- Slowly progressive, painless unilateral vision loss
- Shunt vessels between retinal venous & choroidal
circulation (optociliary shunts)
- MRI/CT: enlargement optic nerve w/ parallel
linear images of thickened meninges (tramtrack
sign)

OPTIC NERVE TUMORS

1. MELANOCYTOMA
- Heavily pigmented nevus that usually occurs on
the inferior temporal portion of the optic disc
- Occurs mainly in deeply pigmented individuals Please support!
- Low malignant potential
Thanks Ian Martinez for doc Fermin’s notes 

5 Specially made for bigote boy 

OCULAR EMERGENCIES
Jesus F. Marin, M.D.
Department of Ophthalmology APRIL 25, 2017

RELEVANCE EXAMINATION PROTOCOLS

The primary care physician needs to recognize conditions 5-POINT EXAMINATION
afflicting or observable in the eye in order to make urgent referrals • Gross examination
to ophthalmologists and/or initiate therapy, whenever appropriate. • Visual acuity testing
• EOM evaluation
OBJECTIVES • IOP determination
1. Be able to evaluate and handle a patient complaining of ocular • Fundoscopy
related conditions potentially requiring immediate attention;
2. To learn EXTENDED VISUAL EXAM
 Pertinent questions to ask • Visual Acuity testing
 Utilize the appropriate examination techniques • Confrontation VF test
 Recognize conditions requiring immediate attention • Periorbital & Gross
• EOM evaluation
FOR WHAT DO PATIENTS CONSULT THEIR DOCTORS URGENTLY • Pupillary reflexes
WITH REGARDS TO THEIR EYES? • AC assessment
1. Red and painful eye • Fundoscopy
• IOP determination
 Red eye differential
 Ocular trauma
INSTRUMENTATION
2. Urgent White Eye
 Sudden asymptomatic visual loss
 Leukocoria

PRESENTATIONS OF OCULAR ER
THE ACUTE RED EYE
 Infection
 Inflammation
 Glaucoma
 Trauma
 Blunt SCENARIO 1
 Penetrating/perforating - Visual loss in an otherwise
- Externally Normal eye
THE ACUTE WHITE EYE
 Acute visual loss ARTERIAL OCCLUSIVE DISEASE
 Vascular occlusion
 Retinal detachment
 Optic neuritis
 Intraocular tumors
 Retinoblastoma
 ROP

BASIC INFORMATION - HISTORY Central Retinal Artery Occlusion Branch Retinal Artery Occlusion
 Demographic data
 Chief complaint COMMON PRESENTATION:
 Evolution of illness Overall pallor of the involved area/s of the retina
 Laterality
 Duration and tempo CENTRAL RETINAL ARTERY OCCLUSION
 Associated signs and symptoms  True ophthalmic emergency
 Medical/surgical history  Sudden painless visual loss
 Medications/allergy  “CHERRY-RED SPOT”; generalized retinal edema and
opacification
 Is the visual loss transient or persistent?  Precipitating factors
 Is the visual loss monocular or binocular? o Arteriosclerosis
 What was the tempo? Did the visual loss occur abruptly, or o Hypertension
did it develop over hours, days, or weeks? o Diabetes
 What are the patients’ age and medical condition? o Inc IOP
 Did the patient have documented normal vision in the o Embolisation
past?  Treatment within 45-90 min (golden period)

1
OCULAR EMERGENCIES
Jesus F. Marin, M.D.
Department of Ophthalmology APRIL 25, 2017

 Vitreous hemorrhage
o Ocular trauma (especially penetrating)
o Child abuse
 Retinal detachment
o Ocular trauma
o Child abuse
o Norrie disease
o Incontinentia pigmenti
TREATMENT:
o Cutis marmorata telangiectatica
 Carbogen, brown paper bag breathing
o Turner syndrome
 Efforts to decrase IOP and dislodge the embolus/clot
o Walker-Warburg syndrome
o Digital massage
o Stickler syndrome
o IV Acetazolamide
 Other retinal abnormalities
o AC Paracentesis
o RETINOBLASTOMA
 Phamaceutical: Systemic antithrombotic agents
o COATS' DISEASE
 Surgical o Persistent hyperplastic primary vitreous
o CV with direct CRA massage (persistent fetal
o PRP for NV
o vasculature)
o Anti-VEGF treatment
o Retinopathy of prematurity
o Ocular toxocariasis
CENTRAL RETINAL VEIN OCCLUSION o Familial exudative vitreoretinopathy
 Sudden painless visual loss o Congenital retinoschisis
 “HOT DOG AND CATSUP” fundus  Optic disc abnormalities
o Venodilation o Colobomata of choroid and optic disc
o Generalized hemorrhage o Morning glory syndrome
o Exudates o Myelinated nerve fibers
 Precipitating factors  Uveitis
o Arteriosclerosis o Juvenile rheumatoid arthritis
o Hypertension o Sarcoidosis
o Diabetes o Toxoplasmosis
o Inc IOP  Infection
o Embolisation o Endophthalmitis
 Complications o Orbital cellulitis
o Macular edema  Tumors
o Neovascularization o Retinoblastoma
o Glaucoma (90 day) o Leukemia (with ocular involvement)
o Vitreous hemorrhage o Intraocular tumors (other than retinoblastoma)
o Traction retinal detachment o Choroidal melanoma
o Metastatic tumors
o Choroidal osteoma
o Medulloepithelioma ("diktyoma")
Treat neovascularization by o Combined hamartoma of the retina and the
panretinal photocoagulation retinal pigment
o epithelium
o Choroidal hemangioma
o Benign astrocytic hamartomas in tuberous
sclerosis

LEUKOCORIA
 Retinoblastoma
 Congenital/Developmental Cataracts
 Retinopathy of Prematurity
 Persistent Hyperplastic Primary Vitreous
- Check every month for 6 months
- Look for rubeosis and angle NV  Others
o Retinal Detachment
o Vitreous Hemorrhage
DIFFERENTIAL DIAGNOSIS OF LEUKOCORIA o Ocular Inflammation
 Lens abnormalities o Congenital Glaucoma
o Cataract (congenital or acquired) o Mesodermal Dysgenesis
o Posterior lenticonus o Neonatal Infection
2
OCULAR EMERGENCIES
Jesus F. Marin, M.D.
Department of Ophthalmology APRIL 25, 2017

CAUSES OF LEUKOKORIA IN PEDIATRIC POPULATION  Newborns with uni- or bilateral cataracts are surgical
ENTITY USUAL AGE OF INCIDENCE OF emergencies which should be referred to an
DETECTION BILATERALITY ophthalmologist immediately.
RETINOBLASTOMA Several months of 1/3
age RETINOPATHY OF PREMATURITY (ROP)
CATARACT At birth Varies PATHOPHYSIOLOGY
RETINOPATHY OF Several months of Very high  Sufficient Cause: IMMATURE RETINAL VASCULATURE
PREMATURITY age o Prematurity
(ROP) o Low Birth Weight
PERSISTENT At birth 1/10  Potentiated by excessive oxygen administration
HYPERPLASTIC  Influenced by maternal and neonatal factors
PRIMARY VITREOUS  Maternal Factors
(PHPV) o Alcohol
o Anemia
COAT’S DISEASE o Diabetes
o Drugs (antihistamines)
 Fundamental causes:
o Duration of ruptured membranes
o Formation of retinal telangiectasia
o Glucocorticoids
o Breakdown of the inner blood-retinal barrier
o Multiple Births
 Progressive exudative changes noted with subsequent
o Threatened Abortion
retinal detachment
o Tobacco
o Toxemia of Pregnancy
 Neonatal Factors
o Acidosis
o Alkalosis
o APGAR score
o Apnea
o Birthweight
RETINOBLASTOMA o Bradycardia
o Bronchopulmonary Dysplasia
 Most common intraocular malignancy of childhood
o Endotracheal Intubation
 LIFE THREATENING
o Exchange Transfusion
 1 in 20,000 live births
o Gestational Age
 Prognosis is directly related to the size and degree of o Vitamin E Deficiency
extension o Hypotension
o Intraocular = possible cure o Hyperoxia
o With orbital extension = poor prognosis o Hypoxia
 IMMEDIATE OPHTHALMOLOGIC REFERRAL o Intracranial Hemorrhage
o Intrauterine Growth Retardation
PRESENTATION o Indomethacin
 Bilateral= within 15 mos.; ave = 8 mos. o Light
 Unilateral= by 20-30 mos.; ave = 25 mos. o Patent Ductus Arteriosus
 90% within 3 years o Respiratory Distress Synd
 Rare after 7 years o Sepsis
 Signs and symptoms o Ventilatory Support
o Leukocoria
o Squint EXAMINATION SEQUENCE
o Photophobia  Screen at about the 4-8th week of age
o Proptosis  Repeat every 1-2 weeks until the ff:
o Inflammation o Normal and complete blood supply develop
o Glaucoma o Successive 2-week exam shows Stage 2 in zone III;
then, every 2-4 weeks
PEDIATRIC CATARACTS o Development of “prethreshold” - weekly
 Most common cause of pediatric leukocoria o ROP disappears
 May be congenital or developmental with variable  Once blood supply completed — every 6-12 months
opacification and visual interference
 Approach is completely different from adult cataract
 May require surgery in the first few weeks of life in the
more opaque cases

3
OCULAR EMERGENCIES
Jesus F. Marin, M.D.
Department of Ophthalmology APRIL 25, 2017

ICROP CLASSIFICATION • POSSIBLE SEQUELAE OF ACUTE PVD

 Stage 3: o Uncomplicated PVD (85%)
o Fibrovascular proliferation on the edge of the ridge
o Mild, moderate or severe vitreous infiltration
o 50% chance of progression to stages 4 and 5 and
blindness
 THRESHOLD
o Stage 3 ROP
o Zone 1 or 2 in 5 or more continuous clock hours
o Zone 1 or 2 with 8 cumulative hours of involvement
with the presence of “plus disease” o Retinal tear formation and haemorrhage (10-15%)
o INTERVENTION W/IN 72 HOURS OF DIAGNOSIS
 Stage 4:
o Fibroproliferative scar contraction and partial RD
o 4A - detached outside of the macula (zone1)
o 4B - retinal detachment involving the macula
o POOR VISUAL PROGNOSIS

o Avulsion of retinal vessel and haemorrhage

(uncommon)

• Stage 5:
o Complete RD with a closed or partially closed funnel,
from the ON to the retrolenticular space
o Essentially no useful vision
o Treatment : SURGICAL
RHEGMATOGENOUS RETINAL DETACHMENT
VR traction at points of adhesion
↓
Transmission of energy to the retina
↓
Break/hole formation relieves traction, but allows
↓
Liquid vitreous access to SR space
↓
Neurosensory retina separates from RPE
• Plus Disease ↓
o With abnormal iris vessels/tortuosity and Retina becomes edematous and opaque
engorgement of retinal vessels ↓
o Rush Disease plus disease involving zone 1 - very Photoreceptor degeneration and atrophy in time
rapid progression
OPTIC NEURITIS
ROP TREATMENT
• Objective: ABLATE ISCHEMIC RETINA
• Modalities:
o Cryotherapy
o Laser Photocoagulation
‒ Indirect Ophthalmoscope
‒ Surgical / Endolaser
‒ Endoptik
‒ Laser Diopexy
Profound visual loss
PVD AND RETINAL DETACHMENT o Inflammation of the optic nerve
• Two components for retinal break formation o Invariably leads to MS
o Acute posterior vitreous detachment (PVD) o 15-20% of MS present with ON
o Predisposing peripheral retinal degeneration o 35-40% of MS ----> ON

4
OCULAR EMERGENCIES
Jesus F. Marin, M.D.
Department of Ophthalmology APRIL 25, 2017

CLINICAL SYMPTOMS THE HISTORY: VISION

 70% , unilateral • Are one or both eyes affected?
 30% , bilateral • Vision at time of examination?
• Vision prior to trauma?
TRIAD:
 Loss of vision THE HISTORY: SYMPTOMS
 Ipsilateral eye pain • Symptoms besides decreased vision ?
 Dyschromatopsia • Duration of symptoms ?
• Any surgery prior to trauma ?
TREATMENT
 OPTIC NEURITIS TREATMENT TRIAL SUPERFICIAL/CONJUNCTIVAL INJECTION
o A large multicenter prospective study conducted from • Superficial ocular affliction
1988-1991 • Bright red/peripheral
o On MRI, presence of 2 or more foci of demyelination • Blanches with pressure or
or if visual loss is severe, give IV corticosteroids adrenaline
• Examples:
MODALITIES o Conjunctivitis
 Oral prednisone o Blepharitis
o Did not have a better outcome than those given
placebo CILIARY INJECTION
o Increased rate of recurrent optic neuritis • Usually connotes deep
o No benefit for typical cases of optic neuritis and may intraocular pathology
even predispose patients to further attack • Violaceous / Perilimbal
 High dose IV Methylprednisolone + oral prednisone • Does NOT blanch on pressure
o IV methylprednisolone (250 mg qid x 3 days) followed or with adrenaline
by oral prednisone (1mg/kg/day x 11 days) • Examples:
o Sl. faster recovery of visual function o Uveitis
o Final VA after 6 mos. did not differ from that of o Glaucoma
placebo-treated patients
o Associated with a reduced rate of development of ACUTE RED EYE DIFFERENTIAL DIAGNOSIS
multiple sclerosis over a 2-yr follow-up period
CONJUNCTIVITIS IRITIS/UVEITIS GLAUCOMA
PROGNOSIS INJECTION Superficial Ciliary Ciliary
 Visual Recovery DISCHARGE Mucoid/Purulent Serous Serous
o Irreversible optic nerve damage occurs in 80% of CORNEA/AC Infiltrates Flare/Cells Bedewed
pateints, but recovery of Snellen acuity is good PUPILS Normal Constricted Mid-dilated
o 65-80%: 20/30 or better IOP Normal Low High
o 45% recover within the first 4 mos VISION Normal ↓/Moderate ↓/Severe
o 35% recover near normal acuity at 1 yr
o 20% fail to make any significant CONJUNCTIVITIS
QUERIES
Scenario 2 • Is the involvement unilateral or bilateral?
- Visual loss in an ACUTELY RED AND CONGESTED • What was the tempo? Did the redness and/or discharge
PAINFUL EYE occur abruptly, or did it develop over hours, days, or
weeks?
THE RED EYE • What are the patients’ age, activities, and medical
• Ocular injection can denote : condition? Was there any exposure?
o Inflammation • Is there pre-auricular lymphadenopathy?
o Hypersensitivity • Is there significant visual loss? Transient or permanent?
o Infection
o Ciliary vs conjunctival DIFFERENTIALS
• Usually associated with • VIRAL
o Pain o Bilateral
o Discomfort o Serous to mucoid discharge
o Swelling o Predominantly
• Onset, duration, and associated signs and symptoms lymphocytic
determine the etiology cellular response
o With pre-auricular
lymphadenopathy
o Self-limiting
5
OCULAR EMERGENCIES
Jesus F. Marin, M.D.
Department of Ophthalmology APRIL 25, 2017

• BACTERIAL • SIGNS
o Monocular o Ciliary injection
o Mucopurulent to purulent o Miosis
discharge o Flare and cells
o Predominantly o Endothelial precipitate
segmenter cellular o Synechiae
reaction o Iris nodules
o NO pre-auricular ‒ Koeppe (pupil)
lymphadenopathy ‒ Busacca (iris)
o Requires antibiotic treatment
• ALLERGIC/HAYFEVER/IRRITATIVE UVEITIS/IRITIS: MANAGEMENT:
o Associated with asthma, allergic rhinitis, exposure to • Work-up
noxious stimulants • Anti-inflammatory agents
o Symptoms: itchiness or o Steroids
burning sensation o NSAIDS
o Stringy discharge • Cycloplegics
with copious serous o Tropicamide/cyclopentolate
secretion, and swelling o Atropine sulfate
o Treatment: isolation from • Anti-infectives (as indicated)
triggers, supportive
ACUTE ANGLE CLOSURE GLAUCOMA
NEWBORN: OPHTHALMIA NEONATORIUM • Sudden, monocular
• Chemical (silver nitrate) • Severe ipsilateral headache with
• Gonnorheal (hyperacute) vomiting, shallow AC, steamy
• Staphylococcal cornea, mid-dilated pupils
• Chlamydial • History of iridescent vision or
activity in a semidarkened
CONJUNCTIVITIS: MANAGEMENT environment
• VIRAL/IRRITATIVE
o Grams/Giemsa stain SIGNS
o Supportive • Shallow anterior chamber
‒ Antiinflammatory agents • Corneal bedewing
‒ Decongestants • Mid-dilated, sluggish to non-reactive pupil
‒ Sulfacetamide • Hard, tender globe to palpation / elevated intraocular
• BACTERIAL pressure
o Grams/Giemsa stain
o Appropriate antimicrobials MEDICAL MANAGEMENT
• OBJECTIVES
ACUTE IRITIS (UVEITIS)/IRIDOCYCLITIS o Constrict pupil/decongest the peripheral angle
***Iridocyclitis: iritis + inflammation of o Improve outflow/decrease aqueous production
ciliary body o Dehydrate the vitreous
• Inflammatory disease • AGENTS
• Usually monocular o Anticholinergic (Pilocarpine)
• Precipitated by: o Betablockers (Timolol/Betaxool)
o Stress o Carbonic anhydrase inhibitors (Diamox)
o Resistance breakdown o Osmotic agents (Glycerol/Mannitol)
o Thunderstorms
• Associated with browache and photophobia SURGICAL MANAGEMENT
• IRIDECTOMY/IRIDOTOMY
UVEITIS: SIGNS AND SYMPTOMS
• SYMPTOMS
o Photophobia
o Deep ocular pain
o Reflex lacrimation
o Mild to moderate visual reduction
o Floaters

6
OCULAR EMERGENCIES
Jesus F. Marin, M.D.
Department of Ophthalmology APRIL 25, 2017

• Hemorrhagic chemosis sever hypotony may imply a

rupture
• Conjunctival injury heal quickly and may mask perforations

BLOWOUT FRACTURE OF THE ORBIT

• Direct blunt injury
• Intact orbital rim
• Presentation:
o Diplopia
o Hypotropia
• Diagnostic modalities:
o EOM evaluation
o Forced duction test
o Imaging techniques
• W/O for fx of the medial wall and optic canal

SUBCONJUNCTIVAL HEMORRHAGE

Surgical Iridectomy Laser Iridotomy

OCULAR TRAUMA
PROTECTIVE MECH Inferior iridodialysis Traumatic aniridia
• Orbital rim
• Lashes and lids
• Blink/Bell’s reflex
• Tears and lacrimal system

EXAMINATION TIPS
• A drop of topical anesthesia may facilitate evaluation
• Exposure/tension may be dangerous when there is Rupture of the globe
perforation
• Retract and fix lids only over the orbital rim and not the TRAUMATIC HYPHEMA
globe

TYPES
• Blunt
• Penetrating/Perforating
• Chemical/Thermal Burns

BLUNT TRAUMA • Grade 1 - Layered blood occupying less than one third of
• Sphincter pupillae muscle may be ruptured, resulting in the anterior chamber
semidilated pupil that does not react to light (iridoplegia) • Grade 2 - Blood filling one third to one half of the anterior
• Iris may be torn from its insertion to the scleral spur chamber
causing iridodialysis • Grade 3 - Layered blood filling one half to less than total of
• Tear a portion of the lens zonule, causing the lens to the anterior chamber
become subluxated • Grade 4 - Total clotted blood, often referred to as
blackball or 8-ball hyphema
CONTUSION HEMATOMA/TRAUMATIC IRITIS
BLACK EYE MANAGEMENT
• Secondary to blunt ocular 1. Light activity or even bedrest (to prevent a rebleed into the
injury anterior chamber, which may cause obstruction of vision, or a
• Presentation: painful rise in pressure)
o BOV 2. Elevation of the head of the bed by approximately 45 degrees
o Photophobia (so that the hyphema can settle out inferiorly and avoid
o Lacrimation obstruction of vision, as well as to facilitate resolution)
o Sphincter rupture
o Iridoplegia

7
OCULAR EMERGENCIES
Jesus F. Marin, M.D.
Department of Ophthalmology APRIL 25, 2017

3. Wearing of an eye shield at night time (to prevent accidental Corneal foreign body removed
rubbing of the eyes during sleep, which can precipitate a
rebleed)
4. Avoidance of pain medications such as aspirin or ibuprofen
(which thin the blood and increase the risk of a rebleed -
instead, acetaminophen can be used for pain control)

CORNEAL ABRASIONS
SYMPTOMS
CONJUNCTIVAL FOREIGN BODY
• Foreign body sensation
• Foreign bodies can always be removed with:
• Pain
o Irrigation
• Tearing
o Spud
• Photophobia
o Cotton-tipped applicator
• Foreign bodies frequently lodge on the upper tarsal
conjunctiva
• Upper eyelid must be everted to remove them

TREATMENT
• Topical cycloplegic
• Topical antibiotic
• Pressure patch over eye

LACERATIONS
SUPERFICIAL LID LACERATIONS
• Avoid lid margin retraction
• Give tetanus prophylaxis
• Remove superficial foreign bodies
• Rule out deeper foreign bodies

EYELID LACERATION
Eye shields Lateral canthal tendon disruption

FOREIGN BODIES
CORNEAL FOREIGN BODY

Canalicular laceration

• Wounds of the eyelid must be carefully cleaned with soap

and water
• Lacerations parallel to eyelid margins are closed with fine
sutures
• Vertical lacerations are divided into:
o Outer five sixths of the eyelid (ciliary) margin
o Inner one sixth of the eyelid (lacrimal) margin which
avulse the cannaliculi leading to the tear sac

CILIARY MARGIN
• Outer five sixths of eyelid margin
• Place first suture through gray line of the eyelid to align
eyelid margin
• Remainder of the eyelid can be closed in layers with catgut
sutures for the tarsus and silk for the skin

8
OCULAR EMERGENCIES
Jesus F. Marin, M.D.
Department of Ophthalmology APRIL 25, 2017

• Usually projectiles
• Careful examination technique
• Requires REFERRAL

INTRAOCULAR FOREIGN BODY

• Present in injuries in which small particles penetrate the
cornea or the sclera
• Large foreign bodies markedly disrupt the globe and cause
LACRIMAL MARGIN
so much associated injury that the eye may be
 Inner one sixth of the eyelid that sever a cannaliculus
disorganized and require eventual enucleation
 Placement of a stent thru the cannaliculus to remain
patent
• A sharp, pointed metallic intraocular foreign body (IOFB)
 Closure of laceration
rests on the retina, covered by a small amount of vitreous
 Prevention of traction by the orbicularis oculi muscle hemorrhage
located lateral to the laceration • Commotio retinae and B-scan ultrasound
o show the shadowing behind the IOFB and the
anechoic zone extending into the sclera (black arrow)
o Note the low-lying retinal detachment caused by a
hole from the IOFB (white arrow).

DIAGNOSIS AND TREATMENT DEPEND ON THE FF FACTORS:

 Lacerations of the bulbar conjunctiva that do not involve • Size of the foreign body
the globe are rarely severe enough to require surgical o Roentgen-ray
closure o Ultrasound
• Usually surrounded by an area of subconjunctival o CT-scan
hemorrhage • Magnetic Properties
• Laceration is evident as a white, crescentic area o Only nickel and iron may be removed by magnet
• Tissue reaction
CORNEAL LACERATIONS o Siderosis
• Location within the eye
• Seidel testing can reveal ocular
wound leaks through the
SYMPATHETIC OPHTHALMIA
use of sterile tetracaine eyedrops
and a fluorescein strip. • A bilateral, chronic, diffuse inflammation of the uveal tract
• Occurs days, months or years after injury to the uvea,
(a) Slitlamp photograph of a small particularly the ciliary body, by a perforation of the sclera
corneal laceration with a moderately by accidental trauma
shallow anterior chamber. • A quiet, insidious uveitis affects the exciting eye with
ciliary injection, decreased vision and photophobia, keratic
• Partial-thickness corneal precipitates, posterior synechiae, inflammatory cells fill
lacerations should be carefully the vitreous
inspected to ensure that Descemet’s membrane is intact.
• Direct appositional sutures are used to close lacerations • “MUTTON-FAT” keratic precipitates
with well-defined margins • Iris is thickened, dilates poorly
• Pupillary margin is bound to the lens with posterior
CORNEOSCLERAL LACERATIONS synechiae (adhesions)
• Inflammatory cells fill the vitreous
• For repair, the lacerated area is exposed by dissecting the
• Ophthalmoscopy discloses small yellowish white nodules
cut edges of the conjunctiva and tenon capsule from the
in the retinal pigment epithelium (Dalen-Fuch’s nodules)
scleral laceration
• Prolapsed uveal tissue is excised and vitreous removed
• Sclera closed with interrupted sutues
• Conjunctiva closed separately

PERFORATING/PENETRATING INJURIES
• Presentation:
o History of fluid gush
o Chemosis/hypotonic • Removal of a severely injured eye within 7 days after a
o Flat/shallow AC penetrating injury prevents the development of
o Prolapsing uveal tissue sympathetic ophthalmia
o Peaked pupil • Topical therapy for uveitis
• Systemic prednisone
9
OCULAR EMERGENCIES
Jesus F. Marin, M.D.
Department of Ophthalmology APRIL 25, 2017

CHEMICAL BURNS
• A true ocular emergency
• Alkali more serious than acid
• Immediate irrigation – essential

IRRIGATION OF CHEMICAL BURNS SHOULD BE INITIATED BEFORE

ARRIVAL AT EMERGENCY CENTER

INITIAL EC MEASURE
• Topical anesthesia
• Copious Irrigation
• Check for foreign bodies

EC TREATMENT FOLLOWING IRRIGATION

• Topical cycloplegic
• Topical antibiotic
• Patch eye
• Prompt referral to ophthalmologist

EYELID THERMAL BURNS

• First-degree eyelid burn
o Erythema and mild edema of the eyelid
o No loss of epidermis
• Second-degree eyelid burn
o Epidermal loss
o More painful
o Blisters and oozing of serous fluid
o Lid contraction
• Third-degree eyelid burn
o Full-thickness skin
o Charring and white-brown waxy consistency
o Usually are not painful

*Purely PPT-based.

RISE UP; TAKE COURAGE AND DO IT.

Ezra 10:4


10
 OPHTHALMOLOGY
3.2 Ocular Manifestations (Dr. Barja)
Date: 13 October 2015
FEU-NRMF Institute of Medicine
---------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------
STRABISMUS
 “to squint” – to look sideways or off center; not straight

ANATOMY AND PHYSIOLOGY

 6 extra-ocular muscles (EOM)
o 4 recti
 Medial rectus (MR)
 Lateral rectus (LR)
 Superior rectus (SR)
 Inferior rectus (IR)  Significance: during eye surgery
 ALL have the same insertion and they form the Annulus of
Zinn Medial rectus (nearest to the 5.5 mm
 Each muscle is approximately 40mm long and 10 mm wide corneal limbus)
o 2 obliques
 Superior oblique (SO)
 Inferior oblique (IO) Inferior rectus 6.5 mm
 The 4 recti and the superior oblique originate from the apex of
Lateral rectus 7.0 mm
the orbit.
 The inferior oblique originates from the floor of the orbit. Superior rectus 8.0 mm

MUSCLE INNERVATIONS

 If you want to view your EOMs, request for a CT Scan or MRI.

LR6 --- SO4 --- R3

 Lateral rectus – Abducens

 Superior Oblique – Trochlear
 The Rest - Oculomotor

EYE MOVEMENTS
1
 Ductions
3 o monocular eye movement
o adduction, abduction,etc
2  Versions
o conjugate binocular eye movement
o eyes move in the same direction
o dextroversion, levoversion
 Vergence
o disconjugate binocular eye movement
o eyes move in opposite directions
o convergence, divergence

 Pictures 1 and 2 show a normal EOM

o Tapering at the origin and at the insertion
 Picture 3 shows problematic EOMs specifically a thyroid eye
problem – there is bulging of the belly

MUSCLE INSERTION

 The EOMs insert in the sclera anteriorly

 Most people would have the same distance of insertion from the
corneal limbus.

Faith Angeli J. Ladia (3A) 1

 Out of the 6 movements, 4 are voluntary movements.  Yoke muscles
Intortion and extertion are involuntary. o 2 muscles one in each eye that are the prime movers
 When you tilt your head to the right, what happens to your eyes? in their respective eyes in a given position of gaze
The RIGHT eye INTORTS and the LEFT eye EXTORTS. o If you look the right, the 2 yoke muscles are? Right LR
 Agonist and Left MR. To the left? Left LR and Right MR. Down
o primary muscle moving the eye in a certain direction and right? Right IR and Left SO. Up and right? Right SR
o when you move your eyes upward, the agonist muscle is and Left IO. Don’t forget dexterity lalo na sa exams! 
the SR. When looking down? IR.
HERING’S LAW OF EQUAL INNERVATION OF MUSCLE
 Synergist
o The “helpers”
 Applied for yoke muscles, for version
o muscle in same eye that acts with the agonist in the
same direction Equal innervation is supplied to
o When moving the eye up: Agonist? SR. Synergist? IO. yoke muscles to move both eyes
 Antagonist into the same direction of gaze.
o muscle in same eye acts in opposite direction as the
agonist
o When moving the eye up: Agonist: SR. Synergist? IO.
Antagonist? IR.

MUSCLE PRIMARY SECONDARY TERTIARY

ACTION ACTION ACTION
MR Adduction
LR Abduction
SR Elevation Incycloduction Adduction
IR Depression Excycloduction Adduction POSITIONS OF GAZE
SO Incycloduction Depression Abduction
IO Excycloduction Elevation Abduction
Table 1. Eye movements. MEMORIZE! 

Mnemonics: SINRAD

ALL Superiors are INTORTERS.

ALL Vertical RECTI are

ADDUCTORS.

Primary position (straight gaze)

SHERRINGTON LAW OF RECIPROCAL INNERVATION Secondary position ( up, down, right, left)

 For monocular eye movement/ductions Tertiary position (right & up, right & down, left & up, left & down)

In a certain movement, there is Diagnostic position (9 positions)

increased innervations of the
agonist, and there is a decreased  Always do all of these so as not to miss the muscle that is
innervations of the agonist. problematic.

The same amount of contraction of BINOCULAR VISION

the agonist has also the same
amount of relaxation of the
antagonist. BINOCULAR SINGLE VISION (BSV)

VERSIONS
An image coming from your L eye is
slightly different from that of the R
eye.

BSV is the ability to fuse these

slightly different images to be able
to see just one single image.

Requirements for BSV:

 clear visual axes

 ability of the retino-cortical elements to fuse slightly different
images
 binocular eye movements
 coordination in movement of the two eyes in different
direction of gaze

Faith Angeli J. Ladia (3A) 2

 AMBLYOPIA  Strabismus
o ocular misalignment of whatever cause
 “lazy eye”  Orthophoria
 In comparison to the other eye, one eye has poor vision o ideal condition of ocular balance/straight eyes
 It is not corrected by glasses
CLASSIFICATION OF STRABISMUS
CLASSIFICATION

 Strabismic
o You grew up with one eye misaligned ACCORDING TO DIRECTION OF DEVIATION
o One eye can see straight ahead while another eye
deviates → creates confusion → disregard other image  Horizontal
(usually patient chooses the image seen straight ahead) o Esodeviation
 Anisometropic o Exodeviation
o An- – negative; -iso – equal; -metropia – measurement  Vertical
o Unequal measurements (grades) of the eyes o Hyperdeviation
o Ex: R eye is +8.00, L eye is -2.00 o Hypodeviation
o Patients tend to use the eye with the lesser grade and
Esotropia – inward deviation
disregard the image coming from the eye with a higher
grade
 Stimulus deprivation Exotropia – outward
o Ex: patients born w/ a cataract in one eye deviation
 Iso-ametropic
o Equal grades but both eyes have very high grades Hypertropia – upward
 Meridional deviation
o Patients having more than 300 astigmatism

 Torsional
o Excyclodeviation
1 2 o Incyclodeviation

ACCORDING TO AGE OF ONSET

 Congenital/infantile
o prior to age 6 months
 Acquired

4 3 ACCORDING TO FUSION STATUS (WHETHER THE DEVIATION

CAN BE CONTROLLED BY FUSION MECHANISM)

In times of fusion, the eyes are aligned; in non-fusion, the eyes are
misaligned

 Phoria
o latent deviation; eyes remain aligned
1 – strabismic o there is a hidden strabismus
2 – stimulus deprivation (cataract)] o when you cover one eye, there is misalignment
3 – congenital ptosis → stimulus deprivation  Intermittent phoria or tropia
4 – severe astigmatism → meridional o Obvious – sometimes straight gaze, sometimes
misaligned
TREATMENT o Fusion control present
 Presents in childhood → must be detected early to be able to  Tropia
treat early because amblyopia can only be treated until age 8. o manifest deviation; fusion control not present
 Present clear retinal image to amblyopic eye o progression from phoria to intermittent to
o in problems of refractive errors or cataracts → correct manifest/permanent
o astigmatism → give astigmatic correction
 Make the child use the amblyopic eye ACCORDING TO VARIATION OF DEVIATION WITH GAZE
o Patching POSITION OR FIXATING EYE
 Cover the good eye so that the bad eye
would start working  comitant
 Usually done 2 hrs every day o patient is cross-eyed: when patient is asked to look to
o Penalization the R or L → still cross-eyed
 Triad of accommodation:  incomitant
 Change in shape of the lens (more o patient is cross-eyed in straight gaze
spherical) o when asked to look to the R → straight. To the left →
 Eye convergence cross-eyed
 Pupillary constriction o there is a change in the amount of deviation in
 Put atropine (dilation) on the good eye → loss different positions of gaze
of accommodation → blurring of vision →
patient has no choice but to use the
amblyopic eye

Faith Angeli J. Ladia (3A) 3

ACCORDING TO FIXATION

 alternating
o sometimes, patient has a deviated gaze in the L,
sometimes in the R; or sometimes an eye is straight,
sometimes deviated from time to time
 monocular

EXAMINATION OF THE PATIENT

A B
A. History taking
 Chief complaint Which one has strabismus? B. Patient A may look cross-eyed but when
 Age of onset you do the Hirschberg Test, the light falls on the center of both pupils.
 Direction of deviation In patient B, the light is displaced on the temporal side → esotropia
 Constant or intermittent
 Alternating or monocular fixation KRIMSKY TEST
 Magnitude of deviation
 Antecedent or concurring illness
o seizure, diabetes, hypertension
 Associated eye complaints
o diplopia, blurring, vision
 Thyroid disease
 Trauma
 Previous consultation or treatment
o patching, glasses, surgery
 Maternal and birth history Makes use of prism glasses to neutralize the deviation. It moves
 Developmental history the corneal light back to the center.
 Family history
COVER TEST
B. Ocular Examination

 Visual acuity
 Ocular motility exam
o Do versions and ductions
o Usually, versions are done first. When normal,
you don’t have to do ductions anymore
 Ocular alignment test
o Corneal light reflex (Hirschberg)
o Prism test (Krimsky)
o Cover test
 cover-uncover test
 alternate cover test (prism and cover
test)
o Ophthalmoscopy To know if patient has phoria (hidden/latent strabismus). Patient
o Refraction comes to you straight gazed → cover 1 eye → when you uncover → eye
movement back to center. L figure – exophoria. R figure - esophoria
HIRSCHBERG TEST/CORNEAL LIGHT REFLEX TEST

Use your penlight. Normally, it should be at the center of the pupil. If Also done to know which eye is fixating. L figure – Right esotropia
it’s slightly off your pupil, then most probably you have an eye w/ Left eye preference. Cover L eye → R eye takes fixation → Uncover
deviation. → L eye takes fixation. The L eye is the better eye because it is always
the one fixating.
 A 1 mm deviation from the center (N pupil size = 2-3mm)
means a 7° eye deviation. R figure: Alternating fixation. R eye deviated → cover L eye → R eye
fixates → Cover R eye → L eye fixates

Faith Angeli J. Ladia (3A) 4

  congenital motility disorder usually
COMMON TYPES OF STRABISMUS
unilateral
 Major problem: paralysis of the LR because
th
the 6 CN did not develop
COMITANT STRABISMUS (NON PARALYTIC/NON-RESTRICTIVE)  limited abduction or limited adduction or
both
 Congenital or infantile esotropia  globe may retract and eyelid fissure may
o Shortly after birth up to 6 months of age narrow on adduction
o Deviation is big and constant  there may be up-shooting or down-shooting
 > 30 prism diopters, > 4mm of the eye
o Cross fixation  face turns to allow patient to use both eyes
 If patient wants to look at the L visual field, together
patient uses the R eye and vice versa
o Over-action of inferior obliques

 Refractive Accommodative Esotropia

o Acquired, usually > 6 mos of age
o 2 years of age
o hyperopia of +3.00 to +10.00 diopters
o magnitude of esodeviation is moderate
o constant non-alternating accommodative esotropia can
cause amblyopia
Left LR palsy: At left gaze, L eye did not move. There is up-shooting of
the IO. There is narrowing of the palpebral fissure bc the aberrant CN 3
w/c innervates the MR may also innervate the LR → abnormal globe
retraction. There is also limitation in the R gaze.

o Brown syndrome
 restriction of superior oblique tendon
sheath limiting elevation in adduction

Patient is asked to look L and up. L

Patient will try to make objects look clearer by accommodating → eye eye is fine. R eye cannot elevate. It
convergence → cross-eye. Over-accommodation can bring about could be a palsy of the IO or a
over-convergence → eye deviation restriction of the SO.

