Quid Refert, Dummodo non Desinas, Tardius Ire

Retina
Opthalmology Dr. Funny yung tawa 

ANATOMY AND PHYSIOLOGY OF RETINA would be the internal limiting membrane. (Picture
st
below) when I say 1 layer, the most external.
st
o 1 Layer: RETINAL PIGMENT EPITHELIUM:
 border b/w choriocapillaries & retinal
layers (Choriocapilliary Narrie)
nd
o 2 Layer: RODS & CONES
 Photoreceptor layer

 CONES
 photopic or day and color
vision
 situated more predominantly at
the macula
o 1.5 mm in size
o located at TEMPORAL
 Retina SIDE of optic nerve
rd st
So, when we say retina, it’s the 3 layer. 1 layer is  RODS
nd
sclera and 2 is choroid.  scotopic or dark vision
What is choroid? It’s the middle coat of the eye. It is the  located more at the PERIPHERY
rd
middlemost vascular layer of the ocular wall. (ang ingay o 3 Layer: EXTERNAL or OUTER LIMITING
ng zipper ng bag ni shiela! Hindi ko marinig…) it goes all MEMBRANE
th
the way to the back, into the front then to the ciliary o 4 Layer: OUTER NUCLEAR LAYER
th
body and what you see as the black of the eye – iris. o 5 Layer: OUTER PLEXIFORM LAYER
th
Choroid is one continuous tissue. A less pigmented o 6 Layer: INNER NUCLEAR LAYER
th
individual tends to have a brighter choroid or more red o 7 Layer: INNER PLEXIFORM LAYER
th
orange while a darker colored individual has dark color. o 8 Layer: GANGLION CELL LAYER
th
Lighter colored individual has lighter iris, blue, while if o 9 Layer: NERVE FIBER LAYER
th
you are from Africa, then you’ll have a dark colored iris. o 10 Layer: INTERNAL LIMITING MEMBRANE
And the reason why I’m saying that is when you do your  inner border that separates the inner
PE, and you see the red orange reflex… the reflex is not vitreous gel & outer nerve fiber layer
actually a neurological reflex it’s actually a reflection of  The layer before the vitreous gel which is
the choroid and not the retina. The retina by itself is a house by the hyaloid membrane.
semitransparent tissue. So why is that important?
Because in most PE, at least for your level, you need to If the photo receptors are shot  view is distorted
see the ROR using your ophthalmoscope. Again, I’m
taking particular attention to iris because; this is the
only visualization we have in the retina. So if you have
cataract, cataratous??? opacity, you won’t have a view
of the retina.
A highly organized structure, with the ability to initiate
processing of visual information before it is transmitted
through the optic nerve to the visual cortex.
neurovascular tissue that lines the vitreous cavity
multi laminar
The most complex of the ocular tissues. The eye
performs as an optical instrument, a complex receptor,
and an effective transducer. Rod and cone cells in the
photoreceptor layer transform light stimuli into nerve
impulses that are conducted through the visual
pathways to the occipital visual cortex.
composed of ten layers – from internal going to the
external. From the sclera, choroid and then retina going
to the vitreous. The last layer, the innermost layer,