 Sensory esotropia It is common in trauma and

o Anything that blocks vision on 1 eye can cause eye improves within 6 months
deviation
o A non-seeing eye would be deviated either inward or
outward
o Corneal opacity, cataract, retinal scars, inflammation, o Mobius syndrome
tumors, optic neuropathy, anisometropia  palsy of CN VI and VII

 Intermittent exotropia mask-like facies and limited

o More common in Asians abduction
o Most number of cases seen
o Starts as intermittent and becomes manifest (fatigue, patient has bilateral LR palsy and a
sleepy, or inattentive) flat face
o Closes 1 eye when exposed to bright sunlight
o Frequency increases as patient grows older

 Sensory exotropia
o Eye that does not see well for any reason may turn
outward o Congenital fibrosis syndrome
 restriction of 1 or more extraocular muscles
 muscle fibers are replaced with fibrous
tissue
usually familial –
they cannot look
up

INCOMITANT STRABISMUS (MUSCLE PARALYSIS/RESTRICTION)

 Paralytic strabismus
o Limitation of action of the involved muscle
o Patients should have neurologic and systemic
evaluation
o Patients may have diabetes and/or hypertension

 Strabismic syndromes
o Duane syndrome

Faith Angeli J. Ladia (3A) 5

SYSTEMIC ILLNESSES ASSOCIATED WITH STRABISMUS o Transposition
 Thyroid disease
o Graves’ ophthalmopathy
o EOMs undergo swelling and inflammation and later
replaced by fibrous tissue
o IR is affected first → Medial → Superior → Lateral →
Obliques (IMSLO)
 Diabetes mellitus
o Acute onset of diplopia
o Most commonly seen here in the Phils.
o Improves within 6 months
 Myasthenia gravis
o Abnormal fatigability of striated muscles
If you have an LR palsy, you can join fibers from your working SR and
 Neurologic
IR → join it with the weak/paralyzed LR → to make the LR straight.
rd
In patients w/ 3 nerve palsy (eye that is down and out), only the SO
and LR are working. In this case, you can manipulate your LR and SO
to make your patient’s eyes aligned again.

Thyroid eye dse: fibrotic Left IR → L hypotopia

Myasthenia: at the end of the day, all muscles are tired

How to diagnose MG in the clinics: tire the patient by asking him to

look up/down continuously. You can also diagnose by putting ice in the
patient’s eyes and then you can see that the eyes will open up.

MANAGEMENT

 Aims
o Good vision
o Binocularity
o Good alignment

PRINCIPLES OF MANAGEMENT OF A STRABISMIC PATIENT

 Enhance vision
o Spectacles
o Treat amblyopia
 Patching
 Manipulation of Accommodation
o Esodeviation
 Anti-accommodative therapy
 plus lenses for hyperopia
o Exodeviation
 Stimulate accommodation
 overcorrect myopia, undercorrect hyperopia
 Prism
o Acute onset of strabismus, diplopia, small deviation
 Surgery
o Recession
 muscle weakening procedure
 from its original insertion, you move it back
→ you lengthen it → weaker pull
o Resection
 muscle strengthening procedure
 you shorten the muscle → stronger pull

Faith Angeli J. Ladia (3A) 6

 Far Eastern University - Nicanor Reyes Medical Foundation
OPHTHALMOLOGY 2018 - OPTICS and OPTICAL DEFECTS
Prepared by: The O.D.

NOTE: This lecture is tailor-made for those who want to Electromagnetic Spectrum
further understand this topic in Ophthalmology. Supplement
it with other transes/ppts.

The Eye as an Optical System

- What the eye does to the light = refraction

The Eye as a Sense Organ

- How the brain perceives the light and forms
images out of it - The entire distribution of the electromagnetic radiation
according to frequency and wavelength
- The stimulus for vision is the visible light or also known as
OPTICS the white light
- Ranges from 380 to 770 micra or nanometers in wavelength
- branch of physics which deals with the study of light and its - Red has the longer wavelength but lower frequency, while
behavior. blue has the shorter wavelength but greater frequency.

BRANCHES OF OPTICS

1.) Physical optics - deals with the wave properties of light.

When we say wave properties, we refer to the diffraction and

interference of light. Diffraction is the bending of light as it
enters an aperture, and interference is the increase or decrease
in the amplitude of light when two waves emitted (In this image, we compare the red from the blue. Wavelength
superimpose on each other. refers to the distance from one deflection to the next one,
while frequency is the number of deflections. Relate it with the
2.) Geometric optics - how the entering light into the eye is previous statement.)
focused exactly on the retina.
- Light falling outside the said range is also known as invincible
This branch deals with the reflection, refraction and absorption light simply because the eye cannot see it. Examples are the x-
of light, most importantly as it is focused on the retina. If ray, ultraviolet light and infrared.
physical optics deals with the wave properties of light, this one
deals with the properties of light as a ray or as a straight line. Characteristics of the Visible Light

3.) Physiologic optics - how light energy is converted or 1.) Velocity

transformed into visual energy. 2.) Wavelength
3.) Frequency
4.) Neuro-ophthalmologic optics - how the visual energy will
be interpreted as an image in the brain, particularly in the - To put in an equation:
occipital lobe which contains the Primary and Secondary
Visual Cortices. 1.1. 𝑉𝑒𝑙𝑜𝑐𝑖𝑡𝑦 = 𝑊𝑎𝑣𝑒𝑙𝑒𝑛𝑔𝑡ℎ 𝑥 𝐹𝑟𝑒𝑞𝑢𝑒𝑛𝑐𝑦, or

𝑉𝑒𝑙𝑜𝑐𝑖𝑡𝑦
Physical Optics 1.2. 𝐹𝑟𝑒𝑞𝑢𝑒𝑛𝑐𝑦 =
𝑊𝑎𝑣𝑒𝑙𝑒𝑛𝑔𝑡ℎ

- deals with the wave properties of light

Page 1 of 10
 Far Eastern University - Nicanor Reyes Medical Foundation
OPHTHALMOLOGY 2018 - OPTICS and OPTICAL DEFECTS
Prepared by: The O.D.
Speed of Light
Refraction
- The speed or velocity of light in air is:
1.1. 186,282.40 miles/sec, OR - the bending of light wave as it travels from one medium with
1.2. 299,792.46 meters/sec a given refractive index to a medium with another at an
oblique angle.
- The speed or velocity of light in a vacuum is:
1.1. 299,792.46 meters/sec Refractive Index

A medium is a space where light travels. This includes air, - a measure of how fast light propagates at a given medium
water, glass and others. Vacuum on the other hand is a
medium devoid of matter. It is just a space that exists in theory.

That is why if you compare the speed of light in air to that in

a vacuum, they are the same.

Geometric Optics

- how the entering light into the eye is focused exactly on the
retina, particularly, at the macula.

The preceding table shows you the different media where light
can travel as well as their indices of refraction. To understand
it further, let us express it in an equation where we want to
know how we came up with 1.33 as the index of refraction of
water:

𝑠𝑝𝑒𝑒𝑑 𝑜𝑓 𝑙𝑖𝑔ℎ𝑡 𝑖𝑛 𝑣𝑎𝑐𝑢𝑢𝑚

𝐼𝑛𝑑𝑒𝑥 𝑜𝑓 𝑟𝑒𝑓𝑟𝑎𝑐𝑡𝑖𝑜𝑛 =
𝑠𝑝𝑒𝑒𝑑 𝑜𝑓 𝑙𝑖𝑔ℎ𝑡 𝑖𝑛 𝑤𝑎𝑡𝑒𝑟

299,792.46 𝑚/𝑠
𝐼𝑛𝑑𝑒𝑥 𝑜𝑓 𝑟𝑒𝑓𝑟𝑎𝑐𝑡𝑖𝑜𝑛 =
226,000 𝑚/𝑠

𝐼𝑛𝑑𝑒𝑥 𝑜𝑓 𝑟𝑒𝑓𝑟𝑎𝑐𝑡𝑖𝑜𝑛 = 1.326 𝑜𝑟 1.33

The macula (e) is the central region of the retina. Anatomically,
this is defined as the 3-mm diameter area containing the
This means that light travels 1.33 times faster in a vacuum
yellow luteal pigment xanthophyll. The fovea (c) is a 1.5mm
compared to water. Take note however, that to be able to
area characterized histologically by thinning of the outer
compute for the index of refraction, the speed of light in a
nuclear area (cell body of the photoreceptors) and absence of
given medium must be provided.
other layers. In the center lies the 0.3mm diameter foveola,
seen as a depression that creates a reflection when viewed
ophthalmoscopically (foveal reflex). It is also the thinnest part
of the retina and provides for the optimal visual acuity (central
vision).

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Snell’s Law of Refraction
Accommodation

- Process by which the crystalline lens varies its focal length in

response to changes in the vergence of incident light.
- Simply put, this is the process by which the crystalline lens
changes its shape in response to near objects.
- This is the reason why the dioptric power of the lens from the
table ranges from 19-35 D.
- At distance, the lens is said to be relaxed, which explains the
19 D, but when focusing at near, the lens becomes more
convex or more spherical, increasing its refractive power up to
almost 35 D.
- This law states that:
Physiologic Optics
“A light-ray will deviate more towards the normal in
the optically denser medium, that is, the medium with a
higher index of refraction. While a light-ray will deviate more - how light energy is converted or transformed into visual
away the normal in the lesser dense medium, that is, the energy.
medium with a lower index of refraction.”
Laws Governing the Transformation of Light into Visual
Referring to the preceding figure, a light ray coming from a Energy
source travels through air, strikes the air-water interface and
is bent toward the normal in the water. On the right, a light ray 1.) Law of Conservation of Energy
coming from a source travels through water, strikes the air- - Photochemistry of vision;
water interface and is bent away from the normal in the air. In - energy can neither be created nor destroyed
numerical terms, we know that the index of refraction of air is - energy can only be converted from one form (light
1.0 and the index of refraction of water is 1.33. If a light ray energy) to another (visual energy).
coming from a source travels through air with a refractive - in this case, the energy that entered the eye is the
index of 1.0, it is expected that it will be bent toward the light energy and the energy that emanates from it is
normal as it hits the water, and the other way around. the visual energy.

Refractive Media of the Eye 2.) Law of Specific Energy

- there is a specific organ for a specific energy.
- there is a characteristic sensation produced by an
Medium Refractive Dioptric
Index Power organ’s adequate stimulus.
Cornea 1.376 42 D
Aqueous Humor 1.336 1D Visual Senses
Crystalline Lens 1.36 19-35 D
Vitreous Humor 1.336 1D 1.) Light Sense
Total Refractive Power of the Eye: 60 D - role of visual pigments in the retina
- Vitamin A + opsin
The primary refractive media of the eye refer to the cornea and - β-carotene
the lens because they provide for most of its refractive or - Vit. A from plants (water-soluble form)
dioptric power compared to the aqueous and vitreous which - Contains 2 molecules of Vit. A
- Forms of vitamin A
only provides 1 D each.
-Aldehyde - retinal or retinene combined
with opsin
- Alcohol – retinol

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- Vit. A ester - stable form released in - Gross form sensitivity
circulation attached to Retinal Binding
Protein (RBP)
- Acid - Cannot be utilized by the retina

2.) Form Sense

- Visual acuity specification in terms of angular size

- Light absorption by the photoreceptor outer segments of the gap for the smallest-sized letter the patient can
isomerizes 11-cis-retinal to all-trans-retinal, which dissociates identify.
it from opsin. - A person can recognize form as long as what he or
- All-trans-retinal is converted to all-trans-retinol in the she sees an object with a minimum visual angle of 1 minute
retinal pigment epithelium in the presence of light. or 1’.
- All-trans retinol is isomerized to 11-cis-retinol and is again
converted to 11-cis-retinal.
- 11-cis-retinal plus opsin thus form the rhodopsin.

Enzymatic Activities

* Trans-retinine/all-trans-retinal (aldehyde) is
converted to all-trans-retinol by retinal reductase + NADH +
H+
* All-trans-retinol is converted to 11-cis-retinol by
retinol isomerase
* 11-cis-retinol (alcohol) is converted to 11-cis-retinal
(aldehyde) by retinol reductase + NAD+

Photoreceptors
As you can see in the previous figure, the gap in the letter C
* Cones subtends 1 minute of an arc, that is, in a person with clear
- Daylight or photopic vision vision at 20 feet, he will be able to distinguish the smallest C
- Color vision in a visual chart if he is able to recognize that gap. Same goes
- Contour resolution or visual acuity with the letter E and others. Also, the whole letter C is divided
- Concentrated at the macula by 5 squares. That means that the whole letter, including the
gap subtends 5 minutes of an arc.
* Rods
- Night or scotopic vision
To put that in a scientific correlation with visual acuity:
- No color perceptive ability
- Faint light intensity
- Movement

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OPHTHALMOLOGY 2018 - OPTICS and OPTICAL DEFECTS
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A person with a visual acuity of 20/40 means that at
20 feet, he can see the smallest letter that subtends an angle
of 5’ of an arc which can be seen by an emmetrope at 40 feet. EXAMINATION OF THE EYE AS AN OPTICAL SYSTEM
AND AS A SENSE ORGAN
3.) Color Sense
- Function of the cones
- Tested by commonly using the Ishihara Color Plates. HISTORY TAKING
Each plate consists of numbers which the patient
would identify and lines which a patient can trace. What you have to elicit during history taking in an eye
examination in the clinic:

1.) Is there blurring of vision with one eye? Both eyes?

2.) If unilateral only, which one, the right or the left?

- This is very important particularly in the pediatric
age groups because most of these patients won’t subjectively
tell you which of their eye is blurred. In this case, amblyopia
could go unchecked.

Amblyopia - aka lazy eye; a condition in which lowered visual

Neuro-ophthalmologic Optics acuity exists, even with the best correction in place, without
any obvious cause. One common example is when one eye is
- how the visual energy will be interpreted as an image in the highly myopic while the other eye has less error. In this case,
brain, particularly in the occipital lobe which contains the since the brain is responsible for fusing images coming from
Primary and Secondary Visual Cortices. both eyes, it will just disregard the blurred one and will just
use the good eye. If this is not taken into consideration, when
This branch of optics also deals with the simultaneous macular that patient reaches the age when all the ocular structures are
perception of images, their fusion, the ability to perceive fully developed, even if you give the best correction, no
three-dimensional depth or solidity known as stereopsis or improvement to 20/20 will be noted.
stereoscopic vision, and the visual field.
3.) How long was the patient experiencing the blurring?
Always remember that in order to appreciate depth perception
or stereopsis, you need binocular single vision. 4.) Is there eye strain?

The Visual Pathway Eye strain aka asthenopia is a feeling of fatigue, discomfort, or
(I did not include the lesions as they were not discussed.) pain localized in or about the eyes or thought to be associated
with the use of the eyes (especially when using the computer
or reading at near).

5.) Is there frequent blinking? How about frequent rubbing of

eyes?

Both of these manifestations are done by an individual with

the hope of improving their eyesight.

6.) Is there headache?

7.) Had any previous eye consultations? Was there any

prescription of corrective lenses? What was the reason for the
previous visit?

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8.) Ask for social history. Does the patient avoid playing Synkinetic Near Triad
outside?
A triad of:

TESTS DONE DURING AN EYE EXAMINATION

1.) Accommodation - the ability of the eye to focus clearly for
objects at various distances especially at near.
Aside from the 5-step basic eye examination (visual acuity is (Parasympathetic division of CN3 to the ciliary muscle)
again included below) discussed previously, the following are
also performed 2.) Convergence - the ability of both eyes to simultaneously
move nasally. (Somatic innervation of inferior division of CN3)
I. VISUAL ACUITY TESTING

- The most logical starting point, as any complaints of 3.) Constriction - the ability of the sphincter pupillae to
blurred vision elicited during the history is confirmed, and contract to focus an object clearly at the center of the macular.
patients typically expect the doctor to have them read the (Parasympathetic division of CN3 to the sphincter pupillae)
“eye chart”
The synkinetic near triad or simply the near triad, is a function
Basic Procedures (For Review) of the inferior division of the ophthalmic nerve and in a normal
person, should be present simultaneously in response to near
1.) Determine the distance and near visual acuity without the stimulus.
correction (DVA and NVA SC), distance and near visual acuity
with correction (DVA and NVA CC), with the right eye first,
then the left.

2.) Caution the patient not to squint as this will cause an

erroneously high acuity in myopes and astigmats.

3.) Record the findings in terms of the smallest complete line

of letters identified (20/20), the number of letter not identified
in the line in question (20/20-1 or 20/40-2), or the number of
letters identified in addition to those in the line in question
(20/25+1 or 20/100+2)

Sample Visual Acuity Testing Charts:

Once the CN 3 enters the SOF, it will divide into two main
branches, the superior division and inferior division. The
superior division will give off a branch that will innervate the
levator palpebrae superioris muscle (LPS) and another branch
that will innervate the superior rectus muscle (SR).

The inferior division will give off three branches going to the
medial rectus (MR), inferior rectus (IR) and inferior oblique
(IO). It also runs along with the parasympathetic division which
will synapse at the ciliary ganglion to help function for
accommodation.

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When is the synkinetic near triad tested during an eye exam?

- When performing the test for PERRLA (pupils equally round,

responding to light and accommodation)
- To observe the near reflex, the patient in a semidarkened
room is first ask to fixate at a distant object then asked to
fixate at a near target. While doing this, the examiner notes for
the presence of the synkinetic near triad.

Presbyopia
- occurs when accommodation has receded to the point that
near work is difficult or impossible without the use of plus
lenses for correction;
-normal aging process. 2.) Subjective Refraction - examiner determines the refractive
state entirely on the basis of the patient’s subjective responses.
II. REFRACTION If you ever had an eye exam or witnessed one, this is the part
where the examiner asks the patient “which is clearer? lens 1
- the determination of the refractive state of the eye or lens 2?”.

Two types: Instruments used:

1.) Objective Refraction - the examiner determines the A. Trial Lens Case
refractive state of the eye on the basis of the optical principles
of refraction without the need to the patient responses.

Instruments used:

A. Retinoscope - a streak of light is flashed on the eye;

refractive state is determined by neutralization. (Compared to
ophthalmoscopy, the examiner should be at a working
distance of 67cm away from the patient or approx. one arm’s
length).

B. Phoroptor

B. Autorefractometer/Autorefractor - patient is asked to place

his chin on a rest and fixate on an object seen inside the
machine (usually a hot air balloon), and the examiner gets the
estimated amount of refractive power displayed on the screen.

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OPHTHALMOLOGY 2018 - OPTICS and OPTICAL DEFECTS
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Phoroptors are mostly used for adults, trial lens cases are
useful for kids. (In my practice however, I prefer the use of trial - particularly useful for the diagnosis of corneal disorders such
lenses over phoropter, as I would be able to elicit right away if as keratoconus where there is too much steepening of the
the patient will have issues walking with eyeglasses, or cornea, those who are undergoing hard contact lens therapies
headache with glasses, etc.) and as a screening for those who will undergo refractive
surgery such as that in LASIK.
Note: An eye examination should include both objective and
subjective refraction to gather accurate refractive results. IV. Biometry

* Cycloplegic Refraction - measures the axial length of the eye to determine its
- Also known as wet refraction because this method refractive power.
uses the use of cycloplegic agents such as tropicamide to - particularly useful in the computation of artificial intraocular
paralyze the accommodation of the patient before performing lenses to be implanted after cataract removal.
refraction. - with the use of topical anesthetics, a probe is used to touch
- In cases of pseudomyopia, less minus power is the eye and readings will then be registered at a screen.
found in cycloplegic refraction than the usual one.

III. Keratometry

- provides information about the curvature and refractive

power of the cornea determined in the two principal corneal
meridians.
- particularly useful in patients with astigmatism and those
who are using or having problems with contact lenses.

CONDITIONS OF THE EYE AS AN OPTICAL SYSTEM

AND AS A SENSE ORGAN

EMMETROPIA
- The normal refractive state of the eye where parallel rays of
light will converge to a sharp focus on the retina.

IV. Corneal Topography (Photokeratoscopy or

Videokeratography)

- a non-invasive imaging technique used to map the surface

curvature of the cornea. Hotter spots appear red and denote
steepness of that corneal area while colder spots appear blue
and denote the flatter areas of the cornea.
AMETROPIA

- A refractive condition other than emmetropia where parallel

rays of light fail to converge to a sharp focus on the retina.
- Also known as error of refraction or refractive anomaly.

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OPHTHALMOLOGY 2018 - OPTICS and OPTICAL DEFECTS
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Types of Astigmatism
Myopia

- Nearsightedness or shortsightedness
- Parallel rays of light converge to a focus in front of the retina
- Eyeball may be too long, or cornea is too steep
- Corrected with concave lenses (minus lenses or diverging
lenses)

Hyperopia

- Farsightedness
- Parallel rays of light converge to a focus behind the retina
- Eyeball may be too short (in normal children), or cornea is
too flat
- Corrected with convex lenses (plus lenses or converging
lenses)

1.) Simple - One focus lies on the retina, the other is in front
(simple myopic) or behind (simple hyperopic).
2.) Compound - Both foci lie either in front of the retina
(compound myopic) or behind (compound hyperopic).
3.) Mixed - One focus lies in front of the retina and the other
lies behind.

Astigmatism

- There is failure to form a point image for a point object, GOALS FOR THE TREATMENT or CORRECTION OF
hence the occurrence of multiple foci in the retina REFRACTIVE ERRORS
- The interval between the two extremes of foci is called the
interval of Sturm or conoid of Sturm 1.) To improve visual acuity;
- Corrected with cylindrical lenses which has different 2.) For muscle balance (to avoid the development of
curvatures strabismus or even the suppression of one eye); and
3.) Relieve ocular discomfort and headache.

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OPHTHALMOLOGY 2018 - OPTICS and OPTICAL DEFECTS
Prepared by: The O.D.

CORRECTIVE OPTIONS correction will be in the form of spectacles, this may induce
aniseikonia if one eye is aphakic and the other one is not,
1.) Spectacles or Eyeglasses hence the need for contact lenses.
- Plus lenses (for hyperopes or presbyopes)
- Minus lenses (for myopes) SURGICAL OPTIONS
- Cylindrical lenses (for astigmats)
2.) Contact Lenses 1.) Radial Keratotomy
- Spherical (for myopes or hyperopes) - 6-8 radial incisions are made on the cornea
- Toric (for astigmats) - goal is to flatten the steep cornea for the correction
- Multifocal lenses (for presbyopes) of astigmatism, keratoconus or myopia

Eyeglasses Contact Lenses

Advantages
* Cheaper * Wide field of view
* Less requirement for care * Less aniseikonia
* Easier to adjust * For aphakic patients
Disadvantages
* Restricted visual field due * Psychologic trauma (due
to the rim of the glasses to the impact of putting it
* Marked aniseikonia on)
* Distorted peripheral * Higher risk for corneal
images for cylindrical lenses complications due to
* Cosmetic and psychologic inappropriate care
impact * Dryness of eyes 2.) Photorefractive Keratectomy
* More expensive - Excimer laser
- Corneal epithelium is removed and discarded while
Aniseikonia the deeper layers are reshaped by the laser
- A difference in the sizes of the retinal images for the two
eyes as a result of anisometropia or astigmatism. 3.) Laser-assisted in situ keratomileusis (LASIK)
- Laser surgery (also excimer laser in practice)
Anisometropia is a condition in which the refractive state - The cornea’s deeper layers are created into a
differs for the two eyes. An example would be: permanent flap, then reshapes the portion where the flap was
partially removed, after which the flap is returned to place.
OD: +10.00
OS: +2.00 4.) Automated Lamellar Keratoplasty
- A microkeratome is used to create a flap in the
There is an 8.0D difference between the two eyes. If you will cornea and is used again to remove a thin disc of corneal
give full correction of plus lenses, the +10D will produce higher stroma below. The flap is then returned to heal.
magnification effect compared to that of the +2.0D hence,
there will be a difference in the sizes of images perceived by 5.) Femtosecond lenticule extraction (FLEx)
the brain. Same goes with the minification induced by minus - Laser-based
lenses. - A thin lenticule is cleaved from the corneal stroma
for manual extraction via a flap.
Aphakia
- The condition in which the crystalline lens has been removed, 6.) Small incision lenticule extraction (SMILE)
hence the need for a strong plus correction to compensate for - Laser-based
the loss of refracting power of the crystalline lens. Again, if the - Same goal with flex except that a flapless technique
is done.

-END of the OUTLINE but NOT the END of your DREAM-

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 Far Eastern University
Nicanor Reyes Medical Foundation
Institute of Medicine
Batch 2020

DISORDERS OF THE UVEAL TRACT

Dr. Pia Regina E. Galvante – August 14, 2018

DISCLAIMER: USE AT YOUR OWN RISK! (Kung may corrections, kaya

nyo na yan. Malaki na kayo. Wag na makulit)

In Filipinos, the less brown is the abnormal eye. In Caucasians,

the bluer eye is the abnormal eye. In those with green eyes, if
the other has a grayish tint, that is the abnormal eye. Top L: iris (key hole)
Top R: Ciliary body (notching in the lens)
Bottom L: indirect fundoscopic exam
Bottom R: choroidal coloboma – absence of the choroid so you see
more of the sclera

2. ANIRIDIA

 Failure of the anterior growth and differentiation of the

optic cup
 Results in a rudimentary iris concealed behind the
corneoscleral limbus
Structures that make up the uveal tract  There can be cases of total aniridia (patient cannot see
 Iris anything)
 Ciliary body  S/Sx: photophobia, VA of 20/200 deteriorates with corneal
 Choroid opacification and glaucomatous optic atrophy, cataracts

Doc didnt discuss the anatomy. Please review your prelim 3. ATROPHY OF THE CHORIOCAPILLARIES
lectures na lang.
BENIGN TYPE Depigmentation in situ
CONGENITAL AND DEVELOPMENTAL ABNORMALITIES OF THE No functional impairment
UVEA Seen in simple myopia & aging

1. COLOBOMA DEGENERATIVE TYPE Choriocapillaries are absent

 Failure of the optic cup to close in the retinal fissure Severe functional impairment
 Involves the inferior nasal quadrant of the uvea
 Types A. Generalized Choroideremia
o Choroid – white sclera (nawawala yung Gyrate atrophy
pigments) Toxic retinal pigment degeneration
o Ciliary body – notching defect of the lens
o Iris – key hole pupil B. Focal Central choroidal sclerosis

Depending on which structures are affected it will appear to have

notchings, absence of muscles, or absence of structures in certain
areas.

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 Normally blood vessels are NOT seen in the iris. Blood vessels can
only be seen in cases of retinal ischemia, ocular inflammatory
diseases, tumors, and sometimes as a complication of traumatic
surgery.

6. RUBEOSIS IRIDIS
 Fine, markedly tortuous anastomosed, tightly
 meshed network of blood vessels on the surface and w/in
the stroma of the iris
(Left) X-linked – A carrier. The retina is red orange in color. White  May cover the trabecular meshwork and eventually
patches defect in choroid  cause neovascular glaucoma (secondary glaucoma)
(Mid) Choroideremia – more severe deep red orange color of retina  Risk factors:
(Right) gyrate atrophy – these are usually hard to identify in the o Retinal ischemia: DM retinopathy, CRVO
clinics → do genetic testing o Ocular inflammatory diseases
o Ocular tumors
o Surgical complications
4. HETEROCHROMIA IRIDIS
 Differences in the color of the iris Blood vessels more concentrated in
o Hypochromia – lighter iris pupillary border. Most patients have
o Hyperchromia – darker iris glaucoma. Patients complain of
severe pain in the affected eye. In
HYPOCHROMIC HYPERCHROMIC this picture, the lens has a cataract
Simple congenital hypochromia Ocular melanosis
Horner’s syndrome Ocular nevus
Fuchs’ Heterochromic Ocular hamartoma
Iridocyclitis Iris ectropion UVEITIS
Waardenburg syndrome Pigmented tumors  A non-specific term used to denote intraocular
Non-pigmented iris tumors Siderosis bulbi inflammation involving the uveal tract (iris, ciliary body,
Trauma Rubeosis iridis choroid) and adjacent ocular structures (retina, optic
Long-standing hyphema nerve, vitreous, sclera, macula)
Drug-induced (Xalatan)
EXAMINING A UVEITIS PATIENT
In brown eyes, the lighter the iris, that’s the abnormal one.  Same as examining a patient with retinal problem or
In blue eyes, the darker eye is usually the abnormal one. glaucoma problem
In green eyes, hypochromic eye becomes grayish in color.  Good patient history and thorough examination are
indispensable
o Saves the patient from undergoing unnecessary
5. IRIS ATROPHY investigations
 Blood vessel and collagen fibers atrophied and replaced by o Provide the basis for the generation of
a sclerosed network of collagen tissues differential diagnosis
 Can be caused by surgery, trauma, or certain autoimmune o Allows determination of response to treatment
conditions  Systemic association is common in uveitis
 Eventually this causes neovascular glaucoma o Joint pains in arthritis-related uveitis
 Examples o Skin changes (AIDS)
o Iridocorneal endothelial syndrome o TB-related uveitis (lung problem)
 Corneal edema + Iris atrophy + o Other systemic infections causing uveitis:
secondary glaucoma Toxoplasma, toxocara, Herpes Virus Infections,
 3 variants HIV-AIDS (CMV Retinitis) etc.
o Chandler syndrome  Important to do a targeted review of systems
o Essential iris atrophy / progressive iris atrophy
o Iris nevus / cogan-resse syndrome COMMON SIGNS AND SYMPTOMS (non-specific)
 Most of the time is seen in children. Can cause blurred  Eye redness
vision, diplopia or distorted image  Blurring of vision
 Tearing
 Photophobia
 Pain or discomfort
 Floaters

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BASIC EYE EXAMINATIONS SLIT LAMP EXAMINATION
 Visual Acuity  Cornea
o Right eye first
o Before putting eye drops, examine visual acuity Layers of cornea
first  Anterior epithelium
o Check the vision to know if this is debilitating to  Bowman’s layer
the patient, has it been a while since the patient  Stroma
having a blurred vision? Is it simply corrected  Dua’s layer
with spectacles? Is it a refractive error?  Descemet’s membrane
 Usually reduced from a combination of problems involving  Endothelium
various eye strictures
o Cornea, lens, vitreous, optic nerve etc. o Keratic precipitates
o Determine the source of poor vision as this helps  MC finding in uveitis
in determining the mode of treatment  Aggregates of inflammatory cells on
the corneal endothelium
Corneal problem or anterior problem – eye drops can do  Indicates inflammatory activity
Posterior problems – you have to do injections or oral medications  ARLT’S TRIANGLE - base down
configuration of keratic precipitates on
 EOM the endothelium
o Generally not affected  After the resolution of inflammation:
o There can be dull pains but can still move the  Disappear completely
eye  Become smaller, translucent,
 Intraocular pressure or pigmented
o Normal  May be fine, medium, or large
o Hypotonic (ciliary body involvement)  Round, or stellate: stellate seen in viral
o Firm/Hard (open angle or angle closure types of infection, and appreciated
glaucoma, steroid induced) more in slit lamp exam
 Pigmented, or non-pigmented
Slit lamp is used to get the IOP. In addition, fingers situated  Mutton-fat KPs – large, round ones.
underneath the orbital rim. Then palpate the eye. Be careful not to Quite oily in appearance.
palpate the eye of a patient with open globe injury. Compare the
right and left eye. Same pressure with the nose is normal, lips are
hypotonic, and chin is hypertonic.

 Pupils
o Irregularly shaped
o Eccentric
o Poor dynamics

o Dendrites
 Inflamed or enlarged corneal nerve
 Infected probably by herpes virus
This means that there is adhesion between the iris and anterior lens o Band keratopathy
capsule. Then you try to shine a light, there is no movement. There is  Calcium deposits on corneal epithelium
poor pupil dynamics already.  Usually in the interpalpebral region of
the cornea
 Conjunctiva  Caused by chronic inflammation, the
o Conjunctival injection pH balance in the surface of the eye
changes and it favors deposition of
calcium

Ciliary redness can be

seen beyond the
limbus

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  Iris FUNDUS EXAMINATION
o “Moth eaten” iris  Indirect Ophthalmoscope
o Absence of crypts o Ideal for defining extent and height of retinal and
o Iris atrophy (depigmented areas) choroidal lesions
o Membranes o Penetrates vitreous haze, media opacities,
o Adhesions (synechia) cataracts
o Nodules o Gives wider view of the fundus
o Heterochromia o Gives you an inverted view (what you see
inferiorly is actually what is in the retina
Nodules located in the pupillary border - Koeppe nodules superiorly)
Nodules in the iris body or stroma – Busacca Nodules  78/90 D Lens
Nodules found in the angles – Berlin’s Nodules o Provide inverted view
o Ideal for viewing vascular abnormalities,
intraretinal lesions, vitreoretinal traction
o
 Hruby Lens
o Prenetrates haze better than 78/90 D
o Better for assessing macular edema
 Mirrored Contact Lens
o Detailed exam of peripheral chorioretinal lesions
 Anterior chamber
o AC cells and Flare VITREOUS
 Cells: immune cells, sign of active  Snowballs
inflammation  Haze – there are inflammatory cells that can
 Flare: increased protein content in cause hazy
aqueous due to damaged iris blood  Strands
 Membranes
 Vitreo-retinal traction

Anterior chamber is the space between the iris and cornea. This is
where the aqueous flows. In patients without inflammation, it is
clean, nothing can be seen. For anterior uveitis or panuveitis, cells
are graded by counting the cells in 1x1 mm

 Anterior vitreous
o Vitreous cells
 Increased cells and protein
 Arise from choroid, retina and ciliary VASCULAR CHANGES
body o Vascular sheathing
 Also a sign of inflammation  Inflammatory
cells around
blood vessels

o Hemorrhages,
exudates, and cotton wool spots
 Related to retinal ischemia

 Lens
o Cataract
 Due to underlying inflammation or
secondary to chronic steroid use or
trauma

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Vasculitis – when you look at the vessels, parang may nakabalot na Retina is a thin film which covers the posterior surface of the
puti eye. In uveitis, it can be affected because when your vessels
Hemorrhages- can be red in color, typically described as dot blot, were damaged or inflammed, there will be fluid collection
pinpoint, flame or spindle shaped underneath the retina. It is called EXUDATIVE/ SEROUS
Cotton wool spots – yellow in color, cotton wool spots are fluffier in RETINAL DETACHMENT.
appearance
Exudates – yellow in color with distinct borders It can be resolve by giving STEROIDS to resorb the fluid. But
incases of tear or hole, it is SURGICAL.
INFILTRATES
 Similar to cotton wool spots SUBRETINAL FIBROSIS
 Deep within the retina –
when vessels crossover it

GRANULOMAS
 Organized collection of
macrophages
 Inner retina as well  A cause of chronic inflammation (may result to
 Often seen in TB uveitis scarring which can be pigmented or non-pigmented,
flat or elevated)
 Appears as plaques and bands of yellow white
tissue (They can be deep in the retina because
vessels travels over it)
DEPIGMENTATION
 There is lighten up of the iris CHOROIDAL LESIONS
 Normally it is red orange
 White scars due to infections

Dalen-Fuchs Nodules in Vogt-Koyanagi-

Harada Disease

 Appear as grayish yellow elevated masses

 Tumors/masses
ATROPHIC LESIONS
 Surrounded by areas of The choroid is pigmented so lesion in the choroid may present
hyperpigmentation to you as pigmented lesions.
 Old inactive uveitis
Looking at the picture:
You’ll know that the lesions is beneath the retina because of
RETINAL DETACHMENT the vessels that travels over it. Vessels also gives you a clue if
the lesions are elevated. (ex. Bending of vessesl)

CYSTIOID MACULAR EDEMA

2 KINDS OF RETINAL DETACHMENT

1. RHEGMATOGENOUS – occurs when a tear/break/hole in

the retina leads to fluid accumulation w/ a separation of the
neurosensory retina from the RPE.