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  So what is the importance of knowing these layers? It’s the
physiology of accepting the light stimulus and transmitting it
to the brain.
 Ano nga ang main receptor? The rods and cones. Then it
sends the message to the different relay station which is the
neurons and axons (the nuclear layer etc.)
 Nerve fiber layer – is the important relay station.
 These nerve fibers coalesce into 1 optic nerve, so sometimes
the eye is fine but the patient is blind, well maybe because
the defect is here, or sometimes there’s a tumor along the
pathway or sometimes you have a retinal detachment or
sometimes the whole vitreous cavity is covered with blood.
 Photoreceptors
Rods – peripheral part of retina
 outside the macula
 Outside the arcades
 Dark adaptation – scotopic vision
 Retinitis pigmentosa – nadedegrade yung
rods receptors.
Cones – center (macula)
 Detect colors – 10 million different colors
 Retinal Pigment Epithelium
Serves as Outer Blood-Retinal Barrier
Extremely adherent to Bruch’s Membrane
Bruch’s membrane – boundary of choroid.
 Blood Supply of the Retina
INNER HALF: Central Retinal Artery – branch of
internal carotid artery.
OUTER HALF: Choriocapillaries of the CHOROID
 So this is a fluorescein angiography of the retina. You can see
here the pattern of the blood vessels.
 Vitreous Humor – like the white of egg.
Transparent gel like structure
Composed mainly of water & proteins
Maintains the tone of the eyeball – maintains the
stability of the eye.
Potential space: Clocae’s canal
 For nutrition
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 VITREOUS BASE
An area of vitreoretinal adhesion which straddles
the pars plana, oro serrata, and most peripheral
retina (3-4mm width)
 2 parts divided by the Band
ANTERIOR HYALOID
 anterior border of the vitreous
POSTERIOR HYALOID
 posterior border of the vitreous
 SCALLOPED at the area of Pars Plana
 What is oro serrata? It is the most anterior termination of
the retina. It is serrated.
 Lattice degeneration – we see this in patients with high
myopia, inflammatory conditions.
 High myopia – higher than 500 grade, there is a high risk of
developing lattice degeneration.
So in high myopia, it is either the eyeball is long or
the curvature of cornea is so curve so that the light
is focus anterior to the retina.
So, the problem here is that the sclera and choroid
is more elastic than the retina so what happens is
na-stretch, and pag manipis mabubutas siya, the
blood will enter the hole, this is one of the reasons
why nagkakaroon ng retinal detachment.
 Back to oro serrata, it adheres to choroid without the retina,
anterior to the oro serrata, you only have 2 layers, the sclera
and the choroid. It actually forms anteriorly into plicated
border.
 So ano naman yang plicated border? It is what we call pars
plicata.
 May flat din, It is important clinically because this is where
our instruments______ the pars plana.
 Pars plana vitrectomy – you can only enter here because
anteriorly you have vascular area that will cause more
bleeding into the vitreous gel. If posterior, you’re creating
hole in the retina causing more problems.
EMBROLOGY OF THE RETINA
 So I’m showing you this picture of embryologic retina just to
show the invagination during of the developmental stage.
And there is a potential space.
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  The potential space is between the dark retino-pigment o no thickening
epithelium and the rest of the layers of the neural sensory o no cotton wool spots
retina. This can be a potential ______ for other conditions in o no hemorrhages & exudates
adult life. Example is most common- retinal detachment.
st nd
 Layer of the retina divided embryologically at the 1 & 2
layer w/c is b/w outer RPE & inner photoreceptor layer
 OPTIC VENTRICLE
 Forms space b/w outer RPE & photoreceptor layer