2. NON-RHEGMATOGENOUS – no retinal tear  Fluid accumulation underneath the macula

2.1 Exudative / Serous / Tractional – often seen in  Presence of “petaloid apperance” characteristic of
uveitis CME
2.2 Bullous – retinal ballooning of the retinad/t
presence of subretinal fluid

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Your macula is the center of your vision. In CME, when you 1. ANATOMICAL CLASSIFICATION OF UVEITIS
look straight or looking at the face your friend, you will not
able to see the details of his face clearly, like the nose. But the
periphery (away from the center) is clearer.

RETINAL PERIPHERY

Anterior Involves only the iris, cornea up to the

pars plicata

HLA-B27-related: ankylosing
spondylitis, Reiter’s, JIA, viral
Intermediate Pars plana involves more of the ciliary
body, vitreous and lens, sometimes
 Pars plana snowbanking the macula is affected but often as
o accumulation of white fibroglial mass a complication
over pars plana and adjacent retina
o usually restricted to inferior pars plana Pars planitis, TB
Posterior Pars plana up to the optic nerve
To assess the periphery, you’ll need to ask the patient to look (retina, sclera, or choroid) During
at the extreme left or right, up and down. Then you will look discussion, doc include MACULA at the
at the sides of the retina. Sometimes there are presence of posterior part
inflammatory cells called as SNOWBANKING.
Posterior scleritis, TB
Panuveitis Combination of the 3
OPTIC NERVE (Normal cup disc ratio 0.3-0.5)
 Neuritis / Swelling TB, VKH (Vogt-Koyanagi-Harada
 Disc edema Disease), toxoplasma, toxocara
 Papilledema
 Neovascularization
 Atrophy (pale) 2. INFECTIOUS VS NON-INFECTIOUS
 Glaucomatous nerve
Infectious Non-Infectious
Toxocara JIA
Toxoplasma Ankylosing spondylitis
Herpetic Behcet’s
HIV-AIDS Vogt-Koyanagi-Harada
TB Malignancies:
Melanomas
Retinoblastoma
Lymphoma

INFECTIOUS UVEITIS

CLASSIFICATION OF UVEITIS
1. Anatomical
2. Infectious vs Non-infectious
3. Onset and Course of Inflammation
4. Granulomatous vs Non-granulomatous
5. Age-group / Race
6. Unilateral vs Bilateral

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NON-INFECTIOUS UVEITIS ANCILLARY EXAMINATIONS

WHY INVESTIGATE?
 Will it identify any underlying systemic disease
process or association?
 Will it provide a “definitive” etiology?
 Will it confirm or reject a diagnosis?
 Will it help in the management of the patient?

GENERAL INVESTIGATIONS
 CBC, ESR, CRP (underlying systemic disease)
 syphilis serology (VRL, RPRP)
 urinalysis
 chest x-ray, PPD (for TB - even if its negative, you
can still have uveitis)

Any other tests that need to be ordered would depend on the

clinical findings and index of suspicion for a particular
diagnosis.
 Color vision testing
 Electroretinogram
 Electrooculogram
 Fluorescein angiography (for problem in the retina,
to know the flow of blood, if there is ischemia,
bleeding, hemorrhage)
 Laser interferometry
(FROM LADIA TRANS)  Laser flare reading
 Ultrasound
Ankylosing Conjunctivitis, irirtis, blurring of vision,  Visual evoked potential
spondylitis eye redness and bamboo spine on  Visual field testing
xray (sacroiliac view)  OCT (Optical Coherence) - to see the layers of the
Toxocara Normally you don't have the white retina
granuloma structure, and there is traction. A  ICG Angiography (Indocyanine Green)
traction band attaches to the  Imaging – xray, CT
granuloma. Dilated fundoscopic exam
– (esp congenital) presents w/ a scar. ULTRASOUND OF THE EYE
Juvenile Eye inflammation, membranes and iris  choroidal thickening
Idiopathic adhesions, may have a cataract  vitreous condensation/ bands
Arthritis (JIA)  retinal detachment
Behcets Oral ulcers, hemorrhages, vasculitis
Disease FLUORESCEIN ANGIOGRAPHY
CMV Retinitis MC seen in HIV (+) patients  Cystoid macular edema
Melanoma Pigmented tumor in the posterior  Neovascularization
chamber  Disc leakage
 Vessel leakage
Herpes Zoster Dermatomal distribution, does not
 Staining and pooling
Ophthalmicus cross the midline. Lesion on nose –
 Retinal lesions
Hutchingson’s sign – there is ocular
involvement and inflammation
IMAGING TESTS
 Cranial CT Scan
 CT scan of sinuses
 Gallium scan
 Hand x-ray
 Cranial MRI
 Sacroiliac x-ray
 Chest x-ray

SKIN TESTING
 Allergy testing
 Anergy testing
 Behcetin/Pathergy
 Histoplasmin
 Kveim – Sarcoidosis
 PPD

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 SURGICAL MANAGEMENT
BIOPSY SPECIMENS  Glaucoma surgery – for uncontrolled, elevated IOP
 Conjunctiva  Cataract surgery
 Lacrimal gland  EDTA chelation – for band keratopathy
 Aqueous humor  Corneal transplant – for corneal decompensation,
 Vitreous ulcers, opacified scars
 Choroid and retina  Retinal Surgery – for retinal complications such as
 Skin retinal detachment, traction membranes,
intraocular infections
INVESTIGATION SUSPECTED ETIOLOGY
sacroiliac joint x-ray HLA-B27 related disease (AS) EMERGING DISEASES
angiotensin converting enzyme sarcoidosis  New and emerging diseases have been reported in
(ACE), Kveim test, Chest CT recent years
 Case reports have documented ocular inflammation
Toxoplasma dye test/ IgG toxoplasmosis in Dengue, Chikungunya, Ebola and Zika infections
antibodies
ELISA toxocara
HLA-B typing, Behcetin Behcet’s disease
ANA, RF, x-rays of joints JRA
Mantoux test, chest x-ray tuberculosis
CT scan of orbits/ B-scan posterior scleritis
ultrasound
MRI head scan demyelination, non-Hodgkins
lymphoma, neurosarcoidosis
CSF studies demyelination, non-Hodgkins
lymphoma, VKH
Polymerase Chain Reaction of herpesviral DNA, propionibacter
Intraocular Fluid DNA

TREATMENT OF UVEITIS
GOALS
 Control the inflammation
 Control the infection
 Treat complications

MEDICAL MANAGEMENT
 Topical (drops, gels, ointments)
o Mydriatic-cycloplegics
o Anti-inflammatory medications (NSAIDS
and corticosteroids)
o IOP lowering medications (anti-glaucoma
medications)
o Antibiotics (anti-bacterials, anti-virals,
anti-fungals)
 Regional/Periocular/Intravitreal injections
o Corticosteroids (triamcinolone,
dexamethasone) - more affordable
o Antibiotics (anti-bacterials, anti-virals)
o Anti-Vascular Endothelial Growth Factor
(Ranibizumab,Bevacizumab) - quite
expensive, dont use often
 Systemic (Oral/Intravenous)
o Corticosterioids (prednisone,
methylprednisolone) - most of the time “Jesus never said it would be easy, but He said it would be
o Immunomodulatory agents worth it”
(antimetabolites, biologics, etc.) - if -Matthew 7:13-14
cannot tolerate corticosteroids
o IOP lowering medications (anti-glaucoma REFERENCES
medications)  Ladia and Pacis Trans
o Antibiotics (anti-bacterials, anti-virals,  Dr. Galvante’s powerpoint
anti-fungals)  Recordings

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 [OPHTHALMOLOGY] DISEASES OF THE CONJUNCTIVA, CORNEA, AND SCLERA

DISEASES OF THE CONJUNCTIVA, CORNEA, AND SCLERA  Bulbar

Pia Regina Espiritu Galvante, MD, DBPO  Lines the anterior sclera
 Includes the caruncle
OUTLINE and semilunar fold (plica
 Conjunctiva semilunaris) at the
 Anatomy and Physiology medial canthus
 Signs and Symptoms
 Conjunctivitis LAYERS
 Subconjunctival Hemorrhage 1. CONJUNCTIVAL EPITHELIUM
 Conjunctival Mass  2-5 layers of stratified columnar epithelial cells
 Cornea  Superficial Epithelium
 Anatomy and Physiology  Mucous secreting goblet cells
 Keratitis  Keeps the conjunctiva moist
 Ulcerative – ex. Microbial Keratitis
 Non-Ulcerative – ex. Dry Eye  Basal Epithelium
 Sclera and Episclera  Contains lymphocytes and melanocytes
 Anatomy and Physiology
 Episcleritis 2. CONJUNCTIVAL STROMA
 Scleritis  Superficial Adenoid
 Trauma  Lymphoid tissue and “follicle-like structures”
 Conjunctiva  2nd – 3rd month of life
 Cornea  Deep (Fibrous)
 Sclera  Connective tissue loosely attached to the tarsus
 Accessory lacrimal glands: Krause and Wolfring
CONJUNCTIVA
ANATOMY AND PHYSIOLOGY CONJUNCTIVAL SIGNS AND SYMPTOMS
 Thin, transparent mucous membrane  Signs:
 Covers the globe anteriorly  Vascular Changes
 3 PARTS:  Hyperemia
 Dilated vessels
 Swelling/Edema (Chemosis)
 Discolorations
 Discharge
 Masses
 Symptoms:
 Discomfort
 Foreign body sensation
 Itching or burning sensation
 Tearing

CONJUNCTIVAL SIGNS
 There are 2 major reactions that occur in the
conjunctiva:
 Follicular Reaction
 Papillary Reaction
 Palpebral
 Lines posterior surface of the eyelid  FOLLICULAR CONJUNCTIVAL REACTION
 Adherent to the tarsus  Follicles  Lymphoid
 Forniceal germinal centers
 Loose, redundant, swells easily  Smooth nodules
 Thrown into folds  Avascular at the apices
surrounded by fine vessels
 This makes it able to move when you blink and at their bases
when you open your lids.  Etiology:
 Adenoviral conjunctivitis
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 [OPHTHALMOLOGY] DISEASES OF THE CONJUNCTIVA, CORNEA, AND SCLERA

 Infection from primary herpes simplex virus  If the patients are already complaining of foreign body
 Molluscum contagiosum sensation or the eye is really swollen  Give mild
 Enterovirus steroids combined with antibiotics
 Chlamydia
 Toxicity from medications
BACTERIAL CONJUNCTIVITIS
 PAPILLARY CONJUNCTIVAL REACTION  Acute onset
 Non-specific response  Manifestations:
 Purulent/mucopurulent
 A lot of etiologies discharge
can cause this type  Photophobia
of reaction  Foreign body sensation
 Seen on the upper tarsal  Matting of eyelashes
conjunctiva  Most Common Etiology:
 Fine mosaic pattern of dilated telangiectatic blood vessels  Staphyloccoccus
 Each papillae has a central fibrovascular core that gives  Streptococcus
rise to a vessel branching out in a spoke-like pattern  Haemophilus
 Neisseria gonorrhoea
 These reactions could occur at the same time in one eye  Chlamydia
 You will be able to appreciate mixed papillary-
follicular reactions  GONOCOCCAL CONJUNCTIVITIS
 Neisseria gonorrheae bacteria
 Hyperacute purulent conjunctivitis
CONJUNCTIVITIS
 Discharge: “Cheesy”
 Conjunctivitis is mainly infection or inflammation of the  If you try to clean the eye, within a few minutes,
conjunctiva you will see discharge coming out again.
 Major Types:  Could be unilateral or bilateral
 Viral
 Bacterial  Direct contact with infected genital secretions of from
 Allergic genital-hand-ocular transmission
 Your goal primarily as medical students is to be a  You will
Could bebe surprisedorhow
unilateral people can be so creative
bilateral
primary health provider when you finish your medical in treating conjunctivitis. Some people who have
education. We should be able to identify the following just had viral conjunctivitis, particularly those from
diseases/disorders so that you will know whether to low income bracket, have a certain practice that
refer to a specialist or not. they use urine as eye drops. They believe that urine
drops would help solve their viral conjunctivitis.
VIRAL CONJUNCTIVITIS They assume that urine is sterile. The problem here
 External ocular adenoviral infection is that some patients don’t know that they have
Gonorrhea, so yes, they still put urine drops into
 Adenovirus Serotypes 8, 11 and 19 their eyes. They also use it as a facial wash, or even
 Acute onset use it as a warm compress.
 Manifestations:  May involve the cornea and progress to melting and
 Watery discharge perforation
 Photophobia
 Mild foreign body sensation  Neisseria gonorrhea is one of those bacteria that
 Pre-auricular could penetrate an intact epithelium.
lymphadenopathy  If you don’t treat it  Cornea could melt
 Mixed papillary-follicular conjunctivitis
 Subconjunctival haemorrhage
 Chemosis
 Pseudomembrane or true membrane

 Resolves on its own within 3-5 days  Treat

symptomatically

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 [OPHTHALMOLOGY] DISEASES OF THE CONJUNCTIVA, CORNEA, AND SCLERA

 Classic cause of neonatal conjunctivitis  TRACHOMA

 Newborns acquire it through the passage of an  Chronic & recurrent chlamydial infections
infected birth canal  Acute: Follicular conjunctivitis & Epithelial keratitis
 Lead to conjunctival scarring & pannus formation
 Gram Stain: Gram (-) intracellular diplococcic
 Pannus  Neovascularization around the limbus
 Routinely, when you see patients with eye
infections, you could do gram stain of their  Arlt’s Line, Herbert’s Pits
discharge  Corneal swab or corneal scrape
Under the microscope, you will see that Neisseria  Arlt’s Line  Scarring on the of the conjunctiva
gonorrhea will present as a gram negative intra  Nice to Know: In Uveitis  Arlt’s Triangle =
cellular diplococci Base down configuration of Keratic
 Usually in pairs Precipitates on the corneal epithelium
 Coffee or kidney bean appearance  Elevated lesions found under the lids  May
be in constant pressure with the cornea or the
limbus  Can cause the development of
Herbert’s Pits
 Herbert’s Pits  Depressions on the corneal
limbus
 Represents areas that are slightly being
thinned out
 At the site where you usually find your follicles
in contact with it  Starts to necrose 
 Concurrently with your Gonorrhea Conjunctivitis, you Depressions
may also have Chlamydia.  Can lead to a secondary bacterial infection
 When you treat Gonorrhea Conjunctivitis, you
usually give them IM Ceftriaxone:
 Adults: 500 mg – 1 g
 Children: 250 mg
 You also include an oral dose of Azithromycin to
target the Chlamydia that could occur with
Gonorrhea Conjunctivitis

 CHLAMYDIA/INCLUSION CONJUNCTIVITIS
 Chlamydia trachomatis D-K bacteria
 Sexually active & in conjunction with urethritis or cervicitis
(although urogenital symptoms may not be present)
 Prominent follicular response
 Non-tender preauricular lymphadenopathy
 Gram Stain: “inclusion bodies”
 Inclusion Bodies  Included in the cell near the
nucleus ALLERGIC CONJUNCTIVITIS
 This is the reason why Chlamydia Conjunctivitis is  Reaction to airborne allergens
also called Inclusion Conjunctivits.  Mediated by IgE antibodies
 Type I Hypersensitivity
 Hallmark is itching
 Signs:
 Hyperemia
 Chemosis
 Mucoid/serous/stringy
discharge
 Attacks are usually short
 Given antibiotics  Usually Azithromycin is given lived & episodic

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 [OPHTHALMOLOGY] DISEASES OF THE CONJUNCTIVA, CORNEA, AND SCLERA

 VERNAL KERATOCONJUNCTIVITIS  Associated with:

 Seasonal, recurring bilateral conjunctivitis  Soft contact lens material
 Young males  Protein debris accumulating on the lens surface
 4-16 years old  Chemicals involved in lens cleaning
 With strong history of atopy  Also seen in:
 Tropical climates  Ocular prosthesis
 Clinical Manifestations:  Loose nylon sutures
 Intense itching  Filtering blebs
 Blepharospasm
 Photophobia
 Blurred vision
 Copious mucoid discharge
 Diffuse papillary hypertrophy develops with giant
(cobblestone) papillae
 When you try to evert the lid, you will see these
large cobblestone papillae
 Very characteristic of Vernal Kertoconjunctivitis  Since this is an inflammatory condition, it could be
 We call it keratoconjunctivitis because it also treated by giving topical corticosteroid combined with
affects the cornea. antibiotics
 For those associated with contact lens wear  Have
 Limbal Vernal in superior limbus them rest from contact lenses
 Limbus thickened, gelatinous  Contact Lens Holiday of 2 weeks combined with
with scattered opalescent medications
mounds and vascular injection
REMEMBER: Horner-Trantas
Dots SUBCONJUNCTIVAL HEMORRHAGE
 Rupture of conjunctival blood vessel due:
 Horner-Trantas Dots  Collection of both active  Trauma
and degenerated eosinophils  Valsava
 Shield Ulcers  Blood dyscrasia

 Cobblestone papillae  Pressure applied to the  Can be due to hypertension

cornea  Development of Shield Ulcers  Could also occur
 Sterile epithelial ulcers with spontaneously
an oval or shield shape and
underlying stromal  Treatment: Conservative
opacification  Cold compress for the 1st 24 hours  Warm compress
for the next succeeding days
 Usually develops in the
 Usually resolves within 7 to 14 days
superior or midsuperior
portion of the cornea  If it only happened once  Nothing to worry about
 If it recurs  Investigate
 Possible blood dyscrasias
 How do we treat Allergic and Vernal Conjunctivitis?  Ask for aspirin use or other blood thinners  Prone to
 Since it is IgE mediated  Topical Anti-Histamines develop subconjunctival hemorrage
and Mast Cell Stabilzers could be given
 Vernal Keratoconjunctivits sometimes need the aid of
topical steroid otherwise inflammation will not be CONJUNCTIVAL MASS
resolved CONJUNCTIVAL NEVUS

GIANT PAPILLARY CONJUNCTIVITIS

 Chronic inflammation of the conjunctiva with prominent
papillary hypertrophy of the superior tarsus

 Usually seen in the upper lid

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 [OPHTHALMOLOGY] DISEASES OF THE CONJUNCTIVA, CORNEA, AND SCLERA

 Could be flat or elevated  Triangular wing-shaped fleshy fibrovascular tissue

 Usually benign if: encroaching upon the cornea
 Present at birth  Usually starts outside the cornea  Can progress and
 Does not progress in size quickly cover the visual axis
 Congenital hamartomas that consists of nests of modified  Most often occurs at the nasal side
melanocytes (nevus cells)  Could also occur in both nasal and temporal side 
 Types: Meet at the center = Called “Kissing Pterygium”
 Junctional Nevi  Risk Factors:
 Compound Nevi  UV light
 Subepithelial Nevi  Wind
 Dust
 Depends on the layer that it affects
 Rarely undergo malignant transformation  Usually find in patients who are exposed to sunlight
 Fishermen, Farmers
CONJUNCTIVAL CONCRETIONS  Sometimes called the “Surfer’s Disease”
 Represent trapped foreign  Histology:
body such as dust in the  Subepithelial fibrovascular tissse
conjunctival epithelium  Elastotic collagen degeneration
 Present as foreign body  Indications for Surgery:
sensation if numerous and  Reduced vision due to invasion of visual axis
very elevated  Irregular astigmatism
 Could be removed by using the needle of your 1 cc  Significant ocular irritation
syringe
 Initially, they are not usually surgical  Do not cause
 Benign  Not painful
any disturbance in the vision
 If they start obscuring the visual axis  Surgical
PINGUECULA  If it becomes inflamed or becomes very very thick
 Elevated, fleshy conjunctival masses located in the inter- that it already causes depression on the cornea 
palpebral region Surgical
 Most commonly on the nasal  Why? Because when something is depressing your
side cornea, it causes the curvature to change 
 Yellow or light brown Induces astigmatism  Leads to blurring of vision
 Associated with:
 Chronic actinic exposure PYOGENIC GRANULOMA
 Repeated trauma  Does not represent
 Dry and windy conditions granulomatous
 Histology  Abnormal collagen bundles with staining inflammation
characteristics similar to elastic tissue  Reactive proliferation of
vascular endothelial cells
 Could manifest symptomatically as foreign body
sensation or with redness and granulation tissue
 Raised, fleshy, red,
pedunculated lesion from skin or conjunctiva
PTERYGIUM
 Could be flat or penduculated
 In Tagalog: Pugita (Octopus in Tagalog)  Looks like an
octopus  After inflammatory conditions such as:
 Chalazia
 Chemical burns
 After conjunctival surgery

 Treatment:
 Flat  Shave Excision
 Pedunculated  Cut or cauterize

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 [OPHTHALMOLOGY] DISEASES OF THE CONJUNCTIVA, CORNEA, AND SCLERA

SUTURE GRANULOMA CONJUNCTIVAL/CORNEAL INTRAEPITHELIAL NEOPLASIA

 Clinically appears similar to a (CIN)
pyogenic granuloma  Corneal extension  Irregular
opalescence with small, white,
 Due to retained intraepithelial opacities and a
sutures central fimbriated edge

 Usually starts at the limbus but

CONJUNCTIVAL/CORNEAL PHLYCTENULES could extend to the cornea
 Focal, translucent lymphocytic nodules located at the limbus  Leukoplakia may overlie a portion of
 Delayed cell-mediated the CIN
hypersensitivity reaction  Associated with certain HPV strains
 At the junction of the  Invasion to basement membrane 
cornea and sclera Squamous cell carcinoma

 Staphylococcal antigens CONJUNCTIVAL PRIMARY ACQUIRED MELANOSIS (PAM)

 Usually occurs with infection of the lids
(blepharitis)
 TB bacilli

 Occurs with Primary TB  Sometimes this is the

sign seen that warrants investigation that a child
might have Primary TB  Intraepithelial melanocytes proliferation  Multiple flat,
 May wander across the cornea producing vascularization & brown patches of unilateral pigmentation within superficial
scarring conjunctiva
 Acquired
 Can resolve on its own but can cause scarring  Occurs in the middle age
 Usually treated with steroids and other anti-  Malignant potential  Melanoma develops in 20-30%
inflammatory agents  Nodules develop in previously flat lesions
 Since it may also cause secondary bacterial infection, it
should concurrently be treated with topical antibiotics  In melanoma, since it is a malignancy, you have to be
aggressive
 Sometimes occur in the upper or lower lid  Wide
CONJUNCTIVAL VIRAL PAPILLOMA
excision of the lid and do reconstructive surgery
 Benign
 If it occurs on the globe itself  More examinations
 Multiple fibrovascular connective tissue cores with an
should be done to see if it has already penetrated the
overlying epithelium
inside of the eye or not
 Sessile or pedunculated
 If it has, you might have to remove the whole eye
 Caused by a papilloma virus otherwise it could spread to other parts of the body
 Can be premalignant in older
adults
 Treatment: CORNEA
 Excision ANATOMY AND PHYSIOLOGY
 Cryotherapy  Unmyelinated nerve endings sensitive to touch,
temperature and chemicals
CONJUNCTIVAL INTRAEPITHELIAL NEOPLASIA (CIN)  No blood vessels
 Localized to the epithelium,  Receives nutrients by diffusion and from neurotrophins
does not invade the
epithelial basement
membrane
 Gelatinous, sessile
appearance with numerous
superficial corkscrew-like
blood vessels typically located at the limbus

LEA THERESE R. PACIS 6

 [OPHTHALMOLOGY] DISEASES OF THE CONJUNCTIVA, CORNEA, AND SCLERA

 Diameter  About 11.5 – 11.7 mm  Central or peripheral

2. NON-ULCERATIVE
 Thickness of:
 Not associated with tissue loss
 0.5 – 0.6 mm at the center
 0.6 – 0.8 at the periphery
There are many subtypes under each. In this lecture,
 Normally curved  Flatter at the nasal side
different types of Microbial Keratitis will be discussed
 Has 5 layers:
under Ulcerative Keratitis type, and Dry Eye Disease
 A – Anterior Epithelium
for the Non-Ulcerative type.
 B – Bowman’s Membrane
Deposition of calcium in the Bowman’s
Membrane as a result of chronic inflammation MICROBIAL KERATITIS
and change in pH  Pankeratopathy Bacterial Fungal Parasitic Viral
 C – Corneal Stroma  Staphylococcal  Aspergillus  Acanthamoeba  HSV
species  Fusarium  Microsporidia  VZV
 D – Descemet’s Membrane  Streptococcus  Mycelia  Toxocara  Adenovirus
 E – Endothelium species  Candida  EBV
 Nice to Know: In 2013  They were able to  Pseudomonas  Others  Poxvirus
 Moraxella
discover an additional layer = Found in between
 Haemophilus
the Corneal Stroma and Descemet’s Membrane   Neisseria
Dua Layer (A-B-C-D-D-E)  Enterobacteria
 Nocardia,
 Composed of collagen fibrils with  Mycobacterium
uniform diameter, spacing and  Others
arrangement
 Type I – 90%  BACTERIAL KERATITIS
 Type V – ~10%  History
 Type III – Descmet’s  Acute, painful, red eye
membrane  Decreased vision
 Type IV – Epithelial Basement  Rapid evolution
Membrane and Descemet’s  Persistent mucopurulent discharge
Membrane  Trauma or contact lens use
 Associated eye disease
FUNCTION  Findings
 Main function is OPTICAL  Dense infiltrates with hypopyon
 Transmission of light  Check borders
 Refraction of light  Brush-like: Pseudomonas
 Provides about 2/3 of the eye’s refractive power (43D)  Distinct: Streptococcus, Staphylococcus, or Moraxella
 Lens provides 1/3  Advancing: Streptococcus
 Other functions:
 Maintains structural integrity of the eye
 Protects ocular contents

CORNEAL DISEASES
KERATITIS
 “Corneal inflammation”
 Due to:
 Microorganisms
 Tear deficiency
 Denervation
 Exposure/drying
 Immune reactions  Sorry wala kong makitang mas okay na picture  Patients daw ‘to
 Ischemia ni Dra eh. Wala naman siguro lalabas na pictures sa exam. For visual
purposes only 
 Trauma
 TWO MAJOR TYPES OF KERATITIS  For ophthalmologists, they are able to identify
1. ULCERATIVE the microorganism just by looking at the
 Associated with tissue necrosis presentation of the ulcer
 May involve all corneal layers

LEA THERESE R. PACIS 7

 [OPHTHALMOLOGY] DISEASES OF THE CONJUNCTIVA, CORNEA, AND SCLERA

 Pseudomonas
 Common in contact lens use  Especially
those who borrow contact lenses
 Very fast growing type of ulcer  Can start
with redness on day 1, and by day 3, it
becomes a full blown ulcer
 Treated with antibiotics
 If scar quieted down  Topical steroids could
be given  Make sure that there are no
epithelial breaks/defect
 Once the eyes quieted down  Can do
corneal transplant  Mild infection  Feathery Borders
 Streptococcus  Only the superficial part of the cornea is
 Borders could be distinct or advancing affected
 Corneal edema could be seen  Characteristic of fungal infections
 Moraxella  If they are quite severe already  Epithelial
 Also associated with angular blepharitis Plaque
particularly on the temporal side  Eventually you will have thinning of the cornea
 Atypical Mycobacterium  Lead to Perforation
 Similar to what causes TB  Iris is already visible underneath
 Seen in post-operative patients  Scleritis  Redness and swelling of the sclera
 Immune Ring (Wesley’s Ring)  Results from
Laboratory confirmation is important! immune reactions
 Hypopyon  Inflammatory cells or pus at the
TREATMENT: anterior chamber
 Topical Antibiotics depending on the severity
and what part of the eye is affected Gram and Giemsa Stain: Hyphal Elements
 Systemic medications might have to be given
as well
 Do not give steroids UNLESS the patient is  PARASITIC KERATITIS
already scarred  Usually caused by Acanthamoeba
 Do not give if there is an active infection
 History
 Slow, protracted progressive course
 FUNGAL KERATITIS  Red eye
 History  Severe pain out of proportion with clinical findings
 Slow
REMEMBER: What is characteristic of
 Red, painful eyes
Acanthamoeba infections is that sometimes
 Decreased vision
the appearance of the eye is not proportional
 Trauma with organic/vegetable matter
to the pain that the patient is complaining of
 Farmers  Natatalsikan ng palay etc.  Kala niyo nag-iinarte lang yung patient
 Topical steroid use  Decreased vision
 +/- Contact lens use
 Long term steroid use  Changes the immune
 Commonly misdiagnosed as HSV
status of the eye  More prone to infection
 Findings
 Findings  Punctate epithelial keratitis
 Gray-white, dense infiltrate  Pseudodendritic keratitis (early phase)
 Sticky hypopyon  Ring infiltrate (late phase)
 Solitary or multiple with satellite lesions, feathery  Radial perineuritis
borders (filamentous fungi)  Gray-white central stromal infiltrates
 Epithelial plaque  Scleritis
 Immune ring
 Scleritis
 May perforate
LEA THERESE R. PACIS 8
 [OPHTHALMOLOGY] DISEASES OF THE CONJUNCTIVA, CORNEA, AND SCLERA

 On the Gram stain or culture of conjunctival REMEMBER:

scrape or corneal scraping, characteristic of  HSV  Dendrites
Acanthamoeba are your double-walled cysts.  VSV  Pseudodendrites
 Calcofluor White Stain
 Non-nutrient Agar with E. coli overlay  You have epithelial defect in both cases  Break
REMEMBER: Commonly seen in those contact in the corneal epithelium
lens wearers with history of swimming in the pool  Do not give steroids!
or river  If you give steroid, it will become geographic 
More difficult to treat
 You may give anti-virals, topical lubricants, or
 VIRAL KERATITIS: HSV AND VZV
opt not to give anything since it is cause by a
 Usually cause by Herpes Simplex Virus family  virus, it could resolve on its own
Including HSV, VZV, CMV, EBV  When your viruses affect the inner layer of the
 History cornea, they may appear as opacities within the
 Subacute cornea
 Red eye  Fluorescein Staining  To see if there are breaks
in the epithelium
 Decreased vision, photphobia
 Stromal Keratitis and Endothelial Keratitis will
 Less painful, mild foreign body sensation
not stain
 +/- Trauma, associated illness or stress
 Endothelial Keratitis or Endothelialitis  Folds in
 Majority of patients have a recurrent ocular disease
the inner part of the cornea (Descemet’s
 How will you know it is recurrent?  You will membrane folds)
have an active lesion and presence of scars  Scar  Patch of opacity in the inner layers of the
 Findings cornea
 Starts as discrete punctate epithelial keratitis  No epithelial defect  Fluorescein will not
stain
 Coalesce, become dendritic, geographic (if with
history of topical steroid use)
DRY EYE DISEASE
 Dendrites  If exposed to steroids can enlarge
and coalesce  Form geographic lesions  Is a multifactorial
disease of the tears and
 HSV  Dendrites, terminal bulbs, dichotomous ocular surface that
branching results in symptoms of
 VZV  Pseudodendrites, no terminal bulbs, heaped discomfort, visual
up epithelium, irregular branching disturbance, and tear
 +/- Previous scars film instability, with
 Epithelial, stromal, endothelial, keratouveitis potential damage to the ocular surface. It is accompanied by
increased osmolarity of the tear film and inflammation of
 Can affect all parts of the cornea
the ocular surface – Dry Eye Workshop (DEWS), 2007
 Epithelium  Epithelialitis or Epithelial
Keratitis  One of the most frequently diagnosed disorders in
 Endothelium  Endothelialitis or ophthalmology
Endothelial Keratitis  Exact prevalence unknown
 Not exclusively associated with aging

LEA THERESE R. PACIS 9

 [OPHTHALMOLOGY] DISEASES OF THE CONJUNCTIVA, CORNEA, AND SCLERA

 Prevalence increases over age 40  TESTS

 Range: 5-40% of the population  Tear Break-up Time (TBUT)
 Frequent cause of ocular irritation
 Could present with dry eye alone or with other
conditions
 Symptoms improve with treatment but usually not cured
 Source of frustration from both the doctor and the
patient
 Important cause of visual morbidity  >10 seconds  Normal
 Compromises results of corneal, cataract and refractive  5-10 seconds  Marginal
surgery  5  Low
 Severe forms ranked equivalent to unstable angina in quality
of life utility assessments  Slit Lamp  Apply Fluorescein dye on the eye of the
patient  Patient blink once, then after that, start
counting until 10. Instruct the patient NOT to blink!
 The moment you see a break in the colored film,
you stop counting  Breakup Time
 Corneal and Conjunctival Staining

 Sign that there are devitalized tissue in the surface

of the eye
 Normally, there should be no stain if you don’t have
dry eye 
 Schirmer’s Test

 Dry Eye is divided into 2 major types:

 Aqueous Deficient
 Evaporative Type  More common
 Of the evaporative type, the most common is
MEIBOMIAN OIL DEFICIENCY due to Meibomian
Gland dysfunction or a type of blepharitis
REMEMBER: Most common: EVAPORATIVE TYPE
caused by MEIBOMIAN OIL DEFICIENCY
 Schirmir’s I
 SYMPTOMS  Without anesthetics
 Irritation  Measures both baseline and reflex tearing
 Redness  Schirmir’s II
 Burning/Stinging  With anesthetics
 Tearing  Measures baseline tear secretion
 Contact lens intolerance
 Increased frequency of blinking  Fold the test strip or filter paper and tuck in the
 Itching lower lid  Patient will close his/her eyes  Time
 Foreign body sensation it for around 5 minutes  Measure the wet part
 Blurred vision (measured in mm)
 Photophobia  If you get <10 mm in Schirmir’s I and <5mm in
 Thick, sticky mucoid discharge Schirmir’s II  ABNORMAL

LEA THERESE R. PACIS 10

 [OPHTHALMOLOGY] DISEASES OF THE CONJUNCTIVA, CORNEA, AND SCLERA

 Tear Meniscus Height  Dense, opaque,

elastic connective
tissue structure
composed of
bundles of collagen
of varying diameters
 Comprised ~90% or
5/6 of the outer coat
of the eye
 Measure the height of your tear film  Main function is to protect the eye and maintain its
 Normal: 0.2 to 0.4 mm shape
 Begins at the limbus and terminates at the optic nerve
 “ARTIFICIAL TEARS”/EYE LUBRICANTS canal
 Key principle in the management of Dry Eye Disease  Thicker in males than in females
 Thickest near the optic nerve (1 mm)
 Augmentation of the tear film through the topical  Thinnest at the insertion of extra ocular muscle (0.3 mm)
administration of artificial tear substitutes  At limbus the
 Enhance tear stability thus reducing loss by evaporation thickness of sclera is
 Helps to retain moisture in the eye and relieve the 0.83 mm
chronic ocular inflammation associated dry eyes  4 layers:
 Help to reduce patient discomfort, improve quality of  Episclera
life and reduce the risk of damage to the corneal  Stroma
epithelium  Lamina Fusca
 Currently the most widely used therapy for dry eye  Endothelium
 Easiest to apply but does not address the more
severe types of dry eye  EPISCLERA
 Fibroelastic structure between the superficial scleral
 Characterized by hypotonic or isotonic buffered solutions stroma and Tenon’s capsule
containing electrolytes, surfactants, and various types of  2 layers:
viscosity agents
 Outer Parietal
 Deeper Visceral
 “MENU OF TREATMENTS”
 Artificial tears substitutes EPISCLERITIS
 Gels/Ointments
 Inflammation of the episclera
 Moisture chamber spectacles
 Self-limiting, resolves within a few days to weeks
 Anti-inflammatory agents (Topical Cyclosporin (CsA) and
 Tissue damage and loss of vision are rare
Corticosteroids, Omega-3 fatty acids)
 Typically recurrent, commonly unilateral
 Omega-3 Fatty Acids  Makes the consistency of  Redness subsides with topical phenylephrine
the tears of a better quality and less evaporative
 In scleritis, redness does not usually disappear with
 Tetracyclines topical phenylephrine
 Plugs
 2/3 without associated systemic condition
 Secretagogues
 Infectious condition extremely rare
 Serum
 If with systemic association, commonly autoimmune
 Contact lenses
 Atopy and Rosacea also associated
 Systemic Immunosuppressives
 Surgery (AMT, Lid surgery, Tarsorrhaphy, MM & SG
SIMPLE EPISCLERITIS
transplant)
 Mild to moderate redness and edema
 Typically no pain or discomfort
SCLERA AND EPISCLERA
ANATOMY AND PHYSIOLOGY  May be regional or span entire episclera
 SCLERA
NODULAR EPISCLERITIS
 “Scleros” – hard
 Focal, well-defined area of intense redness and episcleral
edema
LEA THERESE R. PACIS 11
 [OPHTHALMOLOGY] DISEASES OF THE CONJUNCTIVA, CORNEA, AND SCLERA