 ABNORMAL FUNDUS
ABNORMAL Optic Disc
o Blurred Disc Margin
 Papillitis
 Papilledema
o Enlarged C:D ratio
 glaucomatous process
 Glaucomatous cupping
o Pale optic disc
DIAGNOSTICS
 long standing atrophy
ABNORMAL Retinal Vasculature
 The retina can be examined with a direct or indirect
o A:V ratio < 2 :3 – vein is bigger than artery
ophthalmoscope or with a slitlamp (biomicroscope) and
 Hypertension
contact or handheld biomicroscopy lens. This allows
 Diabetes
identification of the type, level, and extent of retinal disease.
 Vasculitis
Retinal imaging techniques are useful adjuncts to clinical
o Folds of Retinal Tissue
examination, enabling identification of anatomical, vascular
o Hemorrhage – extravasation of blood
(both retinal and choroidal), and functional abnormalities.
 Splinter hemorrhages on optic disc
They include fundus photography, fluorescein angiography,
 leakage of RBC from the vessels secondary to HPN,
optical coherence tomography, indocyanine green
DM, blood dyscrasias
angiography, and autofluorescence.
o IN HYPERTENSION
 Veins are dilated
FUNDOSCOPY
 Arterioles are attenuated or narrower
 AV Ratio increases
 NORMAL FUNDUS – cul de sac  (+) kingking & nicking where the vasculature
Optic Disc: crosses over since they share neurovascular sheath
o CUP:DISC RATIO < 0.5 mm o Sometimes there is whitening of the arteries  GHOST
 THEORETICAL LIMIT: .4 to .5 mm VESSELS d/t atherosclerosis
o well delineated ABNORMAL retina & macula
o healthy pink color o Diabetic Retinopathy
o Disc is the circle around the cup  Red, white & yellow fundoscopy
 Cup is the central depression w/c is paler o Exudates
 Represents the optic nerve  leakage of lipoproteins
Retinal vasculature: o Cotton Wool Spots - graveyard
o AV RATIO 2:3  necrotic cellular organelles
o no kingking and nicking  CENTRAL RETINAL ARTERY
o no occlusions Has 4 main trunks called ARCADES
o no neovascularization POSTERIOR POLE
o Retinal Veins are larger than arteries normally o houses the MACULA
Retina & macula:  Macula is 1.5 mm
o NORMAL Retina  Same size of optic nerve
 Colorless  Located TEMPORAL & SLIGHTLY INFERIOR
 Red orange reflex d/t blood vessels of choroid

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 You look for signs of hypertension, age related macular In comparison to rhegmatogenous retinal detachment,
degeneration & DM traction retinal detachment has a more concave surface and
Look for color is likely to be more localized, usually not extending to the ora
o WHITE
serrata.
 Cotton wool spot
- Necrotic cellular organelles
 No blood supply
 So, magandang malaman to because of the treatment. You’ll be
saving the patient from a hundred thousand pesos.
o RED:
 CAUSES:
- Hemorrhage
- macro/micro aneurysm
 increased vascular permeability causes RBC to leak
out  hemorrhage
o YELLOW
 Increased vascular permeability leaks out proteins
 exudates

 So you can see here wrinkles and folds. The unattached areas
are more whitish than the attached area.
 You can see a horse shoe tear here, that is a non
rhegmatogenous. (ewan ko saan jan sa dalawa).

PATHOLOGIC CONDITIONS OF THE RETINA SYMPTOMS

RETINAL DETACHMENT
 It is very important to see if there are cracks sa retina. If
 is the separation of the sensory retina, ie, the there are cracks kasi it means you are a potential retinal
photoreceptors and inner tissue layers, from the underlying detachment patient.
retinal pigment epithelium. There are three main types:  EARLY
rhegmatogenous, traction, and serous or hemorrhagic Asymptomatic
detachment. Some retinal breaks seals itself spontaneously
 LATE
TYPES: Localized blurring of vision
o When you cover one eye, what you see is not
2 TYPES kay doc, but sa book it’s 3: a total picture; hence part of visual field is
blurred
 RHEGMATOGENOUS
In simple tagalog, rhegmatogenous means may butas o SUPERIOR TEMPORAL VISUAL FIED LOSS
A break in the retina – can be from a lattice degeneration,  Defect inferiomedially
horse-shoe tear, basta meron butas. Pag may butas, papasok “shower” of pigments
ang fluid inside the hole causing detachment. o Choroid has a lot of pigment, if there’s a
May occur when vitreous liquefies known as Syneresis break, you’ll see a shower of pigments
TREATMENT o TYNDAL EFFECT
o Requires SURGERY  Technique used to check
inflammation or retinal detachment
 NON-RHEGMATOGENOUS
Visual loss
no break in the retina but separation takes place – that is so
 You have to remember that when you talk about retina,
because the RPE has a function of pumping out, keeping the
everything is opposite/upside down. If there is superior
potential space to dry but inflammatory conditions may
rd retinal detachment in your R eye, what do you see in the
cause leakage of fluid into it causing 3 spacing.
visual field?
Sometimes tumors may also cause this.
This is a diagnosis of exclusion, we try to find the hole and
then if there’s no hole then we assume na its either hindi
maayos ang pagka-assess or non rhegmatogenous sya.
may occur in inflammation (exudation of fluid)
TREATMENT
o Treat inflammation
 TRACTION RETINAL DETACHMENT
is most commonly due to proliferative diabetic retinopathy.
It can also be associated with proliferative vitreoretinopathy,
retinopathy of prematurity, or ocular trauma.
 Here is your shower of pigment and Tyndal effect

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 TREATMENT  New vessels are of poorer quality –
breakage of blood vessels – bleeding –
retina unable to see light – soon
 So how do you treat that? Parang vulcanizing yan, pag may blindness.
butas tagpian ang butas. Vitreous hemorrhage
 How do we do that? We simply put a chorio-retinal adhesion, Fibrous proliferation
the periphery of the hole; we can either coagulate it by laser Retinal detachment
or freeze it using a cryo-probe.  Diabetic maculopathy manifests as focal or diffuse retinal
 Lasers thickening or edema, caused primarily by a breakdown of the
Increase temperature  photocoagulation  inner blood–retinal barrier at the level of the retinal capillary
adhesion of tissue endothelium, which allows leakage of fluid and plasma
Retina appears white & black constituents into the surrounding retina. It is more common
 Cryotherapy in type II diabetes and requires treatment once it becomes
Decrease temperature  freezes tissue together clinically significant
 Expansile gas
Gas given inside Expansion pushes retina back
into the sclera
When you inject into the eye, it balloons and keeps
the eye attached to the retina.
 Scleral buckles
When sclera is pushed from the outside
i.e. Use of sponge
 Vitrectomy surgery
Pars plana is punctured
If Other areas are punctured can cause retinal
break or detachment
Located 5-8 mm from CORNEAL LIMBUS
Use calipers to measure how you go in
 Silicone oils
To maintain TAMPONADE & attachment
The pressure of the silicon oil keeps the retina
attached to the eye.
Hindi pang breast to ah? LOL
- Red dots are hemorrhages
DIABETIC RETINOPATHY - Small dots are microaneurysms
- Yellow lesions are exudates
 the most important in retina - White are necrotic material
 no. 1 cause of blindness all over the world. - AV ratio somehow changes
 One of the leading causes of blindness in the Western world,  Severe NPDR
particularly among individuals of working age. Chronic  PDR
hyperglycemia, hypertension, hypercholesterolemia, and
smoking are all risk factors for development and progression
of retinopathy. Young people with type I (insulin-dependent)
diabetes do not develop retinopathy for at least 3–5 years
after the onset of the systemic disease. Type II (non–insulin-
dependent) diabetics may have retinopathy at the time of
diagnosis, and it may be the presenting manifestation.

CLASSIFICATION

 Signs of NPDR
Hemorrhages
Microaneurysms
Exudates
Cotton wool spot
 Signs of PDR
All NPDR + neovascularization – attempt of the
body to heal itself.
 VEGF – responsible for angiogenesis;
released due to ischemia.  Fluorescein Angiography in PDR
If you see a lot of leakage, that’s a sign of PDR.

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  Laser panretinal photocoagulation
white dots are due to laser
in effect, the tissues are half dead and the O2
demand is lesser
The factors that increase VEGF production is gone –
new vessels regress.
Side effects: nyctalopia, decrease peripheral vision,
loss of central vision if too early performed.

 macular edema in diabetic retinopathy

extravasation of fluid to the macular area that
causes blurring of vision.
 Neovascularization
HYPERTENSIVE RETINOPATHY
Fine new vessels in the retina
Once you see this PDR na yan.
 It’s good to know how to see it at least you’ll have a good
management.
 Basically same as DM retinopathy
 Sometimes, the effect of this is centro-retinal vein occlusion

 Vitreous hemorrhage

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 AGE-RELATED MACULAR DEGENERATION Neovascular ("wet") age-related macular
degeneration is characterized by the development
of choroidal neovascularization or serous retinal
pigment epithelial detachment. Choroidal new
vessels may grow in a flat cartwheel or sea-fan
configuration away from their site of entry into the
subretinal space to form a choroidal neovascular
membrane. Hemorrhagic detachment of the retina
may undergo fibrous metaplasia, resulting in an
elevated subretinal mass called a disciform scar.
Permanent loss of central vision ensues.