 Usually painless but may be tender on palpation SCLEROMALACIA PERFORANS

 Scleritis “without
SCLERITIS inflammation”
 Inflammation of the sclera  Typical redness, pain, edema
 Occurs more in the 4th to 6th decades of life not apparent
 More common in women  Occurs in long-standing
 Typically leads to destruction of sclera or structural Rheumatoid Arthritis
alterations of the globe if untreated  Scleral thinning revealing a
 Recurrent disease common, usually bilateral blue-gray to dark patch of sclera (underlying uvea becomes
 Does not blanch with topical phenylephrine visible)
 Gradual presentation  Large abnormal vessels cross and surround the area of
 Severe, boring, or piercing pain scleral loss
 May worsen at night  Spontaneous perforation is rare
 May be referred to other regions of the head/face  (+) Hypotony
 Globe is tender to touch
 Sclera is violaceous POSTERIOR SCLERITIS
 Types:  Inflammation of sclera posterior to ora serrata
 Diffuse Anterior Scleritis  In isolation or with anterior scleritis
 Nodular Anterior Scleritis  Symptoms:
 Necrotizing Scleritis  Pain
 Scleromalacia Perforans  Tenderness
 Posterior Scleritis  Proptosis
 Vision loss
DIFFUSE ANTERIOR SCLERITIS  Restricted motility
 Characterized by a zone of  Signs:
scleral edema and redness  Choroidal folds
 Episcleral and deep scleral  Choroidal detachment
vessels injected  Retinal detachment
 Extreme pain especially when  Macular edema
palpated  Myositis
 (+) Bluish translucent area  Orbital inflammation
when recurrent inflammation subsides but scleral thinning  Papilledema
not usually present  Scleral thickening on B-scan Ultrasound, CT scan or MRI
 T-sign on B scan  Edema in subtenon space
NODULAR ANTERIOR SCLERITIS
 Localized scleral inflammation forming
thickened nodules
 Very tender on palpation
 (+) Vascular congestion
 Resolution of inflammation not usually
accompanied by scleral thinning

NECROTIZING SCLERITIS
 Scleral inflammation surrounds whitish, avascular, necrotic
scleral tissue  TREATMENT:
 Overlying conjunctiva also  Anti-inflammatory Drugs
with necrosis  For mild inflammation  NSAID
 Severe pain  If still it does not resolve  Steroids
 Possible perforation  Watch out for complications such as: increase
 Severe tissue loss if not intraocular pressure, secondary bacterial
treated promptly infection and other systemic effects
 40% suffer vision loss  If patient cannot tolerate the side effects of
 Scleral thinning may produce a bluish appearance to the steroids  Immunomodulatory Agents
sclera

LEA THERESE R. PACIS 12

 [OPHTHALMOLOGY] DISEASES OF THE CONJUNCTIVA, CORNEA, AND SCLERA

TRAUMA Common type of collage? Type I

CONJUNCTIVAL TRAUMA Inclusion bodies? Chlamydia
 Chemical Injury What will you see under the microscope if your patient has
 Conjunctival Laceration gonorrhea conjunctivitis? Gram negative intracellular
 Foreign Bodies diplococci, kidney or coffee bean shape
 Subconjunctival Hemorrhage Signs of Vernal Keratoconjunctivitis? Shield Ulcer
Is shield ulcer infectious or not? Not infectious
CORNEAL TRAUMA 20 year old patient, 10 years history of contact lens use,
 Corneal Foreign Body redness, tearing? Giant Papillary Conjunctivitis
 Chemical Injury History of surgery and conjunctival mass, 3 weeks post-
 Corneal Lacerations surgery, retained foreign body? Suture Granuloma
Normal TBUT? More than 10 seconds
SCLERAL TRAUMA Tear Meniscus Height? 0.2 to 0.4 mm
 Chemical Injury Normal in Schirmir’s I? More than 10 mm
 Scleral Lacerations Abnormal in Schirmir’s II? Less than 5 mm
 Scleral Foreign Body
 Penetrating/Perforating injury

 TREATMENT:
 If lacerations are large  Closed using absorbable or
non-absorbable sutures
 Non-Absorbable  Nylon 9-0 or 10-0

INSTA-SAMPLEX 
Immune ring seen in Acathamoeba Keratitis  Wesley’s
Ring
T-sign  Sign of Posterior Scleritis; Edema in the subtenon
space
Test to distinguish Scleritis and Episcleritis  Phenylephrine
Test
Most common type of Dry Eye  Evaporative
Which part of the cornea is flatter? Nasal or temporal 
Nasal
Schirmir’s I  No anesthetic; Test for baseline and reflex
tearing
Dendrites  HSV
Pseudodendrites  VZV
Which one has terminal bulbs – HSV or VZV? HSV
Pain not in proportion with the presentation of the eye?
Acanthamoeba
Gram Stain of Acanthamoeba? Double walled cysts
History of 14 year old patient, with redness of the eye, some
blurring of vision, swollen lids, episodic, seasonal? Vernal
Keratoconjunctivitis
Cobblestone papillae? Vernal Keratoconjunctivitis
Treatment of Vernal Keratoconjunctivitis? Combined topical
steroids and antibiotics
Commonly associated with borrowing of contact lenses?
Pseudomonas
Refractive power of the lens? 1/3 of the total refractive
power of the eye
5 layers of the cornea? ABCDE – Anterior Epithelium,
Bowman’s Membrane, Corneal Stroma, Descemet’s
Membrane, Endothelium Thank you Jon de Luna sa pagpicture and Precious Dy sa pag-encode <3

LEA THERESE R. PACIS 13

 [OPHTHALMOLOGY] CRYSTALLINE LENS

CRYSTALLINE LENS  Zonules of Zinn

Dr. Chua  Connects the lens to the ciliary muscle
 ACCOMODATION
ANATOMY OF THE EYE

 For you to be able to see better, light has to pass through  When you use a slit lamp  The first part that you will
all the optical medias of the eye see is your cornea, followed by your anterior chamber,
 What are the Optical Medias of the eye? then your lens.
 Cornea  You will be able to appreciate if your lens has opacity
 Lens at different levels
 Aqueous Fluid
 Any opacities on these media will yield to poor vision LENS - accomodation & refraction
LENS COMPOSITION Cornea & lens (cornea: 2/3 if refractive power)
 65% Water
THE CRYSTALLINE LENS  35% Proteins
ANATOMY  Trace of minerals common to other tissues
 Transparent  Potassium  Highest concentration
 Biconvex  Ascorbic Acid
 Avascular  Glutathione
 Suspended by Zonules of Zinn
 Birth: 3.5 x 6.4mm, 90 mg REASONS FOR TRANSPARENCY
 Adult: 4 x 10mm, 255mg  Short range spatial correlation between protein molecules
of lens crystalline
PARTS OF THE LENS  Most lens fibers have NO nuclei
 Lens Capsule  Avascular
 Colorless
 Like a membrane covering the lens  Uniform structure, index of refraction
 Deturgescence (Relative Dehydration)
 Epithelial Cells
 Meaning, the lens has no fluid  Dry
 Growth of the lens comes from the epithelial cells
which is situated on the anterior part of the capsule
FUNCTIONS OF THE LENS
 Lens Substance (Cortex)  Sole function of the lens is to focus light rays to the retina
 Composed of recently formed lens fibers thru refraction and accommodation
 Soft portion of the lens  REFRACTION  Bending of light rays that passes thru one
 Nucleus - thickens as we get older medium to another
Bending of light is greater when light passes from gas to solid
 Located at the center
 HYPEROPIA  Far-sightedness
 Composed of mature lens fibers  Eye ball is short or small
 Hard portion of the lens  Object that you see falls at the back of the macula

Cortex - newly formed lens fiber

Nucleus - compressed LEA THERESE R. PACIS 1
 [OPHTHALMOLOGY] CRYSTALLINE LENS

 MYOPIA  Near-sightedness  NO ACCOMMODATION (The patient is looking

 Eye ball is long far/looking at a distance)
 Object that you see falls in front of the macula  Ciliary muscles relaxes  Suspensory ligament
taut  Lens becomes flat
 ACCOMMODATION
 Ciliary muscles contracts  Suspensory ligament
lax  Lens becomes globular

PRESBYOPIA
 Physiologic recession of the near point of accommodation
due to aging
 Not pathologic
 Ciliary muscle is seen to sclerose
-less refractive power  Lens proteins become less deformable with a given change
of ciliary muscle tonus
 Decrease capsule elasticity

 In normal vision, when the lens accommodates, the

object that you are looking at should fall at the macula
 As we age, the lens loses its flexibility  That is why
the object that we see falls out of the macular area
 This is the reason why we use reading glasses as we
age

 SYMPTOMS
 Inability to read fine
 ACCOMMODATION  Physiologic interplay of the ciliary print or discriminate fine
body, zonule and lens that results in focusing of near close objects at about
objects upon the retina age 40 (37 - fil)
- Adolescents: 12-16D
- 40 years old: 4-8D  TREATMENT
- >50 years old: <2D  Corrected by plus lenses

LENS CHANGES WITH AGING

 >40 years old insoluble proteins accumulate in nucleus
 Increase in yellow pigments (tryptophan)
 High molecular weight aggregates accumulate
 Free radicals are generated
 The soft juvenile plastic like lens changes to glass like
character
 Increase high molecular weight protein macromolecules
which contains high concentration of calcium which scatter
light to produce opacity
 Increasing yellow-brown coloration of the human lens

- thicker lens = more refractive power

LEA THERESE R. PACIS 2
Symptomatology - based of refraction & accomodation
 [OPHTHALMOLOGY] CRYSTALLINE LENS

DEVELOPMENTAL LENS ANOMALIES

1. Ectopia Lentis
 Usually bilateral and associated with:
- Marfan’s syndrome
- Homocystenuria
2. Coloboma
3. Spherophakia

 Common Ocular Manifestations

 Partial Dislocation
 Complete Dislocation

ECTOPIA LENTIS
 Lens dislocation due to loss of zonular fiber support
 SYMPTOMS:
 Monocular diplopia (partial)
 Hyperopia (total)
 Loss of accommodation
 SIGN:
 Iridodonesis
 COMPLICATIONS:
 Secondary glaucoma
 If you have lens dislocation, the lens could move
forward, causing closure of the angle

 This just simply shows us that at birth, our lens is  Uveitis

colorless and as we grow old, it becomes brown in  Due to inflammation in the area
color. Once it becomes brown, the cortex will
liquefy.
 ECTOPIA LENTIS IN MARFAN SYNDROME
 Autosomal disorder of connective
SYMPTOMATOLOGY OF LENS DISEASES tissue
 Arises mainly from opacification and lens dislocation  Mutation of fibrillin gene
 Decreased vision  Clinical Manifestation:
 Glare - Heart and aorta changes
 Monocular diplopia - Ectopia Lentis  Major ocular
change; occurs early,
 Meaning, if you cover one eye, you will still have sometimes in utero
double vision - Skeletal defects
 Hyperopia (dislocated lens) - Arachnodactyly
 Pain (complicated) - Pectus excavatum

 Pain is due to secondary glaucoma  ECTOPIA LENTIS IN HOMOCYSTINURIA

 Cystathione beta synthase deficiency
SIGNS OF LENS DISEASES  Urinary excretion of excessive amounts of homocysteine
 Pupillary white reflex in  Clinical Manifestations:
hypermature cataracts - Retardation
- Occlusive Vascular Disease
 Impaired ROR (Central Dark
- Osteoporosis
Reflex)
- Seizures
 Iridodonesis in ectopia lentis
 Subluxation of the lens develops
between 3rd and 10th year of life due to deficient zonule
 In Ectopia Lentis, the lens is not completely supported
 Floppy = Iridodonesis

Remove refractive media -> hyperopic

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COLOBOMA  PATHOPHYSIOLOGY OF AGE-RELATED CATARACT

 Results from loss of zonular attachments in one segment of FORMATION:
the lens equator  Protein denaturation
 Retina may detach  Hydrolysis
 Biochemical Changes:
- Increase sodium and insoluble proteins
- Decrease soluble protein
- Bound water reflecting loss of binding sites
 Widespread Oxidative Changes
- Decrease glutathione concentration and oxidation of
methionine and cysteine

 CLASSIFICATION OF CATARACTS ACCORDING TO THE

 Most of the time it is seen in the inferior portion of the
DEGREE OF OPACITY PRESENT
eye
 Immature - opacity located centally
- Transparent lens fibers present
SPHEROPHAKIA  Intumescent
 Small lens (spherical) with - Swelling of the lens with fluid
increased A-P diameter clefts
 Myopia results  Mature
 Small lens does not adequately - Opacification of all lens fibers
support the iris  Iridodonesis  Hypermature - nucleus is not centrally located (inferiorly)
 Lens subluxation is common due to - Liquefaction of opaque lens fibers (Morgagnian)
weakened & stretched zonules  After-Cataract - primary complication of cataract surgery
 Pupillary block glaucoma may - Opacification of posterior lens capsule
ensue
ACQUIRED CATARACT
TRAUMATIC LENS DISLOCATION 1. Age-related
 Partial or complete may occur following contusion injury 2. Traumatic
(blunt injuries) 3. Associated with Ocular Disease
 Iridodonesis  Uveitis
 Quivering of iris when patient moves the eye  Glaucoma
 A common sign of lens dislocation due to loss of iris-lens  Retinitis Pigmentosa
support  Retinal Detachment
4. Associated with Systemic Disease
 Diabetes Mellitus
 Hypocalcemia
5. Toxic Cataract (drug induced, steroid, miotics)

AGE-RELATED CATARACT
 Diagnosis of Age Related Cataracts
 History
 Gross appearance of whitish pupillary reflex
 1st Picture  Lens is at its normal position  Ophthalmoscopic appearance of black reflex on red
 2nd Picture  Partial dislocation orange background
 Slit lamp findings
 3rd Picture  Complete dislocation
 Symptoms
 Decreased vision
CATARACT  Painless
 Any opacity in the  Reduced vision in bright illumination
crystalline lens
 L. "cataracta" - waterfall  Usually seen in posterior subcapsular cataracts and
 ‘Sheet of falling water’; nuclear cataracts
‘Frosted or fogged up  Not usually seen in cortical cataracts
window’  Spots in the visual field
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 Ability to read without glasses DIABETIC CATARACTS

 Occurs in poorly controlled
 Hyperopics  Becomes myopic because their lens
growth-onset DM
thickened
 Second decade of life
 Myopics  Increases their grade because their lens
 Bilateral and cortical, anterior
got more thicker
and posterior subcapsular
 Increased serum phospholipid and high non-fasting blood region
glucose levels  Adult onset diabetics have earlier onset of age-related
cataracts than non-diabetics
NUCLEAR POSTERIOR  Retinopathy may impair vision
CORTICAL
SCLEROSIS SUBSCAPULAR  Diabetic snow flake cataract
- more common
Hard Soft Soft
Opacity of lens
Condensation of Appears as gold
fibers in spoke
lens nucleus white granules
like pattern
Myopic shift and Decreased near
better near vision vision and glare

Sees better at night, dilated pupils-> more light PATHOPHYSIOLOGY:

OCULAR TRAUMA 1. Increased glucose content in the aqueous humor
 Contusion (vossius ring a pigment on anterior capsule) leads to conversion of glucose by aldose reductase
 Laceration to sorbitol
 Retained Intraocular Foreign Bodies 2. Osmotic hydration due to high sugar content in the
 Iron: Siderosis lens
 Copper: Chalcosis 3. Associated activity of proteolytic enzymes with
 Electromagnetic Radiation consequent proteolysis
 Infrared (glass blower) 4. Disturbance of carbohydrate metabolism of the lens
 Microwave
 Ionizing radiation HYPOCALCEMIC CATARACTS
 UV radiation  Hypocalcemia or hyperphosphatemia
 Anterior Ocular Ischemia (Retinal Detachment Surgeries)  Neuromuscular hyperexcitability
 Small, discreet, iridescent, subcapsular
TRAUMATIC CATARACT  Correction of metabolic defect
 Contusion may produce posterior  PATHOPHYSIOLOGY:
subcapsular cataract months after  Reduction of serum Ca
the event  Increase of PO4
 Rupture of the lens capsule  Relative increase of K
 Extrusion of lens material into the
anterior chamber results in TOXIC CATARACTS
inflammation  Corticosteroids  Posterior
 Intraocular foreign body Subcapsular Cataracts
 Phenothiazines
Laceration/penetration - instant cataract formation

CATARACT ASSOCIATED WITH SYSTEMIC DISEASES:  Miotics

METABOLIC CATARACT  Example: Anti-cholinesterase
 Diabetes mellitus  Anterior Ssubcapsular
 Galactosemia Cataracts
 Hypocalcemia  Amiodarone
 Wilsons disease  Stellate anterior axial pigment deposition
 Myotonic dystrophy  Statins

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LENS-INDUCED OCULAR DISEASE - Metabolic Disorders

PHACOMORPHIC (PHACOGENIC) GLAUCOMA  Galactosemia
 Rapid swelling of lens follows  Lowe’s
hydration of lens fibers in - Maternal Infections
intumescent cataract  Toxoplasmosis
 May follow surgical or accidental  Rubella
rupture of lens capsule  Ocular Development Disorders
 May result in secondary angle - Persistent Hyperplastic Primary Vitreous (PHPV)
closure glaucoma (Pupillary block) - Aniridia
 Ocular Diseases
 Because of its size, iris is pushed forward  Causes - Trauma
narrowing or closing of the angle - Uveitis
- Retinoblastoma
PHACOLYTIC GLAUCOMA
 Leakage of lens proteins from a hypermature cataract cause CONGENITAL CATARACT
uveitis  A common condition but usually are tiny, stationary or non-
progressive that do not cause significant visual loss
 Lens proteins goes out from the capsule  Leakage in  Others progress slowly and may not require surgery until the
the anterior chamber  Causes Uveitis child is 10-15 years of age
 Lens particles, macrophages filled with lipofuscin granules  If you operate on a very young child, especially below
and phagocytes containing lens proteins obstruct the 2 years of age, you cannot put intraocular lens
trabecular meshwork because the lens is still growing at this time, also
because of the possibility of surgical trauma.
 If you can delay it until the child is 10-15 years of age,
better 
 Attention in infancy is directed to cataracts severe enough
to impair vision

EXAMINATION
LENS-INDUCED UVEITIS  At birth, fundoscopy should show a red fundus reflex
 Accidental rupture of the lens capsule liberates lens proteins  Direct or indirect ophthalmoscopy with use of Koeppe lens
 Uveitis sometimes with glaucoma occur to permit visualization of lens and anterior chamber
 Mutton-fat precipitates, posterior synechiae and pupillary
membranes may form LABORATORY STUDIES
 Treatment:  Patient and maternal studies for antibodies against rubella,
 Lens extraction cytomegalaviarus, toxoplasmosis ad syphilis, enzyme testing
 Corticosteroid administration
IMPORTANT ISSUES IN THE MANAGEMENT OF CONGENITAL
ENDOPHTHALMITIS PHACOANAPHYLACTICA CATARACT
1. Associated with other ocular abnormalities
 Sensitization to retained lens material after ECCE in the
2. Associated with systemic disease
second eye may cause endophthalmitis
3. Severity (monocular/bilateral)
 Retention of lens nucleus and or fragments of the lens in the
4. Timing of surgery (monocular/bilateral)
vitreous cavity also cause severe uveitis
5. Type of surgery
 Removal of lens material by vitrectomy is done
6. Aphakic correction
CLASSIFICATION OF CONGENITAL CATARACTS
CATARACT SURGERY IN PEDIATIC PATIENTS
 Primary:
 PROGNOSIS:
 Idiopathic (50% of all congenital cataracts)
 Visual prognosis for congenital cataract is not as good as
 Hereditary (30%)
that for patients with senile cataract.
 Secondary:
 Bilateral cataract has better visual prognosis compared to
 Systemic Disorders
unilateral congenital cataract.
- Chromosomal Disorders
 Down’s syndrome

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INDICATIONS FOR CATARACT SURGERY

 Lens threatens to cause secondary glaucoma or uveitis
 Visual defect interferes with patient’s vocation
 Permit fundus visualization to monitor glaucoma
 Permit adequate visualization of the fundus for
retinal/vitreous conditions
 As a refractive measure
 Cosmetic?

PREOPERATIVE EVALUATION OF CATARACT CASES

 External Exam
1. Motility
 If patient has nystagmus  If you do cataract
 Since the lens is soft in congenital cataract, what they do surgery, the patient will not be as improved as
is they use bimanual technique. compared to those patients without nystagmus
2. Pupils
DIFFERENTIAL DIAGNOSIS  Slitlamp Exam
 Leukoma 1. Conjunctiva
 Retinoblastoma  If you have conjunctivitis, you cannot do cataract
 Retinopathy of Prematurity surgery  Can cause infection post-operatively
 Persistent Hyperplastic Primary Vitreous
2. Cornea
3. Anterior chamber
4. Iris
5. Crystalline lens
 Fundus Evaluation
1. Ophthalmoscopy
2. Optic nerve
3. B-scan
 Ultrasound  See if the retina is attached
MEDICAL TREATMENT FOR AGE RELATED CATARACT  Done if you cannot see the retina
 Accurate frequent refraction to give BCVA (best corrected
visual acuity)  Measurement Of Visual Function
 Aldose-reductase inhibitors in galactosemic or diabetic 1. Visual Acuity Testing
patients 2. Brightness Acuity
3. Contrast Sensitivity
 Iodine salts, vitamins (B,C,E) or ATP, various reducing agents
4. Visual Field Testing
CATARACT SURGERY
PREOPERATIVE EVALUATION OF CATARACT CASES
 Surgery of lens has been practiced for at least several
hundred years
 Couching is the ancient surgical technique of removing
cataract by pushing lens into vitreous
 In middle of 18th century extraction of cataract was
proposed by Daviel which was unchanged for nearly 2
centuries
 In early years of this century increasing attention was paid
to intra-capsular method for cataract extraction
 In intracapsular method for cataract extraction, the
whole lens is taken out
 Most exciting innovation in cataract surgery in this century
is Phacoemulsification introduced by Kelman in 1967 and
latest is the LENSAR femtosecond procedure

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CATARACT SURGERY METHODS ECCE Phacoemul-

SICS
 INTRACAPSULAR LENS EXTRACTION (Traditional) sification
 Entire lens including capsule is removed Nucleus Nucleus
Ultrasonic
 Can make use of: expression expression
fragmentation
TECHNIQUE through through
- Cryoprobe through
medium smaller
- Capsule Forcep incision incision
microincision
- Indian Smith INCISION 6-10 mm <6 mm 2-3 mm
- Erisiphake INDICATIONS Immature to hypermature cataracts
CONTRA- Unstable cataracts
 EXTRACAPSULAR LENS EXTRACTION INDICATIONS Corneal deficiency
 Removal of anterior lens capsule, nucleus and cortex OPTICAL Intraocular lenses – PCIOL: Posterior Capsular
 Different Types: CORRECTION Intraocular Lens (rigid, foldable)
- Traditional ECCE
- Small Incision ECCE (SICS) INTRAOPERATIVE COMPLICATIONS
- Phacoemulsification Suction after Ultrasonic Disruption 1. Retrobulbar Hemorrhage
- Laser Cataract Surgery
 Before doing cataract surgery, they put local
anesthetics in the retrobulbar  If you hit a nerve,
this may cause retrobulbar hemorrhage  Postpone
surgery
 Now, we experience less of this because we now use
topical anesthetics
2. Incision
 Poor incisions  Causes leakage
3. Detachment of the Descemet’s membrane
 If the surgeon goes in and out of the incision site a lot
of times
 INTRACAPSULAR CATARACT EXTRACTION (ICCE) 4. Corneal Endothelial Damage
 10-12 mm incision is done followed by removal of the
 If you use too much phacoemulsification
entire lens
 Phacoemulsification produces heat  Can damage
 EXTRACAPSULAR CATARACT EXTRACTION (ECCE)
the endothelium
 The anterior part of the capsule is torn  Lens,
nucleus, and cortex of the lens is removed, leaving the 5. Iris Prolapse
posterior capsule
 If the incision is too posterior
 PHACOEMULSIFICATION
 Due to straining
 Only a small incision is made  Continuous
curvilinear capsulorrhexis  Using ultrasound, we 6. Hemorrhage
make segments of the lens  Suck out each segment  If you hit a blood vessel
7. Suprachoroidal Hemorrhage
ICCE ECCE
Entire lens is Intact posterior  In cases cataract surgery with glaucoma and glaucoma
TECHNIQUE
removed capsule and zonule is not controlled
INCISION Large (12mm) 3-10mm
8. Expulsive Hemorrhage
Cataracts with intact
INDICATIONS Dislocated cataracts
zonules  The lens, vitreous, and retina are expelled out 
Cataracts <50 years Patient will be blind
CONTRA-
old and ruptured Dislocated cataracts  Very important to make sure that the patient does not
INDICATIONS
cataracts
have any other problem
 Spectacles  Intraocular lens
 Contact Lens 9. Rupture of lens capsule and vitreous loss
OPTICAL
 ACIOL (Anterior
CORRECTION
Chamber
 Common since the posterior capsule is around 5
Intraocular Lens) microns  Easily torn  Vitreous will go out

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10. Operative Loss of Vitreous

11. Dropped Nucleus and Retained Lens Fragments
 Rupture of lens capsule  Lens will fall down/drop to
the vitreous = “Dropped Nucleus”
 Lens Fragments  Mix with the anterior chamber 
Hard to do irrigation and aspiration  “Retained Lens
CATARACT SURGERY COMPLICATIONS
Fragments”
12. Dislocated Intraocular Lens

 Since you have a ruptured capsule, the lens can go

down to the vitreous

 POSTERIOR CAPSULE OPACITY

 Usually because there is retained cortex after cataract
surgery
 Some of the epithelium from the anterior capsule can
migrate down to the posterior capsule
POST-OPERATIVE COMPLICATIONS  INTRAOCULAR LENS DECENTRATION
1. Anterior Chamber Depth Abnormalities  May be due to ruptured capsule
 If your incision is not good  Leakage of aqueous 
Flat chamber  Angles will be closed  Glaucoma VISUAL REHABILITATION OF APHAKIA
2. Hypotension  METHODS OF CORRECTION
 Spectacles
 Because of the incision  Contact Lens
3. Choroidal Detachment  Intraocular Lens
 Lasik
 Because of hypotension
4. Pseudophakic Papillary Block  IOL INSERTION
 Minimizes optical problems of aphakia
 Secondary to hypotension or angle closure  PCIOL (bag/sulcus)
5. Glaucoma  Lens is placed inside the capsule
6. Corneal Edema
 ACIOL
 Usually iatrogenic
 Lens is placed in the anterior chamber
7. Cystoid Macular Edema
8. Endophthalmitis  Scleral fixated

 It is important to clean the eye before you do the  If there is no capsule, we put sutures in the sclera
incisions and the lens is suspended at the back of the iris
 Can be prevented by:  Complications:
 Use of Tegaderm - Posterior Capsule Opacification (after cataract)
 Brushing of lashes  To remove matting - ACIOL may cause endothelial damage and bullous
 Putting iodine or betadine drops keratopathy
9. Uveitis
 Due to retained cortex and/or nucleus

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ADVANTAGES DISADVANTAGES
 Cheaper  25-30% image
 Handling ease size disparity
 Anisometropia
 False spatial
SPECTACLES orientation
 Spherical
aberration
 Restriction of
visual field
 7% image size  Difficulty in
disparity insertion
 No spheric
CONTACT aberration
LENS  Full peripheral field  FOLDABLE ACRYLIC
 Effective for  Injector injects the IOL in the capsule
irregular  MULTIFOCAL INTRAOCULAR LENS
astigmatism  Disadvantage: (+) Glare
 Eliminates  Improper  Advantage: (+) Near vision  Better than
perceptual problems placement may Accommodating IOL
INTRA-  Image size disparity lead to corneal  ACCOMMODATING INTRAOCULAR LENS
OCULAR is reduced to 1-2% complications  Advantage: Less glare
LENS  Useful for those
working in unusual  LASIK
environments  Laser in situ keratomileusis
 Gr. “cornea” (kerato) and “to carve” (mileusis)
 Lamellar flap is formed with a microkeratome or scanning
pulsed laser
 Stromal ablation

 ANTERIOR CAPSULE INTRAOCULAR LENS

 Haptic is S-shaped  Less touch of haptic on the
angles, less irritation, less inflammation
 RIGID PMMA INTRAOCULAR LENS
 Haptic is C-shaped

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CRYSTALLINE LENS produced, the old fibers are pushed towards Accommodation
DR. MARTIN the central portion. - Focusing of near objects upon the retina
- Suspensory zonules of Zinn - Physiologic interplay of the ciliary body,
ANATOMY OF THE LENS zonule, and lens that results in focusing of
TWO FUNCTIONS OF THE LENS near objects upon the retina
Refraction What happens in accommodation? Remember that
- Bending of light rays that passes through the lens is attached to the ciliary body, which is a
The eyeball has 3 different layers: one medium to another circular muscle, through the zonules. When the
External: cornea, sclera 2 Medians: ciliary body contracts, it shortens leading to
Middle: vascular layer (iris, ciliary body, choroid) Cornea – MAIN refractive median relaxation of the zonules. When it does, the lens
Innermost: retina refractive power = 43 diopters (fixed) becomes thicker because the capsule is somewhat
2 chambers of eyeball: Lens elastic.
Anterior chamber refractive power = 17 ± diopters What happens when the lens becomes thicker? The
Posterior chamber “although the lens have lower refractive power, it refractive power becomes higher. So by
Behind the central aperture of the iris, there is a can change through the accommodation” accommodation, you increase the refractive power
transparent biconvex structure which we call an so that you can visualize near objects clearly. When
optical median = LENS - 3 types: you’re looking at a distance, you don’t need
Behind the lens = VITREOUS BODY accommodation. That’s the reason why the ciliary
“lens is a biconvex avascular structure situated just muscle relaxes leading to its elongation.
behind the iris or the pupil, which is attached to the So only the capsule towards the ciliary body, the lens
ciliary body through the zonules.” becomes thinner leading to lesser refractive power
“there is a single layer of epithelium cell just located
behind the anterior capsule, which are the ACTIVELY “you use accommodation when focusing NEAR
PRODUCING CELLS in the lens especially the one that OBJECTS!”
is located in equatorial area.”
Lens fibers are continuously produced throughout
the life in which they contained nucleus.

PART OF THE LENS

- Lens capsule (envelopes the entire lens and is
attached to the zonules)
Anterior lens capsule – the basement
membrane of the epithelial cell
What happens in refraction? As one object is seen
Posterior lens capsule
from space & the light is passing through that object,
- Cortex it is refracted towards the cornea & lens.
Newly-formed fibers Emmetropia – focused in the retina
- Nucleus Myopia – focused in front of the retina (that’s why
Lens fibers – are continuously produced they tend to move the object closer to the eye)
throughout the life in which they contained Hyperopia – focused behind the retina (tendency to
nucleus. So gradually when more fibers are bring away the object farther from the eye)
2|P ag e Reiko N. Santos
PRESBYOPIA - Ophthalmoscopic sign oxidation of methionine & cysteine
- Loss of accommodation due to aging o (+) central dark reflex with peripheral
- Adolescents – 12 to 16 days orange reflex (normally, red-orange CLASSIFICATION OF CATARACT
(accommodating power) reflex) Degree of opacification
- 40 y/o – 4 to 8 days - Spoke-wheel peripheral dark reflex with - Immature
- >50 y/o – <2 days central orange red reflex - Intumescent
Symptoms: - Mature
- Inability to read fine print or discriminate EXAMINATION OF THE LENS - Hyper-mature
fine close objects at about age 40 - Best done with a dilated pupil - After-cataract
40 – Filipino male - Dense cataract MOST COMMON complication of cataract
38 – Filipino female o penlight/slit lamp/ophthalmoscope surgery
Treatment: - less dense cataract “all cataract surgery is now being performed by
- Corrected by plus lenses o slit lamp/ophthalmoscope extracapsular cataract surgery. This technique will
leave the posterior capsule behind so that the
intraocular lens can be inserted. Then this capsule
CATARACT
will become opacified later on. So when there is
- Any opacity of the lens second opacification of the posterior lens capsule as
CAUSES: a result of the cataract surgery, we call it AFTER-
- Acquired CATARACT or POSTERIOR CAPSULAR OPACITY!”
SYMPTOMS OF LENS DISORDERS
o Age-related
Presbyopic symptoms
o Traumatic TYPES OF CATARACTS ACCORDING TO
- Inability to perform near tasks
o Ocular diseases (uveitis, glaucoma) SEVERITY
Loss of lens transparency
o Systemic diseases (DM)
- BOV (blurry of vision)
- Childhood cataract
- Glare
o Congenital
Dislocation
o Acquired
- Refractive symptoms
“this may happen in traumatic injury or
congenitally” AGE-RELATED CATARACT FORMATION
PATHOPHYSIOLOGY
SIGNS OF LENS DISORDERS - Protein denaturation
Immature – If there are transparent lens fibers that
- Whitish pupillary reflex - Hydrolysis
are still present
CATARACT – adult & not always in children - Biochemical changes: Mature – If the whole lens fibers are no longer
RETINOBLASTOMA – pediatrics (<2 y/o) o = Na, insoluble protein present
- Iridodonesis o = soluble protein Hypermature – If there is liquefaction of the len’s
trembling of the eyes when lens are o Bound water reflecting loss of binding cortex leading to whitish pupillary reflex and rippling
dislocated. If there is no lenticular support sites of capsule
for the iris, then this will tend to dislocate. - Widespread oxidative changes: Morgagnian – the len’s cortex has been completely
Usually, it is seen in patients who have o = gluthathione concentration, liquefied that’s why the nucleus is no longer in its
undergone previous cataract surgery. central position
3|P ag e Reiko N. Santos
AGE-RELATED CATARACT ACCORDING TO Symptoms: “progressive painless diminution of DRUG-INDUCED/TOXIC CATARACTS
LOCATION vision” - Corticosteroids
- Decreased vision o Posterior subcapsular cataract (PSC)
- Painless - Phenothiazines
- Reduced vision in bright illumination - Miotics
(usually seen in px with posterior subcapsular o Ex. anticholinesterase – ASC
cataract especially in driving at night) - Amiodarone
- Spots in the visual field o Stellate anterior axial pigment
- Ability to read without glasses deposition
Nuclear sclerosis – elderly patients; aka “second (usually in px with nuclear sclerosis)
sight phenomenon” - Statins
So if the patient complained because of progressive
Remember that epithelial cell produces lens fibers painless diminution of vision but the symptom is Anterior lens deposits
throughout the life. So as you become older, the already present during childhood, then this maybe a due to the long-term
nucleus becomes much thicker & becomes sclerotic different condition. Not all elderly patients that have use of chlorpromazine
(harder). diminished vision has cataract, it may just be
In presbyopic patients, naturally there is a myopia.
problem in focusing near-objects. At the certain age, THREE LENS-INDUCED OCULAR DISEASE
the vision for near sight improves that there is 1. Phacomorphic (Phacogenic) Glaucoma
TRAUMATIC CATARACT - Rapid swelling of lens
myopic shift due to the thickening of nucleus and the
vision for distant sight diminishes, the reason why - Contusion may produce a cataract months follows hydration of lens
the refractive power becomes higher. after the event fibers in intumescent
– SECOND SIGHT PHENOMENON - Rupture of the lens capsule cataract
“this is one of the reason why it’s hard to convince - Extrusion of lens material into the anterior - May follow surgical or
elderly people to undergo cataract surgery, because chamber accidental rupture of lens
their grandparents told them that at a certain age - Intraocular foreign body
capsule
they will regain their vision. BUT note that not all
individual will experience nuclear sclerosis, because - May result in secondary
the most common form of age-related cataract is angle closure glaucoma
POSTERIOR SUBCAPSULAR.” The lens fiber becomes opacified as a result of
Cortical – the location of the cataract is in the protein denaturation & hydrolysis. If more fluid goes
periphery having a “spokewheel-like” appearance. CATARACT ASSOCIATED WITH SYSTEMIC inside the lens, that fluid will be absorbed by the lens
So even if the whole peripheral area is opacified, DISEASES (METABOLIC CATARACT) fibers resulting to its swelling & becomes edematous
your vision still works because the light can pass - Diabetes mellitus which blocks the pupil – PUPILLARY BLOCK secondary
through the central portion. - Galactosemia to glaucoma.
Posterior subcapsular – aka cortical cataract (MOST - Hypocalcemia Acute congestive glaucoma:
COMMON). This is located centrally in front of the - Blurring of vision - Ciliary injection
- Wilsons disease
posterior capsule. This usually gives more disturbing - Severe pain - Corneal edema
vision of illusion in relation to its size. So even if the
- Myotonic dystrophy
Tx: Intravenous mannitol
cataract is small, it gives severe visual disturbance Stellate posterior subcapsular
Oral acetazolamide
because of its location where the visual light passes cataract in myotonic dystrophy
Topical medications (to reduce the pressure)
through the area. seen on retroillumination
4|P ag e Reiko N. Santos
2. Phacolytic Glaucoma CHILDHOOD CATARACT - As a refractive measure
- Leakage of lens Congenital cataract When lasik method cannot be performed due to
- Common condition but usually small and thin cornea, then lens removal is the option & to
proteins from a replace an intraocular lens for correcting the error
not significant (does not require treatment)
hypermature cataract of refraction – REFRACTIVE INTIMATION
- May not require surgery unless visually
cause uveitis significant (>2 mm size) - Philhealth is not an indication
Binocular single vision – if you prevent light from
passing through the retina, then this condition will TECHNIQUES OF CATARACT SURGERY
In hypermature cataract, there is a liposuction of Intra-capsular Cataract Extraction (ICCE)
not develop.
lens proteins in the lens cortex, which are broken
Severe cataract – even if the patient is at pediatric - The entire lens is removed
down into smaller molecules so that they can escape
age, this must be removed especially for binocular The only indication for this is dislocated lens in which
in anterior capsule. When they escape and went to
vision. you removed the whole lens.
the aqueous humor, the eye perceived this protein as
Bilateral immature cataract – which is usually seen Extra-capsular Cataract Extraction (ECCE) –
a foreign body, thus releasing macrophages to attack
as “red-orange reflex” with tiny opacities. If present, (most common)
this. When they engulf the protein, they accumulate
then surgery can be delayed. Contraindicated for dislocated lens
in the trabecular meshwork that blocks the aqueous
Mature cataract – Do surgery right away! - Nucleus and cortex removed, capsule
humor & producing an OPEN ANGLE GLAUCOMA.
There is a sign of inflammation which is uveitis & intact
glaucoma, plus the cataract. The treatment is - Includes:
directed in reducing the pressure or inflammation, in - Hereditary 30% o Traditional ECCE (removing anterior
which steroid can be added. Once the pressure has - Secondary to metabolic/infectious capsule, cortex, nucleus; inserting
been diminished & inflammation has been diseases intraocular lens – POSTERIOR CHAMBER
controlled, then the cataract can be removed. - Undetermined causes INTRAOCULAR LENS PIGMENTATION)
Acquired cataract o Manual Small Incision Cataract
3. Lens-induced uveitis - Trauma - DM Surgery (MSICS)
- Accidental rupture of the lens capsule - Uveitis - Drugs o Phacoemulsification – ultrasound
liberates lens proteins - Infection (Bloodless surgery)
- Uveitis sometimes with glaucoma occur o Laser Assisted Cataract Surgery
- Mutton-fat precipitates, posterior INDICATIONS OF CATARACT SURGERY
synechiae, and pupillary membranes may - Lens threatens to cause secondary
form glaucoma or uveitis
- Treatment: lens extraction and - Visual defect interferes with patient’s
corticosteroid administration vocation
This may happen in cataract surgery when the
- Permit fundus visualization to monitor
nucleus (nuclear material) has not been successfully
glaucoma
removed, which causes uveitis
Lens Anaphylactica – another severe condition as a - Permit adequate visualization of the
result of lens-induced uveitis, which usually happens fundus for retinal/vitreous conditions
on the second eye (more severe than the first
induced inflammation on the first affected eye)
5|P ag e Reiko N. Santos
VISUAL REHABILITATION OF APHAKIA
(METHODS OF CORRECTION)
- Spectacles
- Contact lens
- Intraocular lens
- Lasik
Intraocular lens implantation
Monofocal – specified power is at -1 diopter with
spectacle so that the patient can see a balance of far
or near-object, granting that they have no
astigmatism. (if with astigmatism = use TORIC LENS)
Multifocal – perfect vision for far or near objects
without using spectacle.

“But not all the time you can place intraocular lenses
if there is a complication in the surgery. Hence, you
can correct it later on.”

Monocular cataract = use CONTACT LENS; no

spectacles (because it can cause double vision)
Bilateral cataract = use SPECTACLE or CONTACT
LENS

The End!
 [OPHTHALMOLOGY] GLAUCOMA

GLAUCOMA 2. Acceleration of Apoptosis

Dr. Manolito Reyes - Silent cell death
- No inflammation involved
GLAUCOMA 3. Ganglion Cell Death and Axon Loss
4. Retinal Nerve Fiber Layer Change (Undetectable)
 One thing that is so sad in Glaucoma is that once you - No cupping yet
have lose your sight/vision, you can’t get back what - No visual field defect yet
you’ve already lost  IRREVERSIBLE kind of blindness - Around 30-40% cell death  You are losing a lot
 Our goal is to detect Glaucoma early, so that we could already but yet you don’t have the manifestations
avoid permanent visual loss. Around 50-60% cell death  You will start to
 Glaucoma is now defined as an OPTIC NEUROPATHY have visual field defects  Mild to moderate
with corresponding visual field changes, as well as OPTIC stage of the disease
DISC CHANGES. Catch it early  Control the disease while there
 Before, Glaucoma is known to be a disease of the eye are no visual field changes and no cupping yet 
that has an increasing ocular pressure with Could be detected by certain diagnosing
corresponding visual field loss, but now, we consider instruments
increasing ocular pressure as a RISK FACTOR of  ASYMPTOMATIC DISEASE
Glaucoma. 5. Retinal Nerve Fiber Layer Change (Detectable)
6. Short Wavelength Automated Perimetry Visual Field
Changes
7. Standard Automated Perimetry Visual Field Changes
 FUNCTIONAL IMPAIRMENT
8. Visual Field Changes (Moderate)
9. Visual Field Changes (Severe)
10. Blindness

GLAUCOMA
 Leading cause of blindness  2nd only to cataracts

(Diagram Above) FUNCTIONAL AND STRUCTURAL  Cataracts remains to be the leading cause of blindness
DEFECTS OF GLAUCOMA here in the Philippines.
 Visual field is getting lesser because of retinal ganglion
 Affects 70 million people worldwide
cell death.
 10% estimated blind
 When you lose your retinal ganglion cells, it cannot be
 In the Philippines  3rd most common cause of blindness
reversed  Irreversible loss of vision
 Top 3 Causes of Blindness in the Philippines:
GLAUCOMA CONTINUUM 1. Cataract
2. Diabetic Retinopathy
3. Glaucoma

 UNDETECTABLE DISEASE
1. Normal
- Normal optic disc
- Normal nerve fiber layer
- Normal number of ganglion cells

LEA THERESE R. PACIS 1

 [OPHTHALMOLOGY] GLAUCOMA

 Aqueous humor is produced at the ciliary body  Goes  Number 1 risk factor to develop Glaucoma 
to the anterior chamber  Drain in your trabecular INCREASED INTRAOCULAR PRESSURE
meshwork  Normal IOP = 10-21 mmHg
 There should be an equal production and equal  IOP around 24 mmHg and above  Big chance that
excretion of aqueous humor  There should be a you have Glaucoma
balance between the INFLOW and OUTFLOW  Low Tension Type of Glaucoma  Variant
 In Glaucoma, the balance is altered  There is  With optic nerve damage and visual field damage
INCREASE PRODUCTION or, most of the time, there is a
DECREASE EXCRETION OR OUTFLOW Without the optic nerve damage, you cannot label them
as Glaucoma
 For example: A patient has IOP of 26 mmHg but has no
CONVENTIONAL OR TRABECULAR OUTFLOW optic nerve damage or visual field defect  Glaucoma
Suspects/Ocular Hypertensive

CONCEPT OF GLAUCOMA PATHOGENESIS

 2 Mechanisms Attributed to the Pathogenesis of

 TRABECULAR/CONVENTIONAL OUTFLOW (80%) Glaucoma:
 Goes out to your Trabecular Meshwork  Schlemm’s 1. Vascular Dysregulation
canal  Episcleral vein 2. Mechanical Tissue Damage
 UVEOSCLERAL/UNCONVENTIONAL OUTLOW (20%)  End Result: RETINAL GANGLION CELL DEATH
 Goes to beyond the iris  Uveoscleral Tissue 
Schlemm’s canal
 Bypass the Trabecular Meshwork ETIOLOGY:
 PRIMARY
 No identifiable ocular or systemic conditions
 Affects both eyes

 Asymmetrical  One eye is more affected

 Genetics
 SECONDARY
 Secondary to ocular or systemic disease

 Examples:
 Inflammation of the eye
 Blunt trauma to the eye
 Chronic steroid therapy

 Unilateral or bilateral

 Most are unilateral

 Genetics
 Acquired

LEA THERESE R. PACIS 2

 [OPHTHALMOLOGY] GLAUCOMA

CLASSIFICATION BASED ON MECHANISM AND OUTFLOW NEW CLASSIFICATION SCHEME – ADOPTED BY THE
OBSTRUCTION AMERICAN ACADEMY OF OPHTHALMOLOGY
 Primary Angle Closure Suspects (PACS)
 Appositional contact between peripheral iris and
posterior TM is possible

 No damage and symptoms

 Primary Angle Closure (PAC)

 Symptomatic with signs of disturbed structure but no
significant optic neuropathy

 OPEN ANGLE GLAUCOMA  Symptomatic:

 Trabecular meshwork is visible  Eye pain
 Blurred vision specially in the morning
 Could be seen by means of Gonio Lens
 Trabecular Meshwork is already occluded  Primary Angle Closure Glaucoma (PACG)
 Around less than 10O angle opening  Glaucomatous optic nerve damage is present along with
 Cornea and iris around 40-50 O angle opening VF defects

 Asymptomatic  Optic nerve and visual field defect

 Difficult to diagnose
ANGLE CLOSURE GLAUCOMA
 Do not complain of blurring of vision  CHRONIC
 Visual defect for Glaucoma is PERIPHERAL  Meaning, the patient doesn’t know about it
CONSTRICTION  Clinically, it is the same with Open Angle Glaucoma
 No symptoms but there is an irido-corneal contact
 Errors of Refraction
 Peripheral anterior synechia
 People who has MYOPIA (Near-sighted) tend to
have Open Angle Glaucoma  Due to the chronic contact of iris to the angle
 Have long eyeballs Synechia is an eye condition where the iris adheres
 Problem with optic nerve  Perfusion problem to either the cornea or lens

People who has HYPEROPIA (Far-sighted) tend to  Gradual IOP elevation

have Closed Angle Glaucoma
 Have short eyeballs  Compressed towards the  Little by little until the angle progresses to close 
anterior chamber That is why the patient could tolerate it

 Cataracts  Asymptomatic
 Recurrent short episodes
 Cataracts tends to push the angle forward - Unilateral pain
- Redness
 Focal loss of vision - Blurring of vision with haloes
 Treatment:
 Increase in IOP  Corresponding corneal
 Start with medicine first! haziness/edema due to high pressure
- Medical Therapy  Attacks resolve spontaneously
- Laser Surgery
- Surgical Procedure: Trabeculectomy  Pressure goes down and normalizes

 CLOSED (ANGLE CLOSURE GLAUCOMA)

 ACUTE
 Iris is touching the cornea  Sudden complete obstruction of the outflow tract by
peripheral iris
 Occluded trabecular meshwork when seen  An OCULAR EMERGENCY

LEA THERESE R. PACIS 3

 [OPHTHALMOLOGY] GLAUCOMA

 Sudden IOP increase DIAGNOSING GLAUCOMA

 HISTORY TAKING
 Acute attack  Normal IOP could suddenly rise to  Reason for visit
about 60 or 80 mmHg
 Chronic Angle Closure Glaucoma  Don’t complain
- Blurring of vision of anything but may complain of tearing or blurring
of vision
 Suddenly becomes counting fingers or even hand
movement
 Visual Problems
- Eye redness - Accompanying ocular signs and symptoms
- Severe eye pain  Family History
- Headache  Previous Eye Surgery
- Nausea/vomiting  Trauma
 Other Systemic or Medical Conditions
 Sometimes mistaken as a Neurologic Emergency  Diabetes
 To differentiate it: Look at the eye  Mid-dilated  Late stage of retinopathy  Neovascularization
(Does not react to light) with hazy cornea + red or  Goes to the angle  Could close the angle =
congested conjunctiva Neovascular Glaucoma
 Sometimes mistaken as Conjunctivitis  Hypertension
 To differentiate it: Look at the eye  Conjunctivitis
does not give you a mid-dilated pupil. It always has  Medications Taken (Systemically or Topically)
a normal pupillary reaction. Vision is also intact.
 Chronic Steroid  Can give rise to GAGs 
 MUST BE REFERRED IMMEDIATELY! Obstructs the angles  Increase IOP
 60 mmHg  In 72 hours, the patient could go blind

 EYE EXAMINATION
 TREATMENT  Error of Refraction
 Acetazolamide  Carbonic Anhydrase Inhibitor - Myopia/Hyperopia

 Safe and potent  Hyperopia  Could give rise to Close Angle

 Decreases IOP by decreasing the production of Glaucoma
aqueous humor  Myopia  Could give rise to Open Angle
 Two 15 mg tablets  Can decrease IOP by 40-50% Glaucoma

 Laser Iridotomy  Impaired Vision

- Relieve the obstruction - Cornea

 If there is Angle Closure Glaucoma: Lens and iris  Increase IOP  Cornea is hazy
touch at the level of the pupil  There is a pupillary
- Lens
block  Aqueous humor cannot pass through the
pupil  Trapped at the posterior chamber   Could be a factor in Glaucoma, especially in
Develop high pressure in the posterior chamber cataractous lens  Very white lens  Can push
 Laser Iridotomy  Allow the aqueous humor to the iris forward  Give rise to Phacomorphic
escape the posterior chamber  Goes to the Type of Glaucoma
anterior chamber  Pass through the trabecular
meshwork - Retina
 Definitive management for Acute Angle Closure
Glaucoma  Diabetic Retinopathy

 Fellow eye predisposed to angle closure - Optic Nerve

- Prophylactic laser iridotomy
 Optic Nerve Cupping

- Brain

 Some strokes could cause Glaucoma

LEA THERESE R. PACIS 4

 [OPHTHALMOLOGY] GLAUCOMA

 SLIT LAMP  Use lenses coupled to the eye

 Stereoscopic Examination - Eliminate the total internal reflection at the cornea-air
 Ocular Tissue interface
 Visualize and evaluate tissues and layers of the eye
Structures in the Anterior Chamber Angle:
 For Glaucoma, Gonio lens is used
 These 4 structures must be seen completely
 If only the Anterior Structures (Schwalbe’s line) is
 TONOMETRY seen  Closed Angle Glaucoma
 Clinical measurement of IOP  If you see the Posterior Trabecular Meshwork 
 Range: 10-21 mmHg Open Angle Glaucoma
 Goldmann  Gold standard for taking the IOP
 Slit lamp is needed

 Schiotz
 Slit lamp is not needed
 Foot plate flattens the cornea  Measure
pressure

- Ciliary Body

 Connection of iris to the sclera

- Scleral Spur
- Trabecular Meshwork

 Drainage apparatus

- Schwalbe’s Line

 Termination of the cornea and sclera

 GONIOSCOPY

 Examination of the angles will tell if the Glaucoma is

open or closed
 Examination of the optic disc will tell you if the
Glaucoma is Mild, Moderate, or Advanced

 OPTIC NERVE HEAD EVALUATION

 Direct Ophthalmoscope
- High magnification
 Indirect Ophthalmoscope
 Examination of the anterior chamber angle
- Stereoscopic view
 Angled lenses that focus on the anterior  Posterior Fundus Lens
chamber angle - High magnification
 When you are looking at the superior mirror, you - Stereoscopic view
are looking at the inferior angle
 It is very important that you view the optic disc by
 When you are looking at the nasal mirror, you
both eyes.
are looking at the temporal angle

LEA THERESE R. PACIS 5

 [OPHTHALMOLOGY] GLAUCOMA

 CLINICAL EVALUATION OF THE OPTIC NERVE HEAD Notching of the Inferior Rim
1. Size and shape of the optic disc
Normal Optic Nerve Head
- Optic Disc

 Focal enlargement of the cup

 Localized notching or narrowing of the neuroretinal
rim

 Notching towards the temporal part of the

rim
 Round to slightly oval
 Contains a central cup 4. Configuration and depth of the optic cup
Comparison Between Normal Optic Disc and
 Central Cup  Where retinal vessels exits Glaucomatous Optic Disc
from the optic nerve

2. Size, shape and color of the neuroretinal rim

Neuroretinal Rim

 Border between cup border and disc border

- Tissue between the cup and the disc margin

- Relatively uniform in width
- Orange to pink in color

3. Size of the optic cup in relation to the area of the optic

disc
Cup-to-Disc Ratio
- Normal: 3/10 or 0.3

 Larger than 3/10  Glaucoma 5. Cup-to-disc diameter ratio and cup-to-disc area ratio

- Increase slightly with age 6. Position of the central retinal vessel trunk on the disc

 Central retinal vessels should be fanning

temporally
 Fanning out nasally is abnormal

7. Presence and location of sphincter-shaped

hemorrhages
Splinter Hemorrhage
 Linear streak on or near
Generalized enlargement of the cup the disc surface
- Earliest change detected in Glaucoma  Clears over several
weeks followed by
 Optic cup enlarges  Neuroretinal rim localized notching and
thins out pallor of the
Compare optic cups of both eyes for asymmetry neuroretinal rim
 Visual field loss
LEA THERESE R. PACIS 6
 [OPHTHALMOLOGY] GLAUCOMA

- Diffuse loss of Retinal Nerve Fiber Layer

 Good clue that the patient could have  Very important sign of early Glaucoma
Glaucoma
 Should be worked-up for Glaucoma  NEW IMAGING TECHNIQUE
 Could be absorbed  Not permanently there  Optical Coherence Tomography (OCT)
 Could also be a sign of progression of
Glaucoma
 Re-evaluate the patient’s IOP
 Ask if the patient is compliant with his/her
medications

8. Presence and location of peripapillary chorioretinal

atrophy

9. Visibility of the retinal nerve fiber layer

Retinal Nerve Fiber Layer

 Quantitates nerve fibers

 In Glaucoma, there is THINNING of the nerve fiber

 Ultrasound Biomicroscopy

 4 Parts:
1. Macular Fibers – goes directly to the optic
nerve
2. Superior Arcuate Fibers
3. Inferior Arcuate Fibers
4. Nasal Fibers
Arcuate Fibers  Don’t pass directly the
optic nerve  They make an arc towards
the optic nerve, hence called “arcuate”
fibers
- Do not extend to the median raphe
 What happens in Glaucoma?
 In Glaucoma, because of the high pressure,
the retinal ganglion cells at the retinal nerve
fibers die
 In Glaucoma, most of the time, the first  Looks at the angle of the eye
indication that you are losing the film is the - Capable of early disease detection and monitoring
arcuate defect  Can be superior arcuate
disease progression
- Seen as inferior arcuate loss  Retinal
image is reversed  Structural loss precedes functional loss
- Superior field and inferior field defect 
Do not cross the median raphe

- Appears as a pattern of striations that radiate  VISUAL FIELD TESTING OR PERIMETRY

toward the optic disc  Important tool in Glaucoma
- Retinal Nerve Fiber Layer thins and becomes less  Monitor disease progression
visible in Glaucoma

LEA THERESE R. PACIS 7

 [OPHTHALMOLOGY] GLAUCOMA

- Confrontation Method 2. Octopus

 If the patient has Glaucoma and you test the

peripheral vision, the patient will not see it 
The only thing that the patient could see is his
central vision

 Gross field defect

 Evaluate patients who are unable to perform well
using the more sophisticated instruments used in
perimetry testing
 Unable to detect small defects in early Glaucoma

- Kinetic Visual Field Testing

 Not used anymore

 Uses moving test object usually a light of variable

size and intensity
 Object is moved from a non-seeing area toward a
seeing area  Normal Limits of the Visual Field of the Right Eye
 Recorded when patient sees the object
 Repeated until a boundary seeing and non-seeing
area is determined (isopter)
 Example: Goldmann perimeter

- Static Visual Field Testing

 Use of non-moving test spots (Picture taken from the internet, inferior visual field is 70 degrees in the lecture.
 Fixed test spots of varying intensity of light are Picture intended for visual purposes only)

presented for a short period of time - 60 degrees superior and nasal

 Patient respond to the light perceived - 70 degrees inferior
 Attempts to find the light sensitivity of the eye at - 90-100 degrees temporal to fixation
preselected location in the visual field - Blind spot occupies the area defied by the optic nerve
 15 degrees temporal to fixation
 Automated Static Perimeters
1. Humphrey Visual Field Analyzer  Visual Field Influenced by Other Factors
- Facial Structures

 Europeans  Have some kind of nasal visual field

defect because of their “sharp nose”

- Eyelid Anatomy

 Ptosis  Superior visual field involvement

- Pupil Size

 Decreased pupil size  Decreased visual field

- Ocular Media
 Black spot near the center  Optic Nerve
(Physiologic Blind Spot)  Cataracts  Generalized field defect

LEA THERESE R. PACIS 8

 [OPHTHALMOLOGY] GLAUCOMA

- Refraction  You have to aim at a target pressure corresponding

 Myopia and Hyperopia to the progression of the disease of a particular
patient
- Neurologic

 Glaucoma  Don’t pass through the median

raphe  For Open Angle Glaucoma  Medical Treatment first
 Respects the horizontal raphe  For Close Angle Glaucoma  Laser Treatment first
 Neurologic Field  “Hemianopsia” – Respects
either Temporal or Nasal, not Superior or Inferior  MEDICAL TREATMENT:
 There are times that there would be  Suppression of aqueous production
Quadrantanopsia 1. Beta Adrenergic Blocking Agents
 Respects the vertical raphe
 Can give around 20% decrease in IOP from the
- Neuro-ophthalmic baseline
- Retinal Conditions - Betaxolol
 If you have defects in the macula  Central vision - Levobunol
is lost - Timolol
2. Alpha Adrenergic Agonists

 Arcuate Distribution of the Retinal  Can give around 15% decrease in IOP from the
Nerve Fiber Bundles baseline
- Retinal nerve fiber radiate from - Apraclonidine
the optic nerve head - Brimonidine
- Distribution in an arcuate 3. Carbonic Anhydrase Inhibitors
manner around foveal region
 Topical: Can give around 15% decrease in IOP
 Structure and Function from the baseline

- Brinzolamide
- Dorzolamide
- Oral Acetazolamide

 Most Potent: Oral Carbonic Anhydrase

Inhibitor in the form of Acetazolamide

 Facilitation of aqueous flow

1. Parasympathomimetic Agents
- Pilocarpine

 Side Effects:
 Structure  Optic Nerve  Constricts pupil  Diminution of vision
 Function  Visual Field  Brow ache

2. Prostaglandin Analogs
 Damage of the optic nerve has a corresponding
damage on the visual field  There should be a  GOLD STANDARD  Can give around 30%
correlation between the optic nerve and visual field decrease in IOP from the baseline
 Central vision is intact  Only the peripheral  Safest drug  No systemic side effects
vision is involved  Has OCULAR SIDE EFFECTS  Eyes becomes red
and lashes will grow
MANAGEMENT OF GLAUCOMAS - Bimatoprost
 Lowering IOP - Latanoprost
 To preserve vision by slowing down the progression of the - Travoprost
disease - Tafluprost

LEA THERESE R. PACIS 9

 [OPHTHALMOLOGY] GLAUCOMA

 Reduction of vitreous volume b. Glaucoma Shunts and Filtration Devices

 For very high IOP, especially for Acute Angle Closure

- Hyperosmotic Agents
 Oral Glycerol
 Intravenous Mannitol

 Side Effects:
 Dehydration
 Cardiac Arrest

 SURGICAL AND LASER TREATMENT

1. Peripheral Iridotomy or
Iridectomy
 Last resort
 For Close Angle  Put a tube in the eye  Tube will suction aqueous
Glaucoma  NOT for humor out
Open Angle Glaucoma
4. Cyclodestructive Procedures
2. Laser Trabeculoplasty
 Kill the ciliary body through cryo or laser  Stop it
from producing aqueous humor
 Indicated for those patients with No Light Perceptio
+ Pain or patients with Light Perception + Pain

Generally, Glaucoma cannot be cured, but can be controlled

with topical medications, lasers, new surgical technology
and techniques

SUMMARY
 Glaucoma is a progressive neurodegenerative disease
affecting the eye
 For Open Angle Glaucoma  May result in visual field disturbance or blindness
 Targets the Trabecular Meshwork  Burn the  There is retinal ganglion cell death resulting in a
trabecular meshwork by means of laser  In characteristic optic neuropathy with cupping or excavation
between burns there will be widening of trabecular of the optic nerve head
cells  It can now function more than the usual  Elevated IOP is the most frequent causative risk factor in the
tight trabecular meshwork development of Glaucoma
 There are other risk factors that are also known to play a role
3. Glaucoma Drainage Surgery  Key to successful Glaucoma management is early detection,
a. Trabeculectomy appropriate and adequate treatment and regular
monitoring

 Medication is not effective  IOP is still far from

target pressure
 Aqueous humor gets out from the subconjunctival
space  “Subconjunctival Drainage”

LEA THERESE R. PACIS 10

 [OPHTHALMOLOGY] GLAUCOMA

MECHANISM OF SIDE EFFECTS DURATION OF

DOSE % DECREASE IN IOP CONTRAINDICATION
ACTION Local Systemic ACTION
 Uveitis
 Conjunctival hyperemia
Increase  Caution in eyes with history of
PROSTAGLANDIN/  Increase length, thichness, and
uveoscleral OD 25-35% None herpetic keratitis and eyes at risk for 4-6 weeks
PROSTAMIDE pigmentation of eyelashes
outflow crystaloid macular edema
 Increase iris pigmentation
 Previous cataract surgery
 Decrease tear secretion  Decrease exercise  Patient with bronchial asthma, COPD
Decrease
BETA BLOCKERS (NON- 1-2x  Allergy tolerance  2nd Degree Heart block
aqueous 20-25% 2-4 weeks
SELECTIVE) daily  Superficial punctate keratitis  Dyslipidemia  Bradycardia
production
 Blurring of vision  Decrease libido  Cardia failure
 Similar to non-selective but  2nd Degree Heart block
Decrease absence of β2-Adrenergic  Bradycardia
BETA BLOCKERS 1-2x
aqueous 15-20% Inhibitors makes it better  Cardia failure 2-4 weeks
(SELECTIVE) daily
production tolerated by patient with  Caution in patients with bronchial
asthma and COPD asthma and COPD
Increase  Dimming of vision (Decrease  Salivation
aqueous outflow pupil size)  Nausea
 Uveitis
CHOLINERGIC AGENTS (Constricts pupil,  Brow ache (Stretched sphincter  Vomiting
 Neovascular Glaucoma
 Pilocarpine increase surface 4x daily 20-25% muscle)  Diarrhea 3 days
 Malignant Glaucoma
 1st glaucoma drug area of  Myopia  Intestinal cramps
 Post-drainage surgery
trabecular  Increase pupillary block  Bronchospasm
outflow)  Cataract  Frequent urination
 Dry mouth
 Blepharitis
Decrease  Lid elevation
aqueous
ALPHA-2 AGONIST  Conjunctival hyperemia
production  Drowsiness
 Brimodine 2-3x  Allergy  Patient on oral MAO Inhibitors
20-25%  Dizziness 1-3 seconds
 Only drug with dual daily  Folliculosis  Pediatric patients
Increase  Apnea in children
effect  Conjunctival edema
trabecular
outflow  Foreign body sensation
 Burning sensation
 Blurred vision
 Tingling sensation
 Anorexia
 Stinging sensation  Nausea
CARBONIC ANHYDRASE
 Allergy  Vomiting
INHIBITORS Decrease Topical: 15-20%  Allergy to sulfa class of medication
2-3x  Butter taste  Diarrhea
 Diamox aqueous  Caution in eyes with compromised
daily  Toxic keratitis  Metabolic Acidosis
 Good for Acute Open production Systemic: 40-50% corneal endothelial cells
 Corneal endothelial  Nephrolithiasis
Angle Glaucoma
dysfunction  Bone marrow
depression
 Blood dyscracias
OSMOTIC AGENTS Lowering of IOP Produces greatest decrease
1-2 g/
 Great for Acute Open due to decrease in IOP but duration of action Few hours
kg/BW
Angle Glaucoma vitreous volume is only a few hours
Not discussed but need to STUDY! - Table from MRA trans

LEA THERESE R. PACIS 11

OPHTHALMOLOGY – THE FUNCTIONAL POSTERIOR SEGMENT: VITREOUS & RETINA
FEU-NRMF Institute of Medicine
3B-Medicine 2017
Lecturer: Dr. Marin, July 2015

POSTERIOR SEGMENT VITREOUS EMBRYOLOGY

- The structures of the globe behind the iridolenticular  Primary Vitreous Stage
plane and encased by the scleral coat - The primary vitreous in the central portion of the
eye will become the Cloquet’s canal
 Secondary Vitreous Stage: will become most of the
adult vitreous (Newell)
 Tertiary Vitreous Stage
- Development of the Zolunar System which enables
a person to see near & far (accommodation)
 from developing CB neuroectoderm
 within the lens equator, pars plicata/plana, CB
triangle
 VB development
- Further Regression of the Hyaloid System
POSTERIOR SEGMENT EVALUATION  Late Fetal Development
Instrumentation:  Postnatal Vitreous Changes
 light source and magnifying device
 opthalmoscope – direct and indirect
 slit lamp
 HR lenses – contact and non-contact
 Visual field apparatus
 Electrophysiologic instrumentation
 Ultrasound
 Fundus camera

DIRECT VS. INDIRECT OPTHALMOSCOPY

DIRECT INDIRECT
1. Image
 Orientation Erect Inverted
 Magnification 15x 2-5x
 Field of view 10-15 deg 35-50 deg
 Depth of field Shallow Deep
dimension 2D 3D
2. Working Distance close Comfortable
3. Indication Details Dynamic study
central Peripheral and
PP THE ADULT VITREOUS
- Virtually acellular and spherical viscous content of
THE VITREOUS HUMOR the globe
- Transparent gel composed of a random network of - Framework of collagen fibrils reinforced with
uniformly thin collagen fibrils suspended in a highly hyaluronic acid molecules w/c provide its gel-like
dilute solution of salts, protein & hyaluronic acid state
(Newell) - 98% water
- Makes ¾ of the globe - Volume = 4.5 ml in the emmetropic eye
- Part of the transmission media which is important for - Axial diameter = 16.5 mm
clarity

1
OPHTHALMOLOGY – THE FUNCTIONAL POSTERIOR SEGMENT: VITREOUS & RETINA
FEU-NRMF Institute of Medicine
3B-Medicine 2017
Lecturer: Dr. Marin, July 2015

Vitreous Hyaluronate - Vitreous volume = HA volume

 HA molecules are the most abundant in the posterior 3. MECHANICAL
cortical gel with a decreasing gradient anteriorly &
- Viscoelastic properties, “mechanical buffer”
centrally - Less rigidity built than other CT (i.e. cartilage) but
 Hyalocyte synthesis? can withstand high-frequency stimulus
 Fill spaces between collagen filaments and provide a - Primarily HA elastic response to stimulus with
“stabilizing effect” on the collagen network frequency = 0.4 cycles/sec
- HA stabilizes the collagen filament network
Vitreal Attachments: - Stabilizes the distribution of structural proteins
1. Vitreous Base (VB) and decreases the susceptibility to mechanical
- Strongest point of attachment to the underlying stress
retina (spans the peripheral retina up to the ora
serrata & the pars plana) 4. PHYSIOLOGIC AND METABOLIC
*If pulled, all of the ocular structures here will be pulled - Repository for hyalocytes and neighboring tissues
with it - Repository for amino acids for retinal utilization
- Extends 1.5-2.0 mm anterior and 2.0-3.0 mm - Repository for metabolic wastes
posterior to the ora, and several mm into VB - “highway of materials in the eye”: diffusion and
- Fibrils attach and interdigitate between the basal bulk flow of materials
lamina of retinal glial cells and fibrillar basement
membrane of the NPCE VITREOUS EXAMINATION
2. Weigert’s Ligament (WL): 8-9mm annular lenticular  DIFFICULTIES ENCOUNTERED
attachment w/c came from the primary vitreous w/c  Microscopic
has regressed  Opaque
3. Vitreopapillary Attachment (Weiss’s ring):  Limited access
attachment to the optic nerve  Dynamic interrelationship
4. Macular Attachment
 TECHNIQUES TO OVERCOME DIFFICULTIES
5. Vascular Adhesions
 Dilation of pupils
6. Areas of Vitreoretinal Degeneration  Retroillumination: use of light to reflect
/highlight opacities in the vitreous (e.g. ROR in
FUNCTIONS OF THE VITREOUS
fundoscopy can be used as background to see
1. OPTICAL structures)
A. Clarity  Tyndall effect
o RI = 1.3349; 90% transmission of 300-1400nm  Ascencion phenomenon &Whiplash effect:
spectra agitative movements used to be able to mobilize
o Transparency due to: lesions within the cavity & make them traverse
- Very low concentration of macromolecules the beams of light projected
- Distinctive properties of collagen and HA
- HA – macromolecular and cellular “sieve”, VITREOUS PROBLEMS
inhibits lymphocyte stimulation, macrophage
 AGING CHANGES
phagocytosis, and PG synthesis
- Primary problem
- Matrix inhibition of cellular proliferation
- Dissociation of hyaluronic acid from fibrils
- Protein (MW6200) – anti-angiogenesis factor
- Pooling of Hyaluroonic acid
B. Accommodation
- Fibril degeneration and reduced elasticity
2. DEVELOPMENTAL  Resulting in gel liquefaction or syneresis
- Eye size and proportion, as well as growth of the  Collagen molecules aggregate to form fibrillar
RPE dependent on vitreous development opacities in the vitreous cavity
- Vitreous provides the internal tension critical for - Drainage of Hyaluronic acid into the retrovitreal
anatomic and geometric evolution of internal eye space producing PVD (Posterior Vitreous
structures Detachment)

2
OPHTHALMOLOGY – THE FUNCTIONAL POSTERIOR SEGMENT: VITREOUS & RETINA
FEU-NRMF Institute of Medicine
3B-Medicine 2017
Lecturer: Dr. Marin, July 2015

THE RETINA
- The inner coat of the posterior eye w/c is light
sensitive & transparent
- Have 2 layers: an outer layer, retinal pigment
epithelium & an inner layer, the sensory retina
VITREOUS PATHOLOGY
- Extends from the edge of the optic disc & anteriorly
 MECHANISMS to the ora serrata
- Cells, membranes, or protein aggregates being - Most important portion is the macula, responsible for
imaged on the retina (“floaters”) 75-80% of vision; sharpest vision
- Loss of gel structure *Foveal area: thinnest & gives light direct access to
- Traction of fibrils on the retina the photoreceptors; there is 1:1 of cells &
photoreceptors; there is luteal pigments; has the
 SIGNS AND SYMPTOMS dendest cone
 Blurring of vision - Blood supply:
 Floaters  Inner nuclear layer: ophthalmic artery
 Photopsia: light is perceived even if there is no  Photoreceptors, retinal pigment epithelium &
light (happens because the retina is being outer nuclear layer: the uveal tissue/choroid
stimulated since it is being pulled)
*Newell: shrinkage of the vitreous causes a variety of NEUROSENSORY LAYER
entoptic phenomena that can be seen with the eyes
closed or in the dark. As the eyes move, the shrunken
vitreous gently bumps the retina, initiating a nervous HISTOLOGY
impulse & perception of light.