TREATMENT
 Age-related macular degeneration (AMD) is the leading cause
of irreversible blindness in the developed world. It is a
 Conventional retinal laser photocoagulation
complex multifactorial progressive disease with genetic and
can achieve direct destruction of a choroidal
environmental influences.
neovascular membrane.
 MC in age 55 and up
 Photodynamic therapy
 BILATERAL
a photosensitive dye, verteporfin (Visudyne,
Novartis), which is believed to preferentially
PATHOGENESIS accumulate in active new vessels, is infused
intravenously and then activated by a low-energy
 The pathogenesis is still poorly understood; however, visible laser (689 nm). The resultant reaction
degeneration of the retinal pigment epithelium, linked to produces localized thrombosis of the new vessels.
oxidative stress, seems to be a crucial component.  ANTI-VEGF therapy
 Accumulation of LIPOFUCSIN Pegaptanib
Breakdown product of RPE metabolism as one Ranibizumab
ages Bevacizumab
The products are being deposited overtime in the  Surgery
retina. for late age-related macular degeneration
 2 TYPES continues to be studied with mixed results. Options
Dry include surgical removal of the choroidal
 Non-exudative neovascular membrane, macular translocation, and
Wet retinal pigment epithelial transplantation.
 Exudative
 See YELLOW SPOTS in macula
 Symptoms include: CENTRAL SEROUS RETINOPATHY
CENTRAL vision loss
 Optein – used for the prevention of ARMD.  is characterized by serous detachment of the sensory retina
due to multi-focal areas of hyperpermeability of the
CLASSIFICATION choroidal vessels and alteration in the pumping function of
the retinal pigment epithelium.
 It affects young to middle-aged men and is associated with
 Classification of AMD is controversial. It is most simply type A personality, chronic steroid use, and stress.
classified as early and late, the latter being subdivided into  Presentation is with sudden onset of blurred vision,
geographic atrophy and neovascular disease. The Age- micropsia, metamorphopsia, and central scotoma. Visual
Related Eye Disease Study (AREDS) devised a grading system acuity is often only moderately decreased and may be
based on fundal features, of which a simplified form is also improved to near-normal with a small hyperopic correction.
useful clinically.
 Early Age-Related Macular Degeneration
is characterized by limited drusen, pigmentary
change, or retinal pigment epithelial atrophy. The
level of associated visual impairment is variable
and may be minimal. Fluorescein angiography
demonstrates irregular patterns of retinal pigment
epithelial hyperplasia and atrophy.
 Late Age-Related Macular Degeneration
Geographic atrophy ("dry age-related macular
degeneration") manifests as well-demarcated
areas, larger than two disc diameters, of atrophy of
the retinal pigment epithelium and photoreceptor
cells, allowing direct visualization of the underlying
choroidal vessels. Visual loss occurs once the fovea
is affected.

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  Found only in the center, it does not progress out.
 Fluid accumulation w/in MACULA
Break in the Zonula Occludens in the RPE
 see flouroscein dye in flouroscein
angiogram
break on the RPE cause an inflow of subretinal
fluid into the macula
 UNKNOWN cause
 Common among Type “ A” individuals - si shiela! 
 Has CYSTIC ELEVATIONS in fundoscopy
 Blood vessels bending at areas of cystic elevation
 This disorder occurs most often in elderly patients and is
typically unilateral.
 Biomicroscopy of the symptomatic eye reveals a full-
thickness, round or oval, sharply defined hole measuring
one-third disc diameter in the center of the macula, which
may be surrounded by a ring detachment of the sensory
retina