POSTERIOR VITREOUS DETACHMENT

- Normal, age-related phenomenon (50’s; younger if
diabetic)
- Antero-posterior progression
- Primary sign: observation of the Weiss’s ring
- Effects:
o Vitreoretinal traction
 Photopsia
 Retinal breaks and detachment
o Loss of barrier function
 Floaters
 Cellular and macromolecular infiltration
Clinically & functionally, can be divided into just 4 layers:
 Epi/sub-retinal membrane formation
- ganglion cell layer (innermost)
 Macular pucker
- layer of intermediary neurons
 Macular hole
*Can be infiltrated by amyloid, crystals, calcium crystals, - photoreceptors
blood (in vitreous hemorrhage) or microbial cells - retinal pigment epithelium

3
OPHTHALMOLOGY – THE FUNCTIONAL POSTERIOR SEGMENT: VITREOUS & RETINA
FEU-NRMF Institute of Medicine
3B-Medicine 2017
Lecturer: Dr. Marin, July 2015

PHOTORECEPTORS (cones & rods) RETINAL IMAGE

- main component of how a o Transformation of Light
person can take up light - Energy to membrane potentials”
- rods outnumber cones by about - Primary image from the photoreceptors
20:1 - Secondary image produced in bipolar cells and
modified by horizontal cells
- rods are more sensitive to light,
- Tertiary image produced in ganglion cells and
the reason why it is the one modified by amacrine cells
used for night vision
Light strikes the
photoreceptors &
gets the primary
image there and this
connect with the
bipolar cells forming
your secondary image
w/c is modified by the
The distribution of rods & cones are opposite; cones are more horizontal cells. The
bipolar cells get the
concentrated on the fovea & less in the periphery, whereas
secondary image to the ganglion cells. It is now transferred to
rods are numerous all throughout except the fovea the brain via the optic nerve which is actually a connection of
long ganglion cells.
Cones Rods
- 6M, 25μm long, 85μm - 120M, 50μm long
 PHOTOCHEMISTRY
at fovea - Elongated outer segment
- Photoreceptor outer segments (OC) contain the
- Conical outer segment w/ 1000 stacked discs
visual pigments
w/ stacked saccules separate from the cell
*Visual pigments or “visual purple”: consists of
connected to the cell membrane containing
vitamin A (cis-retinal) & the protein opsin making
membrane visual pigments
rhodopsin
- OS cell membrane allows Na entry while IS secretes
SUPPORT CELLS the ion producing a resting current
o Bipolar Cells: 1st order neuron connecting PR to GC - Light causes the influx of Ca ions to effect a current
o Ganglion Cells: 2nd order neuron connecting BC to disruption and hyperpolarization
LGB
o Horizontal Cells
o Amacrine cells: modify signals coming from the
other cells
o Muller cells: Glial support cells with nutritive repair,
ionic reservoir, support functions

When light strikes the photoreceptors, the visual pigment

disintegrates, forming different types of molecules that
becomes unstable & so dissociates. Trans-retinal is
transported & put up to the retinal epithelium where it is
converted back to cis-retinal by the retinal isomerase &
thrown back into the outer layer of the photoreceptors for
reassembly to rhodopsin.

4
OPHTHALMOLOGY – THE FUNCTIONAL POSTERIOR SEGMENT: VITREOUS & RETINA
FEU-NRMF Institute of Medicine
3B-Medicine 2017
Lecturer: Dr. Marin, July 2015

RETINAL PIGMENT EPITHELIUM

 Single hexagonal, epithelial cells
 in contact with Bruch’s membrane at the base and
with the photoreceptors at its apex
 contains melanin granules
 apical zona occludens – prevents choroidal bacteria
from entering the retina
 variable distribution:
 tall and numerous at the fovea
 heaped up at the papilla
 larger and irregular peripherally

FA Imaging Principles
The dye is injected IV
and will flow
through the blood
Functions: vessels then pictures
would be taken.
 Photoreceptor metabolism maintenance
There is an exciting
 Regeneration of the visual pigment light from the flash
 Absorption of stray light bulb and will pass
 Outer blood-ocular barrier through a filter,
*inner blood-ocular barrier: endothelial cells of blood vessels which is blue. When
 Active transport of metabolites it hits the flouresceine, it emits a yellow blue light which is
 Phagocytosis and immune cellular response then reflected back to the film or digitized.

FA Interpretation Basics:
RETINAL EXAMINATION - Basically a comparison of early & late, previous to
present angiographic patterns
Instrumentation - Temporal sequences:
 Direct opthalmoscope and the ROR  Choroidal phase: 8-15 sec
 Indirect opthalmoscope  Arterial phase: 10-15 sec
 Slit lamp biomicroscope  Capillary phase: 20-25 sec
 High-resolution contact/non-contact lenses  Venous phase: 21-25 sec
 Goldmann lens
 El-Bayadi Kajura lens Results for interpretation:
 Volk couble aspheric lens - Gives you focal, regional & general perfusion status
 Wide-field contact lenses - Shows location, size & relations of lesions
 Visual field Apparatus - Fluorescence patterns are what we look at
 Electrophysiologic Apparatus  2 abnormal fluorescence patterns:
 HYPERFLOURESCENCE – dye is enhanced that
Retinal diagnostics can be because of leakage, transmission
increase or abnormal vessels
1. FLUORESCEINE ANGIOGRAPHY (FA)  HYPOFLUORESCENCE – extreme decrease in
- Used to assess blood vessels & circulation of the amount of fluorescence by the dy
retina

5
OPHTHALMOLOGY – THE FUNCTIONAL POSTERIOR SEGMENT: VITREOUS & RETINA
FEU-NRMF Institute of Medicine
3B-Medicine 2017
Lecturer: Dr. Marin, July 2015

 Treatment and temporal assessment, comparison

and monitoring
Comparison of other Retinal Diagnostic Modalities:
OCT vs FA/ICG
- Whereas FPFFA and ICG visualizes the retina and
choroidal circulation and fundus background, OCT
allows a cross section of structures

3. OCT ANGIOGRAPHY
 New technology that
combines FA & OCT
 Uses retinal structures
(vessels and optic disc) as
stationary landmarks to
visualize relative flow of
RBCs through the lumen of
blood vessels
*similar to retinal perfusion machines
 No dye needed to be injected
- Safer; no allergies/anaphylaxis

4. WIDEFIELD ANGIOGRAPHY
 Same FA procedure
 Uses a more spherical lens/ Fish eye = wider field of
view
2. OCULAR/OPTICAL COHERENCE TOMOGRAPHY (OCT)
- Software compensates for optical aberration in
 “Tomos” (Greek) = section
the periphery
 Cross-sectional imaging of biologic tissue eg.
Macula using light waves
 “Optical biopsy” akin to in-vivo histopathology
sections

 Combination machines
o Can do FA, ICG, and OCT all at the same time
o Less time consuming
o Recording in Video
- Better at detecting pathology, specially leaks

RETINAL DISEASES

SYMPTOMS/ USUAL COMPLAINTS

Uses:  Painless visual disturbance
 Optical biopsy  Loss of acuity
 Retinal profile  Changes in color perception
 Layer by layer analysis  Quality of vision:
 Vitreoretinal initerface  Discoloration
 Thickness/volume measurements  Scotoma – abnormal areas of blindness

6
OPHTHALMOLOGY – THE FUNCTIONAL POSTERIOR SEGMENT: VITREOUS & RETINA
FEU-NRMF Institute of Medicine
3B-Medicine 2017
Lecturer: Dr. Marin, July 2015

 Nyctalopia – night blindness/ lack of sensitivity - Efforts to decrease IOP and dislodge the
of light in a dim areas clot/embolus ie. Digital massage, IV
 Metamorphosia (micropsia or macropsia) – acetazolamide, AC paracentesis
afflicted eye sees objects smaller or bigger - Pharmaceutical: systemic antithrombotic agents
than the object is should be - Surgical: CV w/ direct CRA massage, PRP for NV,
 Sectoral field defect/shadows antiVEGF treatment
 Floaters
 Photopsia FA of central retinal artery occlusion

DISEASES
1. Circulatory/Generalized
A. Arterial Occlusive Diseases: CRAO/BRAO
B. Venous Occlusive Diseases: CRVO/BRVO
C. Hypertensive Retinopathy
D. Arteriosclerotic Retinopathy
E. Diabetic Retinopathy B. VENOUS OCCLUSIVE DISEASE
F. Retinopathy of Prematurity (ROP)
2. Macular
3. Pigmentary Disturbance/Degeneration
4. Retinal detachment
5. Retinoblastoma

1. CIRCULATORY/GENERALIZED
A. ARTERIAL OCCLUSIVE DISEASE
CENTRAL RETINAL VEIN OCCLUSION (CRVO)
 Sudden painless visual loss
 “hot dog and catsup” fundus
 Venodilation
 Generalized hemorrhage
 Exudates
 Precipitating factors
 Arteriosclerosis
COMMON PRESENTATION: Overall pallor of the  Hypertension
involved area/s of the retina  Diabetes
 Inc IOP
CENTRAL RETINAL ARTERY OCCLUSION (CRAO)
 Embolisation
 Only true ophthalmic emergency
 Complications
 Sudden painless visual loss
 Macular edema
 “cherry red spot” (white arrow); generalized retinal  Neovascularization
edema and opacification  Neovascular Glaucoma (60 or 90-day)
 Precipitating factors  Vitreous hemorrhage
 Arteriosclerosis  Traction retinal detachment
 Hypertension
 Diabetes FA of non-ischemic central retinal vein occlusion
 Inc IOP
 Embolisation
 Treatment
- within 45-90min (golden period)
- Carbogen, brown paper bag breathing

7
OPHTHALMOLOGY – THE FUNCTIONAL POSTERIOR SEGMENT: VITREOUS & RETINA
FEU-NRMF Institute of Medicine
3B-Medicine 2017
Lecturer: Dr. Marin, July 2015

- Focal or generalized arteriolar constriction

- Hemorrhages
- Exudates

Clinical Findings
 Dilated and tortuous retinal veins, haemorrhages &
exudates in all quadrants (Hotdog and ketchup
fundus)
 Cotton-wool spots;
 Capillary non-
perfusion;
 Optic disc swelling;
 Macular edema;
 RAPD; *To differentiate Arterial & venous occlusions
 Vein collateralization; - Arterial: emboli usually seen in bifurcation of vessels
 Neovascularization; - Venous: the arteriovenous crossings
Management
D. ARTERIOSCLEORTIC RETINOPATHY
 Treat underlying systemic disease/s;
 Due to thickening of the vessel wall
 Control glaucoma;
 Intimal hyalinization
 Panretinal Photocoagulation (PRP) for extensive
 Medial hypertrophy
ischemia and/or neovascularization;
 Endothelial hyperplasia
 Remedy macular edema;
 Primary Sign – arterovenous crossing changes
 Corticosteroids and anti-VEGF agents;
Grading of Arteriosclerosis
 Check every month for 6 months
Grade
 Look for rubeosis & angle NV
1 Widened median reflex and venous
CRVO Study concealment
 Argon FLT in CRVO with ME reducing VA to <20/50 2 G1+ venous deflection at arteriovenous
- Macular grid treatment ineffective crossings (Saluss’ sign)
 Argon PRP prevention of AS NV and NV Glaucoma 3 G2+ “copper-wire” arterioles and marked AV
- Although prophylactic laser treatment prevented crossing changes ie. Venous banking (Bonnet’s
AS NV, lashing at the time of AS NV development sign) or venous tapering on either side of the
prevented NV glaucoma; crossing (Gunn’s sign)
- Observe only and laser for NV in angle or 2 clock 4 G3+ “silver-wire” arterioles and severe AV
hours of iris; crossing changes
 Anti-VEGFs

C. HYPERTENSIVE RETINOPATHY
 Associated with systemic hypertension
 Very hard to see & diagnose
 Grading
0 – no changes
1 – Barely detectable arterial narrowing
2 – Obvious narrowing with focal constrictions
3 – Grade 2 with exudates and haemorrhages
4 – Grade 3 with disc edema
 Features

8
OPHTHALMOLOGY – THE FUNCTIONAL POSTERIOR SEGMENT: VITREOUS & RETINA
FEU-NRMF Institute of Medicine
3B-Medicine 2017
Lecturer: Dr. Marin, July 2015

E. DIABETIC RETINOPATHY Sensitivity Specificity

 Retinal microvascular changes associated with the Proliferative DR 87% 80%
systemic disease; Moderate-sever NPDR 81% 93%
 Prevalence generally ↑with age & duration of  Utilized views centered & on either side of the
disease & glycemic control; fovea screening for exudates:
 Pathogenesis Sensitivity Specificity
1. Progressive basement membrane thickening; Hard exudate/s within 1 DD
2. Capillary endothelial cell damage of the center of the macula
94% 80%
3. Loss of pericytes defects clinically significant
4. ↑stickiness & macular edema
aggregation of
platelets Clinical Findings
 Can be proliferative or 1. Hemorrhages
non proliferative 2. Exudates (usually in ring-like fashion)
 Features: 3. Fibrovascular proliferation
 Microaneurysms 4. Retinal detachment
(primary lesion) 5. Subretinal fibrosis
 Exudates 6. Intravitreal hemorrhage
 IRMA 7. Synchisis scintillans – characterized by the presence
 Fibrous of bright, shiny particles floating in vitreous
proliferation 8. Rubeosis iridis – blood vessels visualized in iris
 Vitreous 9. Hyphema – presence of blood in anterior chamber
hemorrhages Diabetic retinopathy treatment
 Neovascularization  Non-progressive DR (NPDR)
 Traction - Glycemic control and systemic surveillance
detachment - Observe for ischemic changes and macular edema
 Macular edema - Referral/tx for high risk characteristics
Diabetes is generally a SILENT DISEASE!!!  Progeressive DR (PDR)
Visual loss is a late consequence of the disease process - Laser photocoagulation
and is commonly PERMANENT! What we need to do is - Vitrectomy
SCREEN
DR STUDIES: All are randomized, prospective clinical trials
FOR SCREENING:
Diabetic retinopathy study (DRS)
Diabetic eye symptomatology
Issues:
 Fluctuating vision and variable/unstable refraction  Efficacy of PRP on severe NPDR/PDR
 Early cataractous lenticular changes - 50% or greater reduction in the risk of severe visual loss
 Diplopia and opthalmoplegia (<5/200) in treated vs. non-treated eyes
 Recurrent corneal epithelial breakdown with - Complications:
subsequent edema and opacification a) decreased VA (11%)
b) visual field loss (5%)
Baseline ocular examination
 High Risk characteristics definition
 History of visual symptoms;
 Measurement of visual acuity & intraocular pressure; Early treatment diabetic retinopathy study (ETDRS)
 Ophthalmoscopic evaluation through dilated pupils; Issues:
Diabetic ocular examination – practical fundoscopy  Efficacy of laser treatment for macular edema
- 50% reduction in rates of MVL in treated vs. non-treated
 Screening and Surveillance of Diabetics eyes with clinically significant macular edema
 Utilized views centered & on either side of the  Optimal training for initiation of PRP
fovea screening for hemorrhages &/or - PRP only in sever NPDR/PDR
microaneurysms:  Efficacy of ASA treatment in retarding progression of
retinopathy

9
OPHTHALMOLOGY – THE FUNCTIONAL POSTERIOR SEGMENT: VITREOUS & RETINA
FEU-NRMF Institute of Medicine
3B-Medicine 2017
Lecturer: Dr. Marin, July 2015

Diabetic retinopathy vitrectomy study (DRVS) Examination sequence

Issue:  Screen at 4 weeks post-natally or 32 weeks,
 Early vitrectomy in DR whichever is ealier
- Clearly beneficial in type 1 diabetics with severe vitreous
 Repeat every 1-2 weeks until the ff:
hemorrhage
- normal and complete blood supply develop
- Advantageous in eyes with very sever proliferative
retinopathy - successive 2-week exam shows Stage 2 in zone III;
then, every 2-4 weeks
Diabetic macular edema and anti-vegf - development of “pre threshold” – weekly
 Anti-VEGF (Ranibizumab) with prompt or deferred - ROP disappears
laser superior to Laser alone up to 2 years  once blood supply completed – every 6-12 months
 Visual gains in Anti-VEGF group versus plateau or
loss in laser group ICROP classification
Zone
Diabetic vitrectomy goals 1 Area around the optic nerve about 2x papillo-
 Clear the ocular media foveal radius
 Restore the function and anatomy of the posterior 2 From edge of zone 1 to the anterior nasal edge
pole of the retina
 Stabilize the proliferative neovascular process 3 Remaining temporal crescent of retina from
the edge of zone 2

WHO RECOMMENDATIONS (Please remember!) Stages (ICROP CLASSIFICATION)

BASELINE EYE EXAMINATION DONE IF: STAGE 1
Diabetic <30 yo Diabetes present for 5 yrs  Characterized by a demarcation line separating
Age = 10 years normal vascularized retina from undeveloped retina
Diabetic >30 yo At the time of diagnosis:  Line is typically white
Suggest annual follow-up evaluation  Marked contrast between regions
unless more frequent exams are
indicated due to the presence of
abnormalities
Pregnant As early as preganancy is detected

F. RETINOPATHY OF PREMATURITY (ROP)

Pathophysiology
- Proliferative retinopathy afflicting premature infants
- Sufficient Cause: IMMATURE RETINAL STAGE 2
VASCULATURE (Red flags: Prematurity & Low birth  Rolled pink ridge in place of the demarcation line
weight) that has increased in width & height
- Potentiated by excessive oxygen administration  Limited to a small sector or may encircle the entire
- Influenced by maternal and neonatal factors posterior pole
*babies born full term does not have fully matured
vascularizations of the retina

10
OPHTHALMOLOGY – THE FUNCTIONAL POSTERIOR SEGMENT: VITREOUS & RETINA
FEU-NRMF Institute of Medicine
3B-Medicine 2017
Lecturer: Dr. Marin, July 2015

 Essentially no useful vision

 Tx: SURGICAL

ROP Treatment
Objective: ABLATE ISCHEMIC RETINA
 Modalities:
 Cryotherapy
STAGE 3  Laser Photocoagulation
 Fibrovascular proliferation on the edge of the ridge  Indirect Ophthalmoscope
 Mild, moderate or severe vitreous infiltration  Surgical/Endolaser
 50% chance of progression to Stage 4 and 5 &  Endoptik
blindness  Laser Diopexy
 LASER RETINOPEXY
(sa slide may advantages na natakpan, but I can’t find it sa book )

Surgery in advanced cases of retinopathy of prematuriy

 Cryotherapy/Laser Indirect
 Opthalmoscopy
 Scleral Buckling
 Degree based on vitreous infiltration  Phakic or Lens-sparing Vitrectomy
 THRESHOLD  Lensectomy with Vitrectomy and Membrane
 Zone 1 or 2 in 5 or more continuous clock hours Dissection, Segmentation & Lysis
 Zone 1 or 2 with 8 cumulative hours of
involvement with the presence of “plus 2. MACULAR DISEASES
disease” -Affects the visually sensitive portion of the retina
 INTERVENTION WITHIN 72 HOURS OF -Very symptomatic so patients consult early
DIAGNOSIS -Carries a relatively guarded or grave prognosis
 PRE-THRESHOLD -Central Serous retinopathy (CSR) & Age Related
 Zone I any stage Macular Degeneration (ARMD)
 Zone II stage 2+ or stage 3 CSR ARMD
 LIO WITHIN 48 HOURS OF DIAGNOSIS Age of Onset Middle aged Elderly (40+)
 PLUS DISEASE (20-40)
 With abnormal iris vessels/tortuosity & Pathogenesis Focal RPE leak RPE/Bruchs
engorgement of retinal vessels breakdown
 Rush Disease Feature Sensorineural Accumulation of
o Plus disease involving zone 1 detachment drusen (metabolic
o Very rapid progression garbage)
Course Spontaneous Progressive
STAGE 4 remission involvement
 Retina detaches from the ridge because of exudative Complication Prone to SRNV
effusion, traction or both recurrence scotoma
 4A: retinal detachment is extrafoveal
Chronic edema
 4B: retinal detachment involving the fovea
degeneration
(POOR VISUAL PROGNOSIS)
CENTRAL SEROUS RETINOPATHY
STAGE 5 “retrolental fibroplasia”
Symptoms
 Completer retinal detachment  Blurring of central vision;
with a closed or partially closed  Central gray area of visual diminution
funnel, from the optic nerve to  Micropsia, metamorphopsia;
the retro-lenticular space  Rubout of certain portions of readable text;
11
OPHTHALMOLOGY – THE FUNCTIONAL POSTERIOR SEGMENT: VITREOUS & RETINA
FEU-NRMF Institute of Medicine
3B-Medicine 2017
Lecturer: Dr. Marin, July 2015

 Afterimage persistence; - Lowering of vision only happens in the later stages

that has atrophy or if it transposes to the wet type
Signs
- It takes about 20-30 years for macular degeneration
 Blisterlike sensorineural detachment of the macula;
to decrease the vision functionally
 VA = 6/6 to 6/30, improved with +1.00 Diopter lens
 Positive relative central/paracentral scotoma You can see that
 Red desaturation; in the dry type,
 Delayed photostress test; the drusen is
Angiographic findings illustrated but it
is not really
 Early hyperfluoresccent
harming the eye.
lesion with late pooling The wet type on
pattern corresponding the on the other
to the area of hand, there is
sensorineural formation of new
detachment; blood vessels
 Inkblot or smokestack (10%) which can cause
initial lesion; blindness.
 May be accompanied by areas of altered RPE
pigmentation with or without similar leakage of Clinical Symptomatology
dye;
Central visual field change:
Management: Spontaneous remission but should last  Distortion
only up to 8months but may be recurrent so treatment  Scotoma
using laser for leaks only  Micropsia/metamorphopsia
 Sectoral field loss
AGE/DRUSEN RELATED MACULAR DEGENERATION  Visual acuity loss
(A/DRMD) *it starts as a central field distortion then when new blood
- A leading cause of irreversible central vision loss vessels arise, it progresses to scotoma; but it does not cause
- Prevalence increases with age total blindness.
- 2 types: wet (disciform) & dry (areolar) Subretinal vascularisation
(Newell) - Can cause central visual field blindness but not total
 Disciform (disc-shaped): absence of whole vision (but remember that 80% of
 preceeded by subretinal new blood vessels that cause the functional vision is through the central field)
a serous or hemorrhagic separation of the RPE - There is a triad of neovascularisation, grayish-green
 This is followed by fibrous metaplasia of RPE that membrane & exudates & haemorrhages
displaces the sensory retina in the foveal and
surrounding macular region w/c can cause blindness A/DRMD Focal Points
 Areolar: may be regarded as gradual atrophy of
choriocapillaries
 The etiology is unkown. The effects of diet, UV
exposure and micronutrients are at most uncertain
Clinical Characteristics  It should be emphasized that although central visual
Central Visual loss associated with: loss is common, peripheral visual loss is rare.
 Drusen formation (yellow flakes at the back of the eye)  They should be reassured that using their eyes will
 RPE changes not aggravate their condition.
 Geographic atrophy  All patients should be educated about the prognosis
 Serous/hemorrhagic RPE detachments of the disease and the potential value of treatment.
 Choroidal neovascularization
 Subretinal fibrosis/disciform scar Screening/Monitoring Procedures
 Age group 40+ (but can happen also to younger people  Comprehensive Adult Eye Examination
that’s why its renamed DRMD) (it is very important to detect this disease when present
Natural History (covered text) because if not, like a flower, it blooms, wherever the new
- Most cases are the dry type, they are non-exudative blood vessels goes, it blinds. Also, because these blood
12
OPHTHALMOLOGY – THE FUNCTIONAL POSTERIOR SEGMENT: VITREOUS & RETINA
FEU-NRMF Institute of Medicine
3B-Medicine 2017
Lecturer: Dr. Marin, July 2015

vessels are leaky, they cause fluid that causes edema w/c Anti-VEGF Therapy: Entails the intravitreal injection of
extends the functional disability of the patient) agents known to block the vasoproliferative effect of
 Stereoscopic biomicroscopic posterior fundus VEGF
examination and recording 1. Corticosteroids ie. Triamcinolone, Dexamethasone
 Fundus photography (Failed because 50% ended up w/ cataracts & 50% ended
 Fluorescein angiography up w/ glaucoma)
 Indocyanine green angiography 2. Pegaptanib (Maccugen)
 Home monitoring with Amsler grid and similar 3. Bevacizumab (Avastin) – off label; for colorectal CA
devices 4. Ranibizumab (Lucentis) – gold standard
Management: Future tech
Low-risk Non-Exudative A/DRMD 1. Eyelea (Regeneron): VEGF trap;
 Few small “hard” drusen & some minor atrophic RPE 2. Fovista (Opthotech): combined anti-VEGF and anti-
changes PDGF;
 No special examination, tests, or therapy advocated 3. IRay (Oraya therapeutics Inc.): in-office stereotactic
 Annual check-up may suffice radiotherapy system that delivers voltage x-rays
through the sclera to a single treatment spot on the
High-risk Non-Exudative A/DRMD
macula for the treatment of wet AMD;
 Bilateral softdrusen,large or cconfluent drusen, and
pigment changes/clumping without evidence of
exudation;
3. PIGMENT ALTERATION/DISTURBANCES
- can be as simple as chronic hypertrophic RPE
 1% risk of developing SRNV in 5 years;
 Contralateral exudative changes 10-50% depending where you see this black pigmented lesion which is
on the presence or absence or large drusen or of no consequence
pigment clumps; - can also be combination of traction and
 Amsler grid home monitoring with yearly follow-up pigmentation in the periphery
(1-2x) - can also be a choroidal tumor which can be
 810 nm diode laser macular grid/ (Olk) (Prophylactic diagnosed by ultrasound
treatment of ARMD)
- another one is retinitis pigmentosa
Treatment
*there is no treatment for the wet or exudative type, you can RETINITIS PIGMENTOSA
only damage control; wherever there is neovascularisation,  Group of progressive disorders of the rods & cones
that area is rendered blind already secondary to mutations of different genes
1. Laser Photocoagulation;  Initially, the retinal rods are affected but eventually all
2. Subretinal Membrane Surgery visual cells are impaired (newell)
3. Anti-VEGF therapy;  Nyctalopia during adolescence is the inital sign
 ROP  a ring scotoma develops & then extends peripherally
 Diabetic and Uveitic Macular Edema; & centrally until only a small contricted visual field
 Neovascular glaucoma remains (tubular vision) (Newell)
4. Combination Laser and Anti- VEGF;  Triad in ophthalmoscopic examination:
5. Genetic Manipulation  pale optic disc
6. Up/Downstream regulation  attenuation of
7. Anti-alu RNA vessels
 peripheral
Focal Laser Photocoagulation for SRNV: Macular
paravascular bony
Photocoagulation Study (MPS)
spicule
- Benefit of timely FLT for well-defined extrfoveal
pigmentation
NVM in preventing SVL & stabilizing Va
 characteristically
- 95% of cases do not follow the MPS indication of
extinguished flat ERG
treatment
 retina is dying

13
OPHTHALMOLOGY – THE FUNCTIONAL POSTERIOR SEGMENT: VITREOUS & RETINA
FEU-NRMF Institute of Medicine
3B-Medicine 2017
Lecturer: Dr. Marin, July 2015

 Treatment: Supportive ; Try to analyze the family tree so - Saccadic eye movements/gravity
that you can aadvise patients of occupations to take since a  Mechanism of chorioretinal adhesion weakening by
full blown RP can blind a person at age 20-30 the fluid vitreous
- Glycosaminoglycan dilution
- Overwhelming the RPE pump
4. RETINAL DETACHMENT
VITREORETINAL INTERFACE DISEASES
VR traction at points of adhesion
 HA- Collagen matrix disintegration results in:
 Loss of barrier and inhibitory functions;
 Traction from stereotactic eye movements and
progressive hyaloid stripping; Transmission of energy to retina
 Specific diseases produced:
 Retinal break formation and retinal detachment
 Traction retinal detachment; beak/hole formation relieves traction but allows liquid
 Epiretinal membrane; vitreous access to SR space
 Proliferative retinopathies;
 Cystoid macular edema;
neurosensory retina separates from RPE

retina becomes edematous & opaque

photorecptor degeneration & atrophy in time

Principles of treatment and repair

 Localization and closure of breaks
 Relief of vitreoretinal traction
Retinal Reattachment Surgeries
POSTERIOR VITREOUS DETACHMENT -main culprit of
 Pneumatic
retinal detachment (discussed above)
retinopexy;
RHEGMATOUS RETINAL DETACHMENT  Scleral buckling;
 Closed
Pathogenesis: vitrectomy;
Two Components for retinal break formation
1. Acute posterior vitreous detachment (PVD)
2. Predisposing peripheral retinal degeneration LEUKOCORIA
 Retinoblastoma
 Coat’s disease
 Congenital/Developmental Cataracts
 Retinopathy of Prematurity
 Persistent Hyperplastic Primary Vitreous
 Others: Retinal detachment, Ocular inflammation,
Mesodermal Dysgenesis, Vitreous Hemorrhage,
Congenital Glaucoma, Neonatal infection
 Factors
- Vitreous traction
- Availability of liquid vitreous
14
OPHTHALMOLOGY – THE FUNCTIONAL POSTERIOR SEGMENT: VITREOUS & RETINA
FEU-NRMF Institute of Medicine
3B-Medicine 2017
Lecturer: Dr. Marin, July 2015

Causes of Leukocoria in a Pediatric Population Clinical Presentaion

Entity Usual Age of Incidence - Bilateral cases in 15 months, ave of 8 months
Detection - Unilateral in 25 months
Retinoblastoma Several months 1/3 - Rarely seen after age of 7
of age - Signs & symptoms:
Cataract At birth Varies  Leucokocoria
Retinopathy of Several months Very High  Photophobia (baby tries to press on the eye to aid
Prematuriy (ROP) of age with the perception of light)
Persistent At birth 1/10  Inflammation
Hyperplastic Primary  Proptosis
Vitreous (PHPV)  Glaucoma
- On examination
inside the eye: a
soapy white mass
in the posterior
segment

Genetics
- Recessive, but acts as dominant with 90%
penetrance
- 60% hereditary; 40% nonhereditary
- Deletion of a suppressor gene on chromosome 13
in close association with esterase D enzyme which
encodes a phosphoprotein (pRB) cell cycle
regulator

Treatment
- Laser to ablate tumor in early stages

COAT’S DISEASE SUMMARY OF THE VITREOUS AND RETINA

 Formation of retinal telangiectasia & breakdown of  Anatomy and physiology;
the inner blood-retinal barrier are the fundamental  Examination techniques and instrumentation
causes;  Salient features of common conditions afflicting the
 Progressive exudative changes noted with subsequent organelles
retinal detachment  Current modalities of treatment;
 Can form a tumor like lesion that can be mistaken for
retinoblastoma

5. RETINOBLASTOMA
 Most common intraocular malignancy of childhood
 LIFE THREATENING
 1 in 20,000 live births
 Prognosis is directly related to the size and degree
of extension
 Intraocular = possible cure
 With orbital extension = poor prognosis
(comes through periocular tissue or from the optic nerve &
goes to the brain causing CNS problems)
 IMMEDIATE OPTHALMOLOGIC REFERRAL

15
 [OPHTHAMOLOGY] OPTIC PHARMACOLOGY

OPTIC PHARMACOLOGY  ABSORPTION

Jesilyn Penny E. Lim, MD Depends on the following:
 Molecular properties
CONTENTS  Viscosity of the vehicle
 Pharmacodynamics  Functional status of the tissue forming the barrier to
 Pharmacokinetics penetration
 Ophthalmic Drug Delivery  DISTRIBUTION
 Ocular Pharmacotherapeutics
 The drug distribution affects the drug absorption
 Local Anesthetics
overtime. So the bioavailability of the drug is also
 Analgesics
affected by the compartments and barriers of the
 Mydriatics
eye.
 Cycloplegic
 Ocular Hypotensive Drugs  METABOLISM
 Anti-Infective Drugs  Plays an important part in eliminating drugs
 Anti-Inflammatory Drugs
 Anti-Allergy and Decongestants  The metabolic enzymes convert prodrug to active
 Drugs for Dry Eye and Ocular Surface Disease form or transform an active drug to its inactive form
to lessen its side effects.
OBJECTIVES
 Discuss the ways in which a drug acts on the body  ELIMINATION/EXCRETION
 Discuss the diagnostic and therapeutic uses of ophthalmic
 As the word implies, refers to the elimination of the
drugs
substance from the body or the accumulation of the
 Discuss the effects of systemically administered drugs to
drug in body parts.
ocular function
 The rate of drug clearance can be computed.
PHARMACODYNAMICS
 It is the biological and therapeutic effect of the drug OCULAR STRUCTURES AND PHARMACOKINETICS
(mechanism of action) TEAR FILM
 Pharmacodynamics or the mechanism of action refers
to your biological and therapeutic effect of the drug

 Most drugs act by binding to regulatory macromolecules,

usually neurotransmitters or hormone receptors or enzymes
 If the drug is working at the receptor level, it can be agonist
or antagonist

 A drug is an agonist or antagonist if it binds at the

receptor level
 Example: Neurotransmitters

 If the drug is working at the enzyme level, it can be activator

or inhibitor

 It is an activator or inhibitor if it binds at the enzyme  Composed of 3 Layers:

level  Lipid Layer/Oily Layer
 Example: Hormone Receptors
 Outermost layer of the tear film
 Produced by the meibomian glands of your eyelid
PHARMACOKINETIC  It is 0.1um thick
 Important function is to stabilize the aqueous layer
 The effect of the drugs on the eye is dependent on and prevent it from evaporation
specific pharmacokinetic properties namely absorption,
distribution, metabolism, and excretion/elimination of
the drug

LEA THERESE R. PACIS 1

 [OPHTHAMOLOGY] OPTIC PHARMACOLOGY

 Aqueous Layer IRIS, CILIARY BODY AND AQUEOUS HUMOR

 Iris
 Secreted by the lacrimal gland
 7um thick  The iris has sphincter and dilator muscles for pupillary
 Layer is unstable  Needs the lipid layer so it won’t constriction and dilatation respectively
evaporate  Functions to regulate the amount of light entering your
retina and contains pigments to absorb light.
 Mucinous Layer  Also, the pigment granules of the iris absorbs
lipophilic drugs and again acts as a reservoir for
 Innermost layer of the tear film
some drugs concentrating and re-releasing drugs for
 Secreted by your goblet cells
longer periods.
 A thin hydrophobic layer consist of glycoproteins
 Drug response vary depending on the amount of iris
pigmentation
 Normal Volume of Tear Film = 8-10um

 Normal volume of your conjunctival culde sac is 30um.  Ciliary Body and Aqueous Humor
 A single drop of medication is about 50um 
 Ciliary body produces your aqueous humor is the main
Exceeds the volume of the conjunctival cul de sac
source of metabolizing enzymes for drug
- The excess is either drained by your lacrimal
detoxification and removal.
drainage system or is blinked out of the eye
- Increasing the drop size, therefore, does not
increase drug absorption but rather increase
LENS AND VITREOUS
systemic absorption
 Lens
Do not advise your patient to put 3 drops  1
drop is enough  As you recall the lens anatomy, you have your anterior
and posterior capsule. The epithelial layer of anterior
capsule is the most metabolically active and thus it is
CORNEA, SCLERA, CONJUNCTIVA the most susceptible to damage by toxic subs.
 Cornea
 Barrier for rapid penetration of drugs from aqueous and
 The absorption of topical meds is primarily thru your vitreous humor
cornea
 Lipophilic drugs can penetrate lens slowly but large
 Acts as a major functional barrier for ocular penetration proteins and hydrophilic drugs cannot be absorbed
 Specially for certain subs like in cases of hydrophilic by the lens from the aqueous humor.
drugs  If you remove the lens surgically the drug kinetics of
 Since your cornea is avascular, it permits direct aqueous humor and vitreous changes.
absorption of drugs without systemic absorption,
however the epithelial surface of your cornea is
 Vitreous
lipophilic, resisting the penetration of hydrophilic
 If there is epithelial break, hydrophilic drugs can
drugs such as your Sodium Fluorescein and
easily penetrate the corneal stroma.  Vitreous contains diffused small particles and HMW
diagnostic agent. substances such as gags (hyaluronic acid) and collagen
 For effective corneal penetration, drugs must have  Major reservoir of drugs and temporary storage depot of
hydrophilic and lipophilic properties metabolites

 Conjunctiva and Sclera  Substances with LMW can diffuse freely from the
ciliary body into the vitreous, however, systemic
 Sclera and conjunctiva is continuous with the cornea at administration of hydrophobic drugs such as
the limbus and they are highly vascular. gentamycin does not readily cross the blood retinal
 Major depot for drugs barrier.
 For drug to reach the vitreous, it must be injected
 Allow the active drug to dissolve slowly and be intra-vitreously or surgically implanted.
gradually released into the tears.  The major route of exit of drugs in the vitreous is
thru your aqueous outflow pathway.

LEA THERESE R. PACIS 2

 [OPHTHAMOLOGY] OPTIC PHARMACOLOGY

RETINA AND OPTIC NERVE  The normal tear pH is 7.4 and if the drug pH is much
 Blood-Retinal Barrier different, this will cause reflex tearing.
 Inner BRB is formed by the retinal capillary endothelial
cells  DRUG TONICITY
 Outer BRB is formed by the zonula occludens of the
Retinal Pigment Epithelium  The osmolality of tears is 290mosm this equivalent to
0.9% saline and this is the tonicity of most ocular and
FACTORS AFFECTING DRUG PENETRATION INTO OCULAR IV meds.
TISSUES  Increase tonicity relative to the tears causes osmotic
 DRUG CONCENTRATION AND SOLUBILITY movement of water from the lids and eye causing
immediate dilution of drug concentration.
 The rate of diffusion of a drug across the barrier is
linearly dependent on the concentration difference
between the compartments on either side of the  MOLECULAR WEIGHT AND SIZE
barrier.
 HMW polymers and additives:
 The higher the concentration the better the penetration  Increase the viscosity of the drug
 Increase contact time to the cornea
 Decrease tear film washout
 VISCOSITY
 Increase bioavailability of the drug.
 Molecular viscosity is a function if MW and
concentration of the drug.
OPHTHALMIC DRUG DELIVERY
 Addition of ophthalmic vehicles, such as methylcellulose 1. Solutions and Suspensions
and polyvinyl alcohol, increases drug penetration by 2. Ointments
TOPICAL
increasing the contact time with the cornea and altering 3. Lid Scrubs
corneal epithelium 4. Gels
1. Soft Contact Lens
 These vehicles are water soluble and has hydrophilic 2. Collagen Shields
and lipophilic sites therefore better drug SOLID DELIVERY DEVICES
3. Filter Paper Strips
concentration. 4. Cotton Pledgets
 More viscous drug  Longer contact time  Better 1. Subconjunctival
absorption and alters corneal epithelium 2. Subtenon
PERIOCULAR
3. Retrobulbar
4. Peribulbar
 LIPID SOLUBILITY
1. Intracameral
 Because of the lipid rich environment of the epithelial cell INTRAOCULAR
2. Intravitreal
membranes, the higher lipid solubility the more the
1. Oral
penetration
SYSTEMIC 2. Intravenous
3. Intramuscular
 SURFACTANTS
 The preservatives used in ocular preparations alter cell
membrane in the cornea and increase drug permeability TOPICAL
 Examples: Benzylkonium and Thiomersal  Most ophthalmic drugs are applied topically because it
is simple, convenient, non-invasive, self-administered by
 pH the patient.
 Some of the drugs formulated in acid solution are more
SOLUTION AND  In the form of eyedrops
stable than in alkaline pH because of the increase
SUSPENSION  Most commonly used form of topical
protonation and decrease degradation.
medication
 A change in the normal pH can cause ocular irritation
 Advantages:
and increase lacrimation.
 Easier to instill
 This results in increase tear flow, decrease
 Can cause less blurring of vision 
availability of the drug and decrease drug
Less viscous
penetration.
 Disadvantages:
 Less viscous  Has lesser contact time

LEA THERESE R. PACIS 3

 [OPHTHAMOLOGY] OPTIC PHARMACOLOGY

 Increased risk of contamination may

cause ocular injury from careless
instillation
 Advantage: Prolonged ocular contact
time  Allowing less frequent dosing
of the medication
OINTMENTS
 Disadvantages:
 Patients on this kind of treatment
often complain of blurred vision or
oily skin after application
 Prolonged contact time  Some
may develop hypersensitivity
reaction to the preservatives
 Application of a solution ointment or
detergent such as baby shampoo is
SOLID DELIVERY DEVICES
helpful in treatment of
LID SCRUBING seborrheic/infective blepharitis.  These devices allow for a more regulated release of drug
 This aids in the removal of oils, debris, instead of the pulsed administration of solutions,
and desquamated skin in the inflamed characterized by an initial period of over dosage
lid. followed by relative under dosage.
 This is done using a strip of
ointment/several drops of solution or SOFT CONTACT
detergent on a cotton tip applicator LENS
and applying it on the lid margin.  Absorb more water soluble drugs for
GELS  Gelling agents transform from gel to later release into the tear film
liquid upon contact with your eye
rendering the drug hydrophilic and
COLLAGEN  Similar to your contact lens, they are
minimizing complaints of blurring of
SHIELD package in a dehydrated state and
vision.
rehydrated with a drug solution before
application.
STANDARD COLOR CODING FOR DRUG LABELLING
 Drug is released as the shield dissolves.
 Drug impregnated filter paper strips
allow for easy administration of drugs
in amounts adequate for their
intended purpose.
 The use of this impregnated strips
prevents administration of excessive
amounts of drug and eliminates the
risk of solution contamination like
RED CAP  Mydriatic FILTER PAPER Pseudomonas aeruginosa.
GREEN  Myotic Agents
Agents STRIPS  3 commercially available staining
agents commercially available in filter
paper strips.

TEAL CAP  Prostaglandin

PINK CAP  Steroids Analogues, Anti-Glaucoma
Medications  Lissamine Green and Fluorescein
Orange  Used for diagnosing dry

LEA THERESE R. PACIS 4

 [OPHTHAMOLOGY] OPTIC PHARMACOLOGY

eye disorders, epithelial defects in  This technique is a blind

the cornea procedure where the needle is
 Rose Bengal  Stain devitalized placed near the globe while
tissue in the cornea aiming for the muscle cone which
 Concentration delivered to the ocular contains vital structure such as the
surface depends on the strip soak time optic nerve
and technique.  Potential risk include inadvertent
 A pledget is a small elongated tuft of globe penetration, retrobulbar
cotton by teasing the cotton tip of an hemorrhage, direct injury to the
COTTON applicator. optic nerve
PLEDGETS  The pledgets is saturated with 1-2  Also a blind procedure
drops of solution, usually mydriatics  Involves one or more injections
like tropicamide or phenylephrine, and PERIBULBAR around the globe without directly
placed in the inferior conjunctival cul aiming for the muscle cone
de sac  This is rather a safer technique, it
 Usually used among children provides similar anesthesia and
akinesia but with a lesser rapid
PERIOCULAR ADMINISTRATION onset as compared with the
retrobulbar anesthesia
 Compared to topical administration, local injections into
periocular tissues bypass the conjunctiva and corneal INTRAOCULAR ADMINISTRATION
epithelium and deliver high concentration of drugs with INTRACAMERAL
low lipid solubility. There are 4 main routes of periocular  Involves directly placing a drug in
tissue. the anterior chamber
 Between the iris and cornea
 Injection between conjunctiva
 Done during cataract surgery
and tenon
 Allow for higher local drug
SUBCONJUNCTIVAL  From the word itself involves
concentration with use of smaller INTRAVITREAL
drug quantities directly placing the drug at the
 Eliminates systemic effects of the vitreous chamber
drug  Examples of drugs admistered via
 Avoid the need for local or this route: Anti-VEGF, steroids,
systemic drug administration antibiotic
 Minimizes problem in patient
compliance OCULAR PHARMACOTHERAPEUTICS
LOCAL ANESTHETICS
 Injection between tenons and
sclera  Act on cell membrane to produce reversible conduction
SUBTENONS  Offers little advantage and deliver blockage of nerve impulses resulting in sensory
lower quantities of the drug into anesthesia and skeletal muscle paralysis.
the eye  The duration of the anesthetic effects is proportional to
 Increases the risk of globe the length of time the drug is bound to nerve proteins
perforation which depends on the chemical structure of the drug,
 Used when dealing with sever drug concentration, amount of administered drug and
uveitis, cystoid macular edema the rate of drug removal by diffusion and circulation.
and diabetic macular edema.  In ophthalmology we have injectable and topical
RETROBULBAR  Drugs are injected in the anesthetics.
intraconal space include
anesthetics, steroids, phenols and  Injectable Anesthetics
alcohol
 Can be injected directly into the anterior chamber
 Provides rapid onset of anesthesia
during anterior segment surgery such as cataract
and akinesia for anterior segment
surgery to supplement topical anesthesia.
and vitreoretinal surgery

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 [OPHTHAMOLOGY] OPTIC PHARMACOLOGY

 If you add vasoconsrictors like epinephrine, this  Hydroxyamphetamine

decreases the rate of absorption into systemic  Cocaine
circulation, resulting to longer duration of action, less
local bleeding, lower risk of systemic anesthetic
toxicity
PHENYLEPHRINE HYDROCHLORIDE
 Lidocaine + Bupivacaine  Used for Retrobulbar
 Selective α-receptor agonist
Injection
 Maximum Dilatation: 45-60mins
 Lidocaine – most frequently used  Duration: 6-7 hours
 Bupivacaine
 Procaine
 Etidocaine
 Mepivacaine CYCLOPLEGICS
 Anti-cholinergic agents, anti-muscarinic, and cholinergic
 Topical Anesthetics blocking agents
 Inhibit the action of acetylcholine on muscarinic sites
 Suppresses corneal sensitivity  Cholinergic innervation in the eye:
 Can cause eye irritation and localized to diffuse  Ciliary body
corneal desquamation when used frequently  Iris sphincter muscle
 Onset of action is 10-20 seconds  Lacrimal gland
 Duration of action 10-20 minutes  Can increase IOP in patients with open angle glaucoma and
can precipitate an acute angle closure glaucoma in patients
 Proparacaine with narrow occludable angles
 Tetracaine
 Benoxinate  In the OPD, we usually do gonioscopy first before
 Cocaine administration of these kinds of medications.
 Open Angle Glaucoma  Triclosamide
MYDRIATICS  Close/Narrow Angle Glaucome  Don’t use
cycloplegics – as you can an induce acute attack
 Adrenergic receptors of the ANS are targeted by
catecholamines and adrenaline particularly epinephrine
and norepinephrine respectively.  ATROPINE
 Adrenergic agonists or your sympathomimetic drugs  Non-selective muscarinic antagonist
cause sympathetic response or your fight or flight  Most potent mydriatic and cycloplegic agent
response like increase in HR and pupillary dilatation. - Onset: 12mins; Duration: Up to 10 days (Mydriactic)
 It contracts the iris dilator muscle and smooth muscle of - Onset: 12mins; Duration: Up to 7-12 days (Cycloplegic)
the conjunctival arterioles causing pupillary dilatation  Uses
and blanching of the conjunctiva from vasoconstriction. - Refraction in actively accommodating children with
 Other effects include widening of palpebral fissure from latent hyperopia
sympathetic stimulation of Muller’s muscle and decrease - Inflammatory conditions such as uveitis
IOP for decrease aqueous production by the ciliary body  Adverse Reaction
 Because of its many local and systemic side effects, its - Dose dependent
long term clinical use is unsatisfactory. - Fever
- Hallucinations
 Targets the adrenergic receptors of the autonomic nervous - Decrease salivation
system - Convulsions
 Affects various ocular function like pupil size, palpebral - Death
fissure, blood vessel diameter, aqueous flow and
accommodation  CYCLOPENTOLATE HYDROCHLORIDE
 Adrenergic terminals can be found in the following:  Cycloplegic agent of choice for cycloplegic refraction in
 Ciliary smooth muscle all age group due to its relatively fast onset and short
 Iris dilator muscle duration
 Muller’s muscle - Onset: 20-30mins
 Mydriatic Agents - Duration: 24hours
 Phenylephrine - Recovery of accommodation: 6-12 hours

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 [OPHTHAMOLOGY] OPTIC PHARMACOLOGY

 TROPICAMIDE  Exhibits tachyphylaxis

 Non-selective muscarinic antagonist
 Fast onset (20-40mins)  Decreased response of the drug
 Short duration of action (6 hours)
 Mydriatic > Cycloplegic Effect
 ADRENERGIC AGONISTS
 Adverse systemic effects are rare
 Brimonidine, Apraclonidine
 Decrease aqueous production and increases uveoscleral
OCULAR HYPOTENSIVE DRUGS
outflow
 Glaucoma can be managed pharmacologically and
 Only ocular hypotensive drug that exhibits a dual
surgically by lowering the existing IOP.
action  REMEMBER! Lalabas daw sa exam ;)
 These ocular hypotensive agents each have a unique
mechanism of action so drugs can be used alone or in  20-25% decrease in IOP
combination.  Side Effects:
- Local: Dry mouth, blepharitis, conjunctival hyperemia,
 PROSTAGLANDIN ANALOGUES (“-prost”) foreign body sensation
 Latanoprost, Bimatoprost, Travaprost, Tafluprost - Systemic: Drowsiness, dizziness, apnea in children, and
 Increases aqueous outflow CI in patients taking MAO inhibitors
 25-30% decrease in IOP
 First line drug for open angle glaucoma and ocular  Do not give in children  Prostaglandin Analogues
hypertension are better for children

 Can be also used for juvenile glaucoma

 CARBONIC ANHYDRASE INHIBITORS
 Very convenient to use, good safety profile  Acetazolamide, Brinzolamide, Dorzolamide

 Once a day dosing  Acetazolamide  In the form of tablets

 Brinzolamide and Dorzolamide  In the form of
 Side Effects: Hypertrichosis, increase pigmentation of eyedrops
eyelid skin and iris color, allergy, cystoid macular edema,
corneal erosion.  Reduces aqueous production
 Topical: 15-20% IOP reduction
 Hypertrichosis  Usually women use this to grow  Oral/Systemic: 40-50% IOP reduction
eyelashes  Side Effects:
- Local: Stinging sensation, toxic keratitis, corneal
 No drug tolerance with prolonged use
endothelial dysfunction
- Systemic: Tingling sensation, nausea, vomiting,
 B-ADRENERGIC ANTAGONIST (BETA BLOCKERS – “olol”) diarrhea, metabolic acidosis, blood dyscrasias
 Timolol, Betaxolol, Levobunolol, Metipranol, Carteolol
 Always monitor potassium levels
 Selective: Betaxolol
 Non-selective: Timolol
 CHOLINERGIC AGONISTS
 Decrease aqueous production  Pilocarpine 1-4%
 It increases outflow facility by stimulates the contraction
 Targets the ciliary body of the longitudinal ciliary muscle  Miotic Agent
 20-25% reduction in IOP
 15-20% decrease in IOP  Side Effects:
 Systemic Side Effects: - Local: Brow ache, blurring of vision, increased risk of
 History taking before taking this drug is very pupillary block due to forward shift of the lens, cataract,
important as it can cause systemic side effects. uveitis, retinal detachment
- Systemic: Salivation, nausea, vomiting, bronchospasm,
- Bradycardia intestinal cramps, frequent urination.
- Systemic hypotension
- Heart block and failure
- Bronchospasm
- Diarrhea
- Amnesia
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 [OPHTHAMOLOGY] OPTIC PHARMACOLOGY

SUMMARY OF OCULAR HYPOTENSIVE DRUGS - Fluorinated quinolones like moxifloxacin, ciprofloxacin

% Decrease
Example of
MOA in IOP from  Very important when you want to have an effective
Drugs
Baseline antimicrobial treatment  You have to obtain a
Latanoprost detailed history of the signs and symptoms of the
Bimatoprost Increases patient for you to arrive with a tentative diagnosis
PROSTAGLANDIN
Travaprost aqueous 25-30
ANALOGUES  Example: Gonoccocal Conjuntivits
Tafluprost outflow
- Young adult, male, call center agent, came in with
(“-prost”)
Timolol
these 3 days PTC
Betaxolol Decrease - Note the edema of the lids with profuse yellowish
B-ADRENERGIC eye discharge signifying a severe infection
Levobunolol aqueous
ANTAGONIST/ 15-20
Metipranol production
BETA BLOCKERS
Carteolol
(“-olol”)
DUAL
ACTION:
Decrease
Brimonidine aqueous
ADRENERGIC
Apraclonidine production 20-25
AGONISTS
(“-nidine”) and
increases
uveoscleral
outflow  Reasons for Failure of Treatment:
Topical: 15-  Wrong diagnosis
Acetazolamide 20  Drug resistance
CARBONIC Reduces
Brinzolamide  Inadequate dosage
ANHYDRASE aqueous
Dorzolamide Oral/
INHIBITORS production  Patient non-compliance
(“-zolamide”) Systemic:
40-50
 Inadequate immune response
Increases
CHOLINERGIC
Pilocarpine outflow 20-25
AGONISTS
facility  ANTIVIRAL
 Interfere with viral replication and multiplication
ANTI-INFECTIVE DRUGS - Inhibition of thymidine kinase
 ANTIBACTERIAL  Organisms:
- Herpes Simplex Virus
 Common bacteria causing ocular infection are  Most frequent cause of primary and recurrent eye
Staphylococcus aureus, Streptococcus pneumoniae for disease, stromal keratitis, conjunctivitis, keratitis
gram positive, while Neisseria gonorrhea, Escherichia  Treatment: Trifluridine, Acyclovir, Valacyclovir,
coli, Serratia proteus and Pseusomonas for gram Famcyclovir, Gancyclovir
negative. - Adenovirus (Serotypes 3,7,8,19 and 37)
 Anti-bacterial drugs acts against bacteria thru the  Conjuntivitis, Epidemic Keratoconjunctivitis
following mechanisms: - Cytomegalovirus
 Retinitis, seen in immunocompromised patients
 Inhibit cell wall synthesis of peptidoglycans which is
necessary for structural integrity of the bacteria  ANTI-FUNGALS
- Penicillin, Cephalosporin, Bacitracin, Vancomycin
 Selective disrupting bacterial cell membranes  Fungi can infect ay eye structure including the cornea,
- Polymixin B, Garamicidin conjunctiva, lens, ciliary body, vitreous, retina and the
 Selective binding of drugs to bacterial ribosomes, which entire uveal tract.
differ from that of humans in size, and composition
 Most common fungal pathogens:
- Aminoglycosides, tetracyclines, macrolides and
- Candida (yeast)
chloramphenicol
- Aspergilus, Fusarium and Curvalaria (molds)
 Inhibit folic acid synthesis
 Polyenes  Bind to ergosterol in the cell membrane;
- Sulfonamides, Pyrimethamine, Trimethoprim
fungistatic (low concentration); fungicidal (high
 Inhibition of enzymes DNA gyrase and topoisomerase IV
concentration)
which are specific for bacteria
- Ampothericin B, Natamycin

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 [OPHTHAMOLOGY] OPTIC PHARMACOLOGY

 Pyrimidines  Blocks thymidine kinase; fungistatic OCULAR PHARMACOTHERAPEUTICS

- Flucytosine  PREPARATIONS FOR DRY EYE AND OCULAR SURFACE
 Azoles  Inhibit fungal growth; fungistatic DISEASE
- Ketoconazole, Miconazole, Itraconazole. Voriconazole,
Fluconazol  Dry Eye Syndrome is described as deficiency in the
 Echinocandins  Inhibits glycan synthesis quantity or quality of tears or tear film due to
- Caspofungin, Micafungin, Anidulafungin inadequate aqueous tear prod or due to excessive tear
evaporation.
ANTI-INFLAMMATORY  It is generally not curable and management is
 CORTICOSTEROIDS therefore structured around the control of symptoms
and prevention of surface damage.
 Ocular hypertension and cataract are the most  Signs and Symptoms of DES:
common complication  Blurring of vision
 Ocular irritation
 Prednisolone, Flurometholone, Loteprednol
 Burning sensation
 Classification: (REMEMBER!!)
 Foreign body sensation
Hydrocortisone
 The choice of treatment depends on the severity of
Short Acting Cortisone
the disease and involves one or more of the following
Prednisolone
measures alone or in combination.
Trimcinolone,  Secretagogues – Lacrimomimetics – Stimulate lacrimal
Intermediate Acting
Fluprednisolone gland to enhance tear production
Dexamethasone  It includes cholinergic agents (Carbachol, Bethanecol
Long Acting
Betamethasone and pilocarpine) and mucolytics (Bromhexine,
 Indications: Ambroxol)
- Topical
 Allergic conjunctivitis  Treatment for OSD
 Scleritis - Relieving ocular symptoms
 Uveitis - Healing the ocular surface
 Allergic keratitis - Preventing serious complication
 After intraocular and extra ocular surgeries  Treatment of DES
- Systemic (Pathology behind the LENS) - Category:
 Posterior uveitis  Tear Supplementation  Artificial tears
 Optic neuritis  Tear Conservation  Ointments or punctal occlusion
 corneal graft rejection  Tear Stimulation  Secretagogues, Anti-
- NEVER GIVE STEROID IF YOU ARE SUSPECTING ACTIVE inflammatories or Immunomodulators
INFECTION
MANAGEMENT FOR DRY EYE SYNDROME:
 NSAIDS  Artificial Tears  Should reproduce the metabolic,
optical, and physical characteristics of tears
 Reduce inflammation but without the side effects of
 Ointments  For moderate to severe dry eye and
steroid
especially in cases with lagophthalmos (inability to
 Used to reduce pain and discomfort after cornea
close the eye), exposure keratitis with severe corneal
surgery
compliance
 Ketorolac, Diclofenac  Punctal Occlusion  Reduces drainage and thereby
 Topical Use preserves natural tears and prolongs the effect of
- Flurbiprofen artificial tears.
- Indomethacine  It is of greatest value in patients with moderate to
- Ketorolac severe KCS (keratoconjunctivis sicca) who have not
 Indications responded to frequent use of topical treatment.
- Episcleritis and scleritis  Anti-Inflammatory Agents  Suppress cytokine and
- Uveitis receptor mediated inflammatory process of the
- CME lacrimal gland that leads to decrease tear production
- PRE operatively to maintain dilation of the pupil

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 [OPHTHAMOLOGY] OPTIC PHARMACOLOGY

1. Low Dose Topical Steroids are effective OCULAR TOXICOLOGY

(Not discussed, but still, please study )
supplementary treatment for acute exacerbations. AMIODARONE
The risks of long-term treatment must be balanced  A cardiac arrhythmia drug
against the potential benefits of increased comfort
 Causes optic neuropathy (mild decreased vision, visual field
2. Topical Ciclosporin (0.05%, 0.1%) reduces T-cell
defects, bilateral optic disc swelling)
mediated inflammation of lacrimal tissue, resulting
 Also causes corneal vortex keratopathy (corneal verticillata)
in an increase in the number of goblet cells and
which is whorl-shaped pigmented deposits in the corneal
reversal of squamous metaplasia of the conjunctiva.
epithelium
3. Systemic Tetracyclines may control associated
blepharitis and reduce inflammatory mediators in
DIGITALIS
the tears.
 A cardiac failure drug
 Causes chromatopsia (objects appear yellow) with overdose
TEAR FILM ABNORMALITIES IN DRY EYE
CHLOROQUINES
 E.g. Chloroquine, Hydroxychloroquine
 Used in malaria, rheumatoid arthritis, SLE
 Cause vortex keratopathy (corneal verticillata) which is
usually asymptomatic but can present with glare and
photophobia
 Also cause retinopathy (bull’s eye maculopathy)
Thin marginal tear
meniscus and inferior CHLORPROMAZINE
Mucous debris  A psychiatric drug
punctate erosions
stained with fluorescein  Causes corneal punctate epithelial opacities, lens surface
opacities
SEVERE CORNEAL COMPLICATIONS OF DRY EYE  Rarely symptomatic
 Reversible with drug discontinuation

THIORIDAZINE
 A psychiatric drug
 Causes a pigmentary retinopathy after high dosage
Bacterial
Melting Perforation ETHAMBUTOL
Infection
 An anti-TB drug
OCULAR DIAGNOSTIC DRUGS  Causes a dose-related optic neuropathy
FLUORESCEIN DYE  Usually reversible but occasionally permanent visual
 Available as drops or strips damage might occur
 Uses:
 Stain corneal abrasions
 Applanation tonometry
 Detecting wound leak
 NLD obstruction
 Fluorescein angiography
 Caution:
 Stains soft contact lens
 Fluorescein drops can be contaminated by Pseudomonas
sp.

ROSE BENGAL STAIN

 Stains devitalized epithelium
 Uses:
 Severe dry eye
 Herpetic keratitis

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 Far Eastern University – Nicanor Reyes Medical Foundation DIABETIC RETINOPATHY
OPHTHA: SYSTEMIC DISEASES - Type 2 or NIDDM – similar but lower prevalence of
retinopathy
o Significant retinopathy at the time of diagnosis
OBJECTIVES - Risk factors
- To understand o Duration of the disease – MOST IMPORTANT
o The systemic diseases that may result to serious ocular o Poor control of diabetes – 2ND MOST IMPORTANT
sequelae o Pregnancy
o The basic principles in the management of the o Hypertension
above conditions o Nephropathy
- To recognize o Others: Smoking, Cataract Surgery, hyperlipidemia,
o The ocular symptoms of certain systemic diseases obesity
o When it is appropriate to refer the patient to an - Pathogenesis
ophthalmologist o Sorbitol accumulation and oxidative stress leading to
cellular damage
CATEGORIES OF SYSTEMIC DISEASES o Death of pericytes
- Metabolic o Neovsascularization
- Autoimmune - Classification
- Vascular o Non-proliferative Diabetic Retinopathy
- Neoplastic o Diabetic Maculopathy
- Infectious o Proliferative Diabetic Retinopathy
- Drugs/Toxins
- Idiopathic NON-PROLIFERATIVE DIABETIC RETINOPATHY
- Congenital - Diabetic retinopathy is a progressive microangiopathy
- Traumatic characterized by small-vessel damage and occlusion.
- Earliest pathologic changes are thickening of the capillary
EYE EXAMINATION endothelial basement membrane and reduction of the
- Visual Acuity number of pericytes.
- External Eye examination - The capillaries develop tiny dot-like outpouchings called
- Pupils microaneurysms.
o Relative Afferent Pupillary defect - Staging of Non-proliferative diabetic retinopathy (NPDR):
- Ocular Motility o Mild
- Anterior Segment Examination o Moderate
- Dilate Fundoscopy o Severe
- Visual Fields o Very Severe
STAGING
DIABETES MELLITUS
STAGE CLINICAL FINDINGS
SIGNIFICANT OCULAR COMPLICATIONS
- Refractive changes
Mild NPDR - At least 1 microaneurysm (MA) and 1 or
- Cataract
more of the ff: retinal hemorrhage,
- Retinopathy – most important
hard exudate, cotton wool spot (CWS)
o Duration of the diabetes is the most important risk
factor
Moderate NPDR - Hemorrhages and MAs in at least 1
o IDDM/type 1 DM – 23% with retinopathy after 5 years;
quadrant and 1 or more of the ff:
80% after 15 years; 50% with sever type of venous beading, CWS, IRMA
retinopathy after 20 years
o
CATARACT IN DIABETES Severe NPDR - One of the ff (4-2-1 Rule): Hemorrhages
- Snowflake Cataract** and MAs in 4 quadrants Venous
- Glucose – aldose reductase - sorbitol beading in at least 2 quadrants IRMAs
in at least 1 quadrant

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SYSTEMIC DISEASES AD ASTRA PER ASPERA
 PROLIFERATIVE DIABETIC RETINOPATHY
Very Severe NPDR - 2 or more of the severe NPDR criteria - Leading cause of blindness in diabetic patients
- Neovascularization - as a response to continued retinal
Mild Non-proliferative Diabetic Retinopathy ischemia

Moderate Non-Proliferative Diabetic Retinopathy

Severe Non-Proliferative Diabetic Retinopathy

MANAGEMENT
- Strict blood glucose and blood pressure control
- Laser Photocoagulation
- Intravitreal Anti-VEGF Injection
- Pars Plana Vitrectomy

DIABETIC MACULOPATHY/DIABETIC MACULAR EDEMA** TIMETABLE BASED ON RETINOPATHY FINDINGS**

- Most common cause of visual impairment in diabetic
RETINAL ABNORMALITY SUGGESTED FOLLOW-UP
patients, particularly
- type 2. Normal or rare microaneurysms Annually
- Manifest as focal or diffuse retinal thickening or edema
caused by the breakdown of inner blood retinal barrier Mild NPDR Every 9 months
- Fluid accumulates initially between outer plexiform and Moderate NPDR Every 6 months
inner nuclear layer and
Severe NPDR Every 4 months
- nerve fiber layer
o Further accumulation – fluid in the fovea assumes a CSME Every 2-4 months (careful follow-
cystoid appearance up)
- Angiography should NOT be used to evaluate the presence
of macular edema PDR Every 2-3 months (careful follow-
- Macular edema is primarily a slit-lamp biomicroscopic up)
diagnosis
- Treatment if already clinically significant THYROID OPHTHALMOPATHY
- Not always correlated with serum thyroid hormone levels
CLINICALLY SIGNIFICANT MACULAR EDEMA - Can progress after thyroid function is normal
- Any retinal thickening within - Inferior rectus: first muscle affected by thyroid disease**
500 microns of the fovea - Grave’s Disease
- Hard exudates within 500 o Hyperthyroidism due to autoimmune process
microns of the fovea o The major clinical risk factor for developing thyroid
associated with retinal eye disease (TED) is smoking
thickening
- Retinal thickening greater SPECTRUM OF THYROID EYE DISEASE
than one disc diameter in - Soft tissue involvement
size, of which any part lies - Lid Retraction
within one disc diameter of - Proptosis
the fovea.

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SYSTEMIC DISEASES AD ASTRA PER ASPERA
 - Ophthalmoplegia/Extraocular muscle dysfunction GRAVE’S DISEASE
- Optic Neuropathy - PATHOGENESIS OF OCULAR SIGNS
- Corneal Exposure o Main feature is gross distention of the ocular muscles
- Conjunctival erythema due to the deposition of mucopolysaccharides
(hygroscopic- increased water content)
SOFT TISSUE INVOLVEMENT - TREATMENT
o A. Medical Treatment
§ Control of hyperthyroidism
o B. Surgical Treatment
§ Decompression of the orbit by removing the
inferior and medial walls via an ethmoidal
LID RETRACTION approach

HYPERTENSIVE RETINOPATHY
- Fundus appearance is determined by the degree of
elevation of blood pressure and state of retinal arterioles
- Mild to moderate systemic hypertension
o Focal attenuation of a major retinal arteriole
o Diffuse arteriolar attenuation
o broadening of the arteriolar light reflex
o arteriovenous crossing change
EXOPHTHALMOS
MODIFIED SCHEIE CLASSIFICATION (MEMORIZE)**
- Grade 0: No changes
- Grade 1: Barely detectable arterial narrowing
- Grade 2: Obvious arterial narrowing with focal
irregularities
RESTRICTIVE MYOPATHY - Grade 3: Grade 2 plus retinal hemorrhages, exudates,
cotton wool spots, or retinal edema
- Grade 4: Grade 3 plus papilledema

SCHEIE CLASSIFICATION
- Stage 1: Widening of the arteriole reflex
- Stage 2: Arteriovenous crossing sign
- Stage 3: Copper-wire arteries (copper colored arteriole
light reflex)
- Stage 4: Silver-wire arteries (silver colored arteriole light
OPTIC NEUROPATHY reflex).

CLINICAL FINDINGS (AMERICAN THYROID ASSOCIATION)**

- 0 No signs or symptoms
- 1 Only signs which include upper lid retraction, with or
without lid lag or proptosis to 22 m. No symptoms
- 2 Soft tissue involvement
RETINOPATHY OF PREMATURITY
- 3 Proptosis >22mm
- A disease of pre-term infants where the immature retina
- 4 EOM involvement
undergoes changes related to / caused by ischemia and
- 5 Corneal involvement
insufficient retinal vascularization
- 6 Sight loss due to optic nerve involvement

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SYSTEMIC DISEASES AD ASTRA PER ASPERA
 - Risk Factors: CRYO-ROP STUDY
o Birth weight of less than 1500 grams - THRESHOLD DISEASE: Zone 1 or 2, stage 3 with plus disease
o AOG of less than 32 weeks of 5 contiguous or 8 cumulative clock hours
o selected infants between 1500 and 2000 grams with - PRE-THRESHOLD DISEASE:
unstable clinical course (high risk infants o Zone 1, any stage
- Staging (MEMORIZE) o Zone 2, stage 2 with plus
o Stage 1 - demarcation line between posterior vascular o Zone 2, stage 3 but less than threshold
and peripheral avascular retina
o Stage 2 - elevated ridge ETROP STUDY
o Stage 3 - extraretinal neovascularization - TYPE 1 (NEW THRESHOLD)
o Stage 4a - subtotal retinal detachment not involving o Zone 1, any stage with plus
macula o Zone 1, stage 3 without plus
o Stage 4b - subtotal retinal detachment involving o Zone 2, stage 2 or 3 with plus
macula - TYPE 2
o Stage 5 - total retinal detachment o Zone 2, stage 3 without plus
o Zone 1, stage 1 or 2 without plus
STAGE 1
- thin, white demarcation line MALIGNANCY
between the vascularized and - Primary cancer originating within the eye or ocular adnexa
avascularized retina is rare.
- NEOPLASTIC DISEASE**
o May involve the eye and optic pathways by direct
spread or metastasis
STAGE 2 o Most frequent metastatic tumor seen in the eye
- line thickens and becomes o Rarely primary, usually metastasis
elevated by additional o In women, carcinoma of the breast
mesenchymal tissue to form a o In men, bronchial carcinoma
ridge
VITAMINS AND EYE DISEASES
STAGE 3 ROP
- VITAMIN A
- Extraretinal fibrovascular
o Maintenance of epithelium
proliferation along the ridge
- VITAMIN B
o Beriberi
o Epithelial changes in the conjunctiva and cornea
produces dry eyes
o Visual loss may occur as a result of optic atrophy
STAGE 4
o NICOTINIC ACID DEFICIENCY (PELLAGRA)
- subtotal retinal detachment
§ Ocular involvement is rare
macula sparing (4a) or
§ Optic neuritis or retinitis may develop
involving the macula (4b)**
o RIBOFLAVIN DEFICIENCY
§ Rosacea keratitis, vascularization of the limbal
cornea, seborrheic blepharitis, and secondary
STAGE 5
conjunctivitis
- total retinal detachment - VITAMIN C
(funnel-shaped) fibrovascular
o Hemorrhages may develop in a variety of sites ( skin,
proliferation
mucous membrane, lids, anterior chamber, retina
etc.)