MANIFESTATIONS

slight blurring of vision like scotoma

TREATMENT

 Laser
 Corticosteroids  Circular break in the retina centrally
 Central Scotoma
BEST’S DISEASE
STAGES OF DEVELOPMENT
 Juvenile-Onset Vitelliform Dystrophy
 Autosomal dominant disorder with variable penetrance and  In stage 1, occult hole, there is a yellow spot at the foveola
expressivity. with loss of the foveal reflex. This stage is reversible if a
 Onset is usually in childhood. posterior vitreous detachment occurs.
 In stage 2, there is enlargement with a deep perifoveal
yellow ring.
 In stage 3, the well-circumscribed full-thickness macular hole
is surrounded by a cuff of subretinal fluid.
 In stage 4, the full-thickness hole is associated with a
posterior vitreous detachment.

TREATMENT

 Vitrectomy
 Injection of expansile gas

RETINITIS PIGMENTOSA

 is a group of heterogeneous hereditary retinal degenerations

 Seldom seen
 accumulation of material in the Subretinal Space
 appears as a “Yellow Egg-Yolk Lesion” in the macula
 this is an inflammatory conditon
characterized by progressive dysfunction of the
photoreceptors, associated with progressive cell loss and
eventual atrophy of several retinal layers.
 Inheritance of the typical form can be autosomal recessive,
autosomal dominant, or X-linked recessive.
 Digenic and mitochondrial inheritance may also be
responsible.

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Jay: Young, ano ang pinakamagandang disease sa lahat
Me: huh? (meron bang ganon?)
Jay: oh, young sagot! Ano?
Me: ewan, ano nga?
Jay: eh di Best’s disease, kasi nga best diba! :D :D :D
Ang corny ni Jay! 

MACULAR HOLE

 is a full-thickness absence of the sensory retina in the

macula.