TUBERCULOSIS
- Caused by Mycobacterium tuberculosis
- Most commonly transmitted by aerosolized droplets
- Affinity for highly oxygenated tissues

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SYSTEMIC DISEASES AD ASTRA PER ASPERA
 OCULAR MANIFESTATION OF TUBERCULOSIS HIV MICROANGIPATHY
- Primary ocular TB - eye is the primary portal of entry
o Conjunctival
o Corneal
o Scleral disease
- Secondary ocular TB - hematogenous dissemination or by
contiguous spread from adjacent structures
o Uveitis – most common manifestation

CMV RETINITIS
- Clinical manifestations
o Patients may complain of minor visual symptoms such
as floaters, flashing lights or mild blurred vision, or
be totally asymptomatic.
o It presents with a wide range of clinical appearances.
From cotton wool spots which may look like HIV
Retinopathy to confluent areas of full thickness retinal
necrosis and vasculitis. CMVR can progress in a
“brushfire” pattern from the active edge of an active
lesion. The retinal vessels in an affected area show
attenuation, becoming ghost vessels eventually.
- Treatment
o The treatment of CMVR in patients with AIDS requires
the use of specific antiviral agents,
o ganciclovir, foscarnet or cidovir in conjunction with
HAART.
AIDS
OCULAR MANIFESTATIONS
- AROUND THE EYE
o Molluscum Contagiosum
o Herpes Zoster Ophthalmicus
o Kaposi’s Sarcoma KAPOSI SARCOMA
o Conjunctival Squamous Cell Carcinoma - Vascular neoplasm which is almost exclusively seen in
o Trichomegaly patients with AIDS.
- FRONT OF THE EYE - Most common anterior segment lesion seen in AIDS
o Dry Eye - Appears as a violaceous non-tender nodule on the eyelid or
o Anterior Uveitis conjunctiva.
- BACK OF THE EYE - Typically KS involves only the skin but when there is a
o Retinal Microangiopathy reduced CD4 count it can progress rapidly to other sites
o CMV Retinitis such as the gastrointestinal tract and CNS
o Acute Retinal Necrosis - Treatment of ocular adnexal KS may be necessary for
o Progressive Outer Retinal Necrosis cosmesis and to relieve functional difficulties.
o Toxoplasmosis Retinochoroiditis - The mainstay of treatment is radiotherapy.
o Syphilis Retinitis o Other options include cryotherapy or chemotherapy.
o Candida albicans endophthalmitis
- NEURO-OPHTHALMIC

DRY EYES
- Sicca syndrome is common with HIV infection
- Patients complain of burning uncomfortable red eyes.
- There are several causes of dry eye in HIV infection from
blepharitis to destruction of the lacrimal glands.
- Treatment is with tear supplements

OPHTHALMOLOGY: OCULAR MANIFESTATIONS OF VISION 20|20

5 OF 6
SYSTEMIC DISEASES AD ASTRA PER ASPERA
 TOXIC OPTIC NEUROPATHY
- Characteristic finding is scotoma that includes both the
blind spot and the fovea
- Cecocentral scotoma
- Progressive visual loss, bilateral
- Papillomacular retinal nerve fiber atrophy
- Temporal disc pallor

ETIOLOGIC AGENTS
- Methanol - Digitalis
- Ethylene glycol - Chloroquine
- Chloramphenicol - Streptomycin
- Isoniazid - Amiodarone
- Ethambutol (visual - Quinine
loss) - Vincristine
- Methotrexate
- Sulfonamides - Mercury
- Melatonin - Thallium
- high-protein diet - Malnutrition with
- Carbon monoxide vitamin B-1
- Lead - deficiency
- Pernicious anemia
- Radiation (unshielded
exposure to >3,000
rads)

**Highlighted in Red, MUST KNOWS!!!**

Notes from Lecture PPT and some recordings only.

OPHTHALMOLOGY: OCULAR MANIFESTATIONS OF VISION 20|20

6 OF 6
SYSTEMIC DISEASES AD ASTRA PER ASPERA
FEU-NRMF Ocular Pharmacology
CORNEA, SCLERA, CONJUNCTIVA
 Pharmacodynamics
 Cornea
 Pharmacokinetics
 Acts as a major functional barrier for ocular
 Ophthalmic Drug Delivery
penetration
 Ocular Pharmacotherapeutics
 For effective corneal penetration, drugs
 Local anesthetics
must have hydrophilic and lipophilic
 Analgesics
properties
 Mydriatics
 Conjunctiva and Sclera
 Cycloplegic
 Major depot for drugs
 Ocular hypotensive drugs
 Anti-infective drugs
IRIS, CILIARY BODY AND AQUEOUS HUMOR
 Anti-inflammatory drugs
 Iris
 Anti-allergy and decongestants
 Drug response vary depending on the
 Drugs for Dry eye and ocular surface
amount of iris pigmentation
disease
 Ciliary body and Aqueous humor
Pharmacodynamics
LENS AND VITREOUS
 It is the biological and therapeutic effect of the drug
 Lens
(mechanism of action)
 Barrier for rapid penetration of drugs from
 Most drugs act by binding to regulatory
aqueous and vitreous humor
macromolecules, usually neurotransmitters or
 Vitreous
hormone receptors or enzymes
 Major reservoir of drugs and temporary
 If the drug is working at the receptor level, it can be
storage depot of metabolites
agonist or antagonist
 If the drug is working at the enzyme level, it can be
RETINA and OPTIC NERVE
activator or inhibitor
 Blood-retinal barrier
 Inner BRB is formed by the retinal capillary
Pharmacokinetics
endothelial cells
 Absorption
 Outer BRB is formed by the zonula
 Molecular properties
occludens of the Retinal Pigment Epithelium
 Viscosity of the vehicle
 Functional status of the tissue forming the
FACTORS AFFECTING DRUG PENETRATION INTO OCULAR
barrier to penetration
TISSUES
 Distribution
 Drug concentration and solubility
 Metabolism
 the higher the concentration the better the
 Plays an important part in eliminating drugs
penetration
 Elimination/Excretion
 Viscosity
 addition of methylcellulose and polyvinyl
OCULAR STRUCTURES and PHARMACOKINETICS
alcohol increases drug penetration by
TEAR FILM
increasing the contact time with the cornea
 Composed of 3 layers
and altering corneal epithelium
 Lipid layer
 Lipid solubility
 Aqueous layer
 because of the lipid rich environment of the
 Mucinous layer
epithelial cell membranes, the higher lipid
 NV – 8-10um
solubility the more the penetration
(Notes: Lipid/oily layer – outermost layer of the tear film, produced
by the meibomian glands of your eyelid, it is 0.1um thick, the imp fxn  Surfactants
is to stabilize the aqueous layer and prevent it from evaporation  the preservatives used in ocular
Aqueous layer – secreted by the lacrimal gland, 7um thick. This layer preparations alter cell membrane in the
is unstable cornea and increase drug permeability e.g.
Mucinous layer – this is the innermost layer of the tear film, secreted benzylkonium and thiomersal
by your goblet cells. it is a thin hydrophobic layer consist of  pH
glycoproteins.  the normal tear pH is 7.4 and if the drug pH
Normal volume of you tearfilm in 8-10um and the normal volume of
is much different, this will cause reflex
your conj culde sac is 30um. Therefore a single drop of medication, is
about 50um, exceeds the volume of the conj cul de sac.
tearing
The excess is either drained by your lacrimal drainaige sys or is  Drug tonicity
blinked out of the eye.  Molecular weight and size
Increasing the drop size, therefore, does not inc drug absorption but
rather increasing systemic sbsorption. )
  Subtenons
 Retrobulbar
 Peribulbar
(NOTES: Compared to topical administration, local injections into
periocular tissues bypass the conjunctiva and corneal epith and
deliver high conc of drugs with low lipid solubility. There are 4 main
routes of periocular tissue.
Subconj – injection between conj and tenon allow for higher local
drug conc wit use of smaller drug quantities. This eliminates systemic
effects of the drug, avoid the need for local or systemic drug
administration and minimizes prob in px compliance
Subtenons – between tenons and sclera offers little advantage and
deliver lower quantities of the drug into the eye and increases the
OPHTHALMIC DRUG DELIVERY risk of globe perforation. This type of administration is used when
 TOPICAL dealing with sever uveitsi, cystoid macular edema and diabetic
 Solution and suspensions macular edema
Retrobulbar – drugs are injected in the intraconal space include
 Ointments
anesthetics, steroids, phenols and alcohol.
 Lid Scrub This provides rapis onset of anes and akinesia for ant seg and
 Gels vitreoretinal surgery
(NOTES: -Most ophthalmic drugs are applied topically because it is This technoque is a blind procedure where the needle is placed near
simple, convenient, non invasive, self administered by the patient the globe while aiming for the muscle cone which contains vital
-Solution and suspension in a form of eyedrops are the most structure such as the optic nerve. Potential risk include inadvertent
commonly used form of topical medication globe penetration, retrobulbar hge, direct injury to the optic nerve
-Advantages: easier to instil, can cause less blurring of Peribulbar teqnique is also a blind procedure , this involves one or
vision however bec it is less viscous, it has lesser contact more injections around the globe without directly aiming for the
time, inc risked of contamination may cause ocular injury muscle cone. This is rather a safer technique, it provides similar
from careless instillation. anesthesia and akinesia but with a lesser rapid onset as compared
- Ointments on the other hand has an advantage of prolonged ocular with the retrobulbar anesthesia)
contact time allowing less frequent dosing of the medication
-However patients on this kind of tx often complain of  INTRAOCULAR ADMINISTRATION
blurred vision or oily skin after application and because of  Intracameral - involves directly placing a drug in
its prolonged contact time, some may develop the anterior chamber
hypersensitivity reaction to the preservatives  Intravitreal - directly placing the drug at the
-Application of a solution ointment or detergent such as baby vitreous chamber anti vegf, steroids, antibiotic.
shampoo is helpful in tx of seborrheic/infective blepharitis.
This aids in the removal of oils, debris, desquammated skin in the OCULAR PHARMACOTHERAPEUTICS
inflammed lid.  LOCAL ANESTHETICS
-Gelling agents transform from gel to liquid upon contact with your  Injectable anesthetics
eye rendering the drug hydrophilic and minimizing complaints of  Lidocaine – most frequently used
blurring of vision.)  Bupivacaine
 SOLID DELIVERY DEVICES  Procaine
 Soft Contact lens  Etidocaine
 Collagen shield  Mepivacaine
 Filter paper strips  Topical Anesthetics
 Cotton pledgets  Proparacaine
(NOTES: These devices allow for a more regulated release of drug  Tetracaine
instead of the pulsed administration of solutions, char by an initial  Benoxinate
period of overdosage followed by relative under dosage  Cocaine
-Soft contact lens – absorb more water solubke drugsfor later release  MYDRIATICS
into the tear film  Targets the adrenergic receptors of the
-Collagen shield – similar to your contact lens, they are package in a autonomic nervous system
dehydrated state and rehydrated with a drug solution before  Affects various ocular function like pupil size,
application. Drug is release as the shield dissolves. palpebral fissure, blood vessel diameter, aqueous
-Drug impregnated filter paper strips allow for easy administration flow and accomodation
of drugs in amounts adequate for their intended purpose  Adrenergic terminals can be found in the
The use of this impregnated strips prevents administration of following:
excessive amounts of drug and eliminates the risk of solution  Ciliary smooth muscle
contamination of Pseudomnas aeruginosa.  Iris dilator muscle
-A pledget is a small elongated tuft of cotton by teasing the cotton  Muller’s muscle
tip of an applicator. The pledgets is saturated wit 1-2 drops of  Mydriatic agents
solution usualy mydriatics like tropicamide.)  Phenylephrine
 Hydroxyamphetamine
 PERIOCULAR ADMINISTRATION  Cocaine
 Subconjunctival
  CYCLOPLEGICS  First line drug for open angle glaucoma and
 Anti-cholinergic agents, anti-muscarinic, and ocular hypertension
cholinergic blocking agents  Very convenient to use, good safety profile
 Inhibit the action of acetylcholine on muscarinic
 Side effects: Hypertichosis, inc.
sites
pigmentation of eyelid skin and iris color,
 Cholinergic innervation in the eye:
 Ciliary body allergy, cystoid macular edema, corneal
 Iris sphincter muscle erosion.
 Lacrimal gland  No drug tolerance with prolonged use
 Can increase IOP in patients with open angle
glaucoma and can precipitate an acute angle
closure glaucoma in patients with narrow
occludable angles

 Atropine
 Non-selective muscarinic
antagonist
 Most potent mydriatic and
cycloplegic agent
 Onset: 12mins;duration:  B-adrenergic antagonist
up to 10 days (mydriatic)  Timolol, Betaxolol, Levobunolol,
 Onset: 12mins;duration: Metipranol, Carteolol
up to 7-12 days (cyclo)  Decrease aqueous production
 Uses  15-20% decrease in IOP
 Refraction in actively  Systemic side effects:
accommodating children with  Bradycardia
latent hyperopia  Systemic hypotension
 Inflammatory conditions such as  Heart block and failure
uveitis  Bronchospasm
 Adverse reaction  Diarrhea
 Dose dependent  Amnesia
 Fever  Exhibits tachyphylaxis
 Hallucinations
 Decrease salivation
 Convulsions
 Death

 Cyclopentolate Hydrochloride
 Cycloplegic agent of choice for
cycloplegic refraction in all age
group due to its relatively fast
 Adrenergic agonists
onset and short duration
 Brimonidine, Apraclonidine
 Onset: 20-30mins
 Decrease aqueous production and increases
 Duration: 24hours
uveoscleral outflow
 Recovery of
 20-25% decrease in IOP
accommodation: 6-12
 Side effects
hours
 Local: Dry mouth, blepharitis,
 Tropicamide
conj.hyperemia, foreign body
 Non-selective muscarinic
sensation
antagonist
 Systemic: Drowsiness, dizziness,
 Fast onset (20-40mins)
apnea in children, and CI in
 Short duration of action (6 hours)
patients taking MAO inhibitors
 Mydriatic>cycloplegic effect
 Adverse systemic effects are rare

▪ OCULAR HYPOTENSIVE DRUGS

 Prostaglandin anlogues
 Latanoprost, Bimatoprost, Travaprost, Taflupost
 Increases aqueous outflow
 25-30% decrease in IOP
 Carbonic anhydrase inhibitors  Most frequent cause of
 Acetazolamide, Brinzolamide, Dorzolamide primary and recurrent eye
 Reduces aqueous production disease, stromal keratitis,
 Topical: 15-20% IOP reduction conjunctivitis, keratitis
 Oral/Systemic: 40-50% IOP reduction  Tx: Trifluridine, Acyclovir,
 Side effects: Valacyclovir, Famcyclovir,
 Local: stinging sensation, toxic Gancyclovir
keratitis, corneal endothelial  Adenovirus (Serotypes 3,7,8,19 and
dysfunction 37)
 Systemic: tingling sensation,  Conjuntivitis, Epidemic
nausea, vomiting, diarrhea, Keratoconjunctivitis
metabolic acidosis, blood  Cytomegalovirus
dyscrasias  Retinitis, seen in
 Cholinergic Agonists immunocompromised
 Pilocarpine 1-4% patients
 It increases outflow facility by stimulates
the contraction of the longitudinal ciliary  Anti-Fungals
muscle  Most common fungal pathogens:
 20-25% reduction in IOP  Candida (yeast)
 Side effects:  Aspergilus, Fusarium and Curvalaria (molds)
 Local: brow ache, blurring of  Polyenes - bind to ergosterol in the cell membrane;
vision, increase risk of pupillary fungistatic (low conc); fungicidal (high conc)
block due to forward shift of the  Ampothericin B, Natamycin
lens, cataract, uveitis, retinal  Pyrimidines – blocks thymidine kinase; fungistatic
detachment  Flucytosine
 Systemic: salivation, nausea,  Azoles – inhibit fungal growth; fungistatic
vomiting, bronchospasm, intestinal  Ketoconazole, Miconazole, Itraconazole.
crapms, frequent urination. Voriconazole, Fluconazol
 Echinocandins – inhibits glycan synthesis
 ANTI-INFECTIVE DRUGS  Caspofungin, Micafungin, Anidulafungin
 Antibacterial
 Inhibit cell wall synthesis of peptidoglycans
which is necessary for structural integrity of  ANTI-INFLAMMATORY
the bacteria  Corticosteroids
 Penicillin, Cephalosporin,  Prednisolone, Flurometholone, Loteprednol
Bacitracin, Vancomycin  NSAIDS
 Selective disrupting bacterial cell  Ketorolac, diclofenac
membranes
 Polymixin B, Garamicidin CLASSIFICATION
 Selective binding of drugs to bacterial  Short acting
ribosomes, which differ from that of  hydrocortisone, cortisone, prednisolone
humans in size, and composition  Intermediate acting
 Aminoglycosides, tetracyclines,  Trimcinolone, Fluprednisolone
macrolides and chloramphenicol  Long acting
 Inhibit folic acid synthesis  Dexamethasone,betamethasone
 Sulfonamides, Pyrimethamine, Topical
Trimethoprim  allergic conjunctivitis,
 Inhibition of enzymes DNA gyrase and  scleritis,
topoisomerase IV which are specific for  uveitis,
bacteria  allergic keratitis
 Fluorinated quinolones like  after intraocular and extra ocular surgeries
moxifloxacin, ciprofloxacin Systemic (pathology behind the LENS)
 Antiviral  Posterior uveitis
 Interfere with viral replication and  Optic neuritis
multiplication  corneal graft rejection
 Inhibition of thymidine kinase NEVER GIVE STEROID IF YOU ARE SUSPECTING ACTIVE
 Organisms: INFECTION
 Herpes Simplex virus
NSAIDS
 Topical use
 Flurbiprofen
 Indomethacine
 Ketorolac
 Indications
 episcleritis and scleritis
 Uveitis
 CME
 PRE operatively to maintain dilation of the
pupil

OCULAR PHARMACOTHERAPEUTICS
 PREPARATIONS FOR DRY EYE AND OCULAR
SURFACE DISEASE
 Treatment for OSD
 Relieving ocular symptoms
 Healing the ocular surface
 Preventing serious complication
 Treatment of DES
 Category
 Tear supplementation – artificial
tears
 Tear conservation – ointments or
punctal occlusion
 Tear stimulation – secretagogues,
antiinflammatories or
immunomodulators

Ocular diagnostic drugs

 Fluorescein dye
 Available as drops or strips
 Uses: stain corneal abrasions, applanation
tonometry, detecting wound leak, NLD
obstruction, fluorescein angiography
 Caution:
 stains soft contact lens
 Fluorescein drops can be
contaminated by Pseudomonas sp.

 Rose bengal stain

 Stains devitalized epithelium
 Uses: severe dry eye, herpetic keratitis
THE VITREOUS AND THE RETINA must be differentiated from neurologic
POWERPOINT TRANS MGA ANIHAO! in origin which respect the vertical
meridian), vitreous or retinal
hemorrhages (scotomata)
POSTERIOR SEGMENT
• Night blindness/ Nyctalopia
• The structures of the globe behind the
• Inherited Rod disorders/ Retinitis
iridolenticular plane and encased by the
pigmentosa
scleral coat.
• Decreased VA and color vision
• Inherited retinal disorders (cone
THE RETINA
dystrophy etc.)
• transparent, light-sensitive membrane
• Retinal detachments affecting the
• inner ocular coat extending from the ora
fovea
serrata to the optic nerve
• divided into the inner neurosensory layer and
THE RETINA NEUROSENSORY LAYER
the retinal pigment epithelium
(PHOTORECEPTORS)
• primary function = VISION
• harness light energy and converts it to
CONES
neurochemical impulses
• 6 M, 25 um long, 85 um at fovea
• conical outer segment with stacked saccules
THE RETINA HISTOLOGY
connected to the cell membrane
RODS
• 120 M. 50 um long
• elongated outer segment with 1000
o stacked discs separate from the cell
membrane & containing visual
pigments

THE RETINA NEUROSENSORY LAYER

(SUPPORT CELLS)

Bipolar Cells
• first order neuron connecting PR to GC
Ganglion Cells
• second order neuron
• connecting BC to LGB
Horizontal Cells
Amacrine Cells
Mullers Cells
• glial support cells with nutritive, repair, ionic
reservoir, support functions
VITREAL ATTACHMENTS
THE RETINA NEUROSENSORY LAYER
• Vitreous Base (VB)
(RETINAL IMAGE)
o extends 1.5-2.0 mm anterior and 2.0-3.0
Transformation of light energy to membrane
mm posterior to the ora, and several
potentials:
mm into VB
• primary image from the photoreceptors
o fibrils attach and interdigitate b/w the
• secondary image produced in bipolar cells and
basal lamina of retinal glial cells and
modified by horizontal cells
fibrillar basement membrane of the
NPCE • tertiary image produced in ganglion cells and
modified by amacrine cells
• Weigert’s Ligament (WL)
o 8-9 mm annular lenticular attachment
• Vitreopapillary Attachment (Weiss’s ring) THE RETINA NEUROSENSORY LAYER
(PHOTOCHEMISTRY)
• Macular attachment
• Vascular Adhesions • photoreceptor outer segments (OS) contain the
• Areas of Vitreoretinal Degeneration visual pigments
• OS cell membrane allows Na entry while IS
secretes the ion producing a resting current
SYMPTOMATOLOGY OF RETINAL DISEASE
• Blurring of vision or visual disturbance without • Light causes the influx of Ca ions to effect a
pain current disruption and hyperpolarization
• Retina has no pain receptors
• Visual field defects RETINAL PIGMENT EPITHELIUM
• Retinal detachment (black curtain), • single layer, hexagonal, epithelial cells
• in contact with Bruch’s membrane at the base
BRVO & BRAO (sectional field defects -
and with the photoreceptors at its apex
1
 • contains melanin granules o 3 - grade 2 with exudates and hemorrhages
• apical zona occludens o 4 - grade 3 with disc edema
o Barrier function • features
• variable distribution: o focal or generalized arteriolar constriction
o tall and numerous at the fovea o hemorrhages
o heaped up at the papilla o exudates
o larger and irregular peripherally
FUNCTIONS HYPERTENSIVE & ARTERIOSCLEROTIC RETINOPATHY
• photoreceptor metabolism maintenance • Breakdown of the inner blood ocular barrier.
• regeneration of the visual pigment Intraluminal pressure is too great, leading to
• absorption of stray light (improves vision) fluid egress together with solutes like lipids
• outer blood-ocular barrier (hard exudates)
• active transport of metabolites
• phagocytosis and immune cellular response ARTERIOSCLEROTIC RETINOPATHY
• Due to thickening of the vessel wall
SYMPTOMATOLOGY OF RETINAL DISEASE • Intimal hyalinization
• Night blindness/ Nyctalopia • Medial hypertrophy
• Inherited Rod disorders/ Retinitis • Endothelial hyperplasia
pigmentosa • Primary sign= arterovenous crossing changes
• Decreased VA and color vision • GRADING
• Inherited retinal disorders (cone • Grade 1: widened median reflex and
dystrophy etc.) venous concealment;
• Retinal detachments affecting the • Grade 2: G1+ venous deflection at
fovea arterovenous crossings (Salus’ sign);
• Diseases that affect respective cells, produce • Grade 3: G2 + “copper-wire” arterioles
corresponding symptoms and marked AV crossing changes, i.e.
• Rods dysfunction à nyctalopia venous banking (Bonnet’s sign) or
• Cone dysfunction à color vision venous tapering on either side of the
defects crossing (Gunn’s sign);
• RPE dysfucntion à affect both rods • Grade 4: G3 + “silver-wire” aarterioles
and cones (since RPE supports and severe AV crossing changes;
photoreceptors)
• Symptomatology of retinal disease
• Metamorphopsia, micropsia or
macropsia
• Photopsia (sparks, rings, lightning
flashes)
• If retinal in origin, affect one eye
at a time only
• *as opposed to temporal or
occipital lobe lesions, both eyes

CLASSIFICATION OF RETINAL DISEASES

• Systemic disease affecting the retina
• Macular diseases
• Retinal detachment
• Tumors

BLOOD-OCULAR BARRIERS
• Outer: RPE zona occludens
• Inner: Endothelium of retinal blood vessels DIABETIC RETINOPATHY
• Dysfunction of these barriers leads to leakage • retinal microvascular changes associated with
of contents either into the subretinal space as the systemic disease;
in the case of the outer layer and into the • prevalence generally increases with age,
retinal substance for the inner blood retinal duration of the disease, and poor glycemic
barrier. control;
• pathogenesis
HYPERTENSIVE RETINOPATHY 1. Progressive basement membrane
• associated with systemic hypertension thickening;
• grading 2. Capillary endothelial cell damage
o 0 - no changes 3. Loss of pericytes
o 1 - barely detectable arterial narrowing 4. 4, increased stickiness and aggregation
o 2 - obvious narrowing with focal of platelets
constrictions • proliferative or non-proliferative
2
 • Features • advantageous in eyes with very severe
o microaneurysms (primary lesion) proliferative retinopathy
o exudates
o hemorrhages DIABETIC MACULAR EDEMA AND ANTI-VEGF
o IRMA • DRCR.net
o neovascularization • Anti-VEGF (Ranibizumab) with prompt
o fibrous proliferation or deferred laser superior to Laser alone
o traction detachment up to 2 years
o vitreous hemorrhage • Visual gains in Anti-VEGF group versus
o macular edema plateau or loss in laser group

DIABETIC EYE - SYMPTOMATOLOGY DIABETIC VITRECTOMY GOALS

• Fluctuating vision and variable/unstable • clear the ocular media
refraction • restore the function and anatomy of the
• Early cataractous lenticular changes posterior pole
• Diplopia and ophthalmoplegia • stabilize the proliferative neovascular process
• Recurrent corneal epithelial breakdown with
subsequent edema and opacification WHO RECOMMENDATIONS
o Diabetic < 30 yrs of age
TREATMENT BASELINE EYE EXAMINATION
• NPDR • diabetes present for 5 years
• glycemic control and systemic • age of 10 years
surveillance o Diabetic > 30 yrs of age
• observe for ischemic changes and BASELINE EYE EXAMINATION
macular edema • at the time of diagnosis
• referral/tx for high risk characteristics
• PDR RETINOPATHY OF PREMATURITY
• laser photocoagulation o proliferative retinopathy afflicting premature
• vitrectomy infants
o Sufficient Cause:
DIABETIC RETINOPATHY STUDY (DRS) IMMATURE RETINAL VASCULATURE
• randomized, prospective clinical trial Prematurity and Low Birth Weight
• Issues o potentiated by excessive oxygen administration
• Efficacy of PRP on severe NPDR/PDR o influenced by maternal and neonatal factors
• 50% or greater reduction in the
risk of severe visual loss (<5/200) EXAMINATION SEQUENCE
in treated vs. non-treated eyes • screen at 4 weeks postnatally or 32 weeks
• complications: whichever is earlier
• a) decreased VA (11%) • repeat every 1-2 weeks until the ff:
• b) visual field loss (5%) • normal and complete blood supply
develop
EARLY TREATMENT DIABETIC RETINOPATHY STUDY • successive 2-week exam shows Stage 2
(ETDRS) in zone III; then, every 2-4 weeks
• randomized, prospective clinical trial • development of “prethreshold”- weekly
• Issues • ROP disappears
• Efficacy of laser treatment for macular • once blood supply completedà every 6-12
edema months
• 50% reduction in rates of MVL
in treated vs. non-treated eyes ICROP CLASSIFICATION
with clinically significant • Zone 1 - area around the optic nerve about 2x
macular edema papillo-foveal radius
• Optimal timing for initiation of PRP • Zone 2 - from edge of zone 1 to the anterior
• PRP only in severe NPDR/PDR nasal edge of the retina
• Efficacy of ASA treatment in retarding • Zone 3 - remaining temporal crescent of retina
progression of retinopathy from the edge of zone 2
• Laser Photocoagulation

DIABETIC RETINOPATHY VITRECTOMY STUDY

(DRVS)
• randomized, prospective clinical trial
• Issue : Early vitrectomy in DR
• clearly beneficial in type 1 diabetics with
severe vitreous hemorrhage
3
Stage 1 • less pain and swelling
• characterized by a demarcation line separating • less ocular damage
normal vascularized retina from undeveloped • less cardio-respiratory effect
retina • less myopia
• line is typically white
• marked contrast between regions Disadvantages
Stage 2 • limited trial
• rolled ridge in place of the demarcation line • technical difficulties of focus and ablation
• limited to a small sector or may encircle the • requires completely flat retina and lesions
entire posterior pole
Stage 3 MACULAR DISEASES
• fibrovascular prolife-ration on the edge of the ✔ Affects the visually sensitive portion of the
ridge retina;
• mild, moderate, or severe vitreous infiltation ✔ Very symptomatic;
• 50% chance of pro-gression to stages 4 and 5 ✔ Relatively early consultation;
and blindness ✔ Carries a relatively guarded or grave prognosis;
• degree based on vitreous infiltration

THRESHOLD CSR ARMD

• Stage 3 ROP Age of Onset middle aged elderly
• Zone 1 or 2 in 5 or more continuous clock hours (20-40) (40 +)
• Zone 1 or 2 with 8 cumulative hours of Pathogenesis focal RPE leak RPE/Bruchs
involvement with the presence of “plus disease” breakdown
• INTERVENTION W/IN 72 HOURS OF Feature sensorineural drusen
DIAGNOSIS detachment
Course spontaneous progressive
PRE-THRESHOLD remission involvement
• Zone I any stage Complication recurrence SRNV
• Zone II stage 2 + or stage 3 chronic edema scotoma
• LIO W/IN 48 HOURS OF DIAGNOSIS degeneration

PLUS DISEASE CSR SYMPTOMS

o with abnormal iris vessels/tortuosity and • Blurring of central vision;
engorgement of retinal vessels • Central gray area of visual diminution;
o Rush Disease plus disease involving zone 1 • Micropsia, metamorphopsia;
very rapid progression • Rubout of certain portions of readable text;
• Afterimage persistence;
Stage 4
• fibroproliferative scar contraction and partial SIGNS
RD • Blisterlike sensorineural detachment of the
• 4A detached outside of the macula macula;
(zone1) • VA = 6/6 to 6/30, improved with +1.00 Diopter
• 4B ret detachment involving the lens;
macula; POOR VISUAL PROGNOSIS • Positive relative central/paracentral scotoma;
Stage 5 • Red desaturation;
o complete RD with a closed or partially closed • Delayed photostress test
funnel, from the ON to the retro-lenticular
space ANGIOGRAPHIC FINDINGS
o essentially no useful vision • Early hyperfluorescent lesion with late pooling
o Tx : SURGICAL pattern corresponding to the area of
sensorineural detachment;
ROP TREATMENT • inkblot or smokestack (10%) initial lesion
Objective: ABLATE ISCHEMIC RETINA • may be accompanied by areas of altered RPE
❍ Modalities: pigmentation with or without similar leakage of
• Cryotherapy dye;
• Laser Photocoagulation
• Indirect Ophthalmoscope AGE/DRUSEN RELATED MACULAR DEGENERATION
• Surgical / Endolaser ✔ a leading cause of irreversible central visual
• Endoptik loss
• Laser Diopexy ✔ prevalence increases with age

LASER RETINOPEXY A/DRMD - CLINICAL CHARACTERISTICS

Advantages Central visual loss associated with
• less need for anesthesia v drusen formation
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 v RPE changes High-risk Non-Exudative A/DRMD
v geographic atrophy o bilateral soft drusen, large or confluent drusen,
v serous/hemorrhagic RPE detachments and pigment changes/clumping without
v choroidal neovascularization evidence of exudation;
v subretinal fibrosis/disciform scar o 1% risk of developing SRNV in 5 years;
v age group 40+ o contralateral exudative changes 10-50%
depending on presence or absence of large
NATURAL HISTORY drusen or pigment clumps;
• Most cases are non-exudative o Amsler grid home monitoring with yearly
• significant visual loss only if they have follow-up (1-2 x)
exudative or severe atrophic changes: o AREDS 2 supplementation
• 60-70% with SVL in untreated well-
defined extrafoveal neovascularization FOCAL LASER PHOTOCOAGULATION FOR SRNV
• 40% with SVL in those with untreated Macular Photocoagulation Study (MPS)
ill-defined membranes Ø benefit of timely FLT for well-defined
• presence of exudative disease extrafoveal NVM in preventing SVL and
significantly increases the likelihood of stabilizing VA;
a similar progression in the Ø 95% of cases do not follow the MPS indication
contralateral eye for treatment
Photodynamic Therapy
CLINICAL SYMPTOMATOLOGY
CENTRAL VISUAL FIELD CHANGES ANTI-VEGF THERAPY
• distortion • Entails the intravitreal injection of agents
• scotoma known to block the vasoproliferative effects of
• micropsia/metamorphopsia Vascular Endothelial Growth Factor (VEGF)
• sectoral field loss 1. Corticosteroids, i.e. Triamcinolone,
• visual acuity loss Dexamethasone;
• A/DRMD Focal Points 2. Pegaptanib (Macugen)
o etiology is unknown. 3. Bevacizumab (Avastin
o diet, UV exposure/ blue light 4. Ranibizumab (Lucentis)
o Genetics (caucasian race) 5. VEGF trap (Aflibercept)
o Micronutrients (role=AREDS)
o central visual loss common ARMD Treatment
o Using their eyes will not aggravate their 1. Laser Photocoagulation;
condition. 2. Subretinal Membrane Surgery/macular
translocation
SUBRETINAL NEOVASCULARIZATION 3. Anti-VEGF Therapy;
o choroidal new vessels penetrating through • *ROP;
breaks in the Bruch’s membrane-RPE complex • *Diabetic and Uveitic Macular Edema;
o features: grayish-green membrane exudates • *Neovascular glaucoma
and hemorrhages 4. Combination Laser and Anti-VEGF;
o treatment = early recognition 5. *Genetic Testing (Cheek swab)
o + anti-VEGF Tx
• Screening/Monitoring Procedures
o Comprehensive Adult Eye Examination Future Tech
o Stereoscopic biomicroscopic posterior • Fovista (Ophthotech): Combined anti-VEGF and
fundus examination and recording anti-PDGF;
o Fundus photography • IRay (Oraya Therapeutics Inc.): in-office
o Fluoresceine angiography stereotactic radiotherapy system
o Indocyanine Green Angiography • low-voltage x-rays through the sclera to
o Optical coherence tomography a single treatment spot on the macula
o Home monitoring with Amsler grid and
similar devices RETINITIS PIGMENTOSA
o group of progressive disorders with nyctalopia,
MANAGEMENT field defects, and typical fundal pigmentary
Low-risk Non-Exudative A/DRMD appearance;
Ø few small “hard” drusen and some minor o triad :
atrophic RPE changes 1. pale optic disc
Ø no special examinations, tests, or therapy are 2. attenuated vessels
advocated 3. bony spicule/ pigmentation
Ø annual check-up may suffice o Flat/extinguished ERG
o treatment : supportive, genetic testing?,
cataract extraction, ACE inhibitors; Vit. A?;
Retinal chip
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VITREORETINAL INTERFACE DISEASES SYMPTOMS
• HA-Collagen matrix disintegration results in: o Pneumatic retinopexy;
• Loss of barrier and inhibitory functions; o Scleral buckling
• Traction from stereotactic eye o Closed vitrectomy
movements and progressive hyaloid
stripping;
• Specific diseases produced:
• Retinal break formation and retinal
detachment;
• Traction retinal detachment;
• Epiretinal membrane;
• Proliferative retinopathies;
• Cystoid macular edema;

RHEGMATOGENOUS RETINAL DETACHMENT

• Two components for retinal break formation
• Acute posterior vitreous detachment
(PVD)
• Predisposing peripheral retinal
degeneration

RETINOBLASTOMA
❍ Most common intraocular malignancy of
childhood
❍ LIFE THREATENING
❍ 1 in 20,000 live births
❍ prognosis is directly related to the size and
degree of extension
• Factors
❍ intraocular= possible cure
• vitreous traction
❍ with orbital extension= poor prognosis
• availability of liquid vitreous
❍ IMMEDIATE OPHTHALMOLOGIC REFERRAL
• saccadic eye movements/gravity
❍ PRESENTATION
• Mechanism of chorioretinal adhesion
❍ bilateral= within 15 mos.; ave= 8 mos.
weakening by the fluid vitreous
❍ unilateral= by 20-30 mos. ave= 25 mos.
• glycosaminoglycan dilution
❍ 90% within 3 years; rare after 7 years
• overwhelming the RPE pump
❍ signs and symptoms
❍ leukocoria
PATHOPHYSIOLOGY
❍ squint
• VR traction at points of adhesion à
❍ photophobia
transmission of energy to the retina à
❍ proptosis
break/hole formation relieves traction, but
❍ inflammation
allows liquid vitreous access to SR space à
❍ glaucoma
neurosensory retina separates from RPE à
retina becomes edematous and opaque à
Retinoblastoma Genetics
photoreceptor degeneration and atrophy in
❍ recessive, but acts as dominant with 90%
time
penetrance
❍ 60% hereditary; 40% nonhereditary (mutations)
Principles of Treatment and Repair
❍ deletion of a suppressor gene on chromosome
o localization and closure of breaks
13 in close association with esterase D enzyme
o relief of vitreoretinal traction
which encodes a phosphoprotein (pRB) cell
o scleral buckling
cycle regulator
o vitrectomy
o production of neuroretinal adhesion
o laser
o diathermy
o cryopexy
o internal tamponade
o air
o PFC gas
o silicone oil
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