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 Condition w/c affects the RODS of photoreceptors – mga hindi
makakita sa dilim.
 night-vision loss and visual field constriction
 TRIAD seen on FUNDOSCOPY
WAXY PALLOR of disc and PIGMENT CLUMPS
ATTENUATION or NARROWING of retinal arterioles
BONY SPICULES appearance
o Sharp & irregular shapes
 Nyctalopia: night vision loss - HALLMARK
 Disease is variable
From SLIGHT visual problems to LOSS of vision
MYOPIC DEGENERATION
 PAPILLARY AREA shows atrophic pigment crescent
Appears as crack
 Retina is “Tigeroic” In Appearance – parang skin ng tiger
 Retina periphery is thinner w/c enhances visibility of choroid
MANAGEMENT
 annual check-up is warranted for ages 50 and up
 prophylactic laser treatment
RETINAL VEIN OCCLUSION
 is a common and easily diagnosed retinal vascular disorder
with potentially blinding complications.
 The patient presents with sudden painless loss of vision.
 The clinical appearance varies from a few small scattered
retinal hemorrhages and cotton-wool spots to a marked
hemorrhagic appearance with both deep and superficial
retinal hemorrhage which rarely may break through into the
vitreous cavity.
 Patients are usually over 50 years of age, and more than 50%
have associated cardiovascular disease.
 CENTRAL RETINAL VEIN OCCLUSION
Macular dysfunction occurs in almost all eyes with
central vein occlusion
 BRANCH RETINAL VEIN OCCLUSION
The vein occlusion usually occurs at the site of an
arteriovenous crossing.
TREATMENT
 If peripheral retinal neovascularization develops, SECTORAL
RETINAL LASER PHOTOCOAGULATION to the area of ischemic
retina reduces the risk of vitreous hemorrhage by one-half.
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 When vision loss due to macular edema persists for several
months without spontaneous improvement, GRID-PATTERN
MACULAR ARGON LASER PHOTOCOAGULATION may be
indicated. Intravitreal injection of steroids or anti-VEGF
agents may be useful in macular edema unresponsive to
laser treatment.
 Clinical trials are investigating the role of VITRECTOMY, WITH
OR WITHOUT ARTERIOVENOUS SHEATHOTOMY, to facilitate
reperfusion of the retina and reduction of macular edema.
RETINAL ARTERY OCCLUSION
 Central retinal artery occlusion
causes painless catastrophic visual loss occurring
over a period of seconds; antecedent transient
visual loss (amaurosis fugax) may be reported.
Visual acuity ranges between counting fingers and
light perception in 90% of eyes at initial
examination.
An afferent pupillary defect can appear within
seconds, preceding the fundus abnormalities by an
hour.
Twenty-five percent of eyes with central retinal
artery occlusion have cilioretinal arteries that spare
macular retina, potentially preserving central
vision.
 Branch retinal artery
is usually embolic in origin and results in visual field
loss. Visual acuity is only reduced if there is foveal
involvement.
TREATMENT
 Sudden decrease in intraocular pressure resulting in
increased retinal perfusion can be achieved with ANTERIOR
CHAMBER PARACENTESIS AND INTRAVENOUS
ACETAZOLAMIDE. This is particularly indicated in embolic
central retinal artery occlusion.
 INHALED OXYGEN–CARBON DIOXIDE MIXTURE induces
retinal vasodilation and increases the PO2 at the retinal
surface.
 THROMBOLYTIC THERAPY, infused directly into the
ophthalmic artery or administered systemically, continues to
be evaluated. Systemic anticoagulants are generally not
employed.
RETINOSCHISIS
 Degenerative retinoschisis is a common acquired peripheral
retinal disorder that is believed to develop from coalescence
of preexisting peripheral cystoid degeneration.
 The cystic elevation is most commonly found in the
inferotemporal quadrant, followed by the superotemporal
quadrant.
 The surface of retinal detachment is usually corrugated with
pigment cells in the vitreous ("tobacco dust")
 It develops into one of two forms, typical or reticular,
although clinically the two are difficult to differentiate.
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 2 FORMS
 Typical degenerative retinoschisis
forms a round or ovoid area of retinal splitting in
the outer plexiform layer. Posterior extension and
hole formation in the outer layer is uncommon and
therefore poses low risk of progression to retinal
detachment.
 Reticular degenerative retinoschisis
is characterized by round or oval areas of retinal
splitting in the nerve fiber layer forming a bullous
elevation of an extremely thin inner layer. Retinal
holes occur in 23%, and posterior extension or
progression to rhegmatogenous retinal
detachment may occur and requires treatment.
MACULAR EDEMA
 Retinal edema involving the macula may be due to
intraocular inflammatory disease, retinal vascular disease,
epiretinal membrane, intraocular surgery, inherited or
acquired retinal degeneration, or drug therapy, or it may be
idiopathic.
 It may be diffuse when nonlocalized intraretinal fluid results
in thickening of the macula.
 Focal macular edema, due to fluid accumulation in
honeycomb-like spaces of the outer plexiform and inner
nuclear layers, is known as cystoid macular edema (CME).
 It has a characteristic appearance on optical coherence
tomography, which is a good noninvasive method of
monitoring response to treatment
TREATMENT
 Topical steroid and/or nonsteroidal anti-inflammatory
therapy may accelerate improvement in visual acuity in
patients with chronic postoperative macular edema.
 In resistant cases, treatment with orbital floor or intravitreal
triamcinolone may be beneficial. If there is vitreous traction,
early YAG laser vitreolysis or vitrectomy should be
considered.
 If an intraocular lens implant is the cause of postoperative
macular edema, due to its design, positioning, or inadequate
fixation, removal of the lens implant should be considered.
INFLAMMATORY RETINAL DISORDERS
 Presumed Ocular Histoplasmosis Syndrome
 Acute Multifocal Posterior Placoid Pigment Epitheliopathy
(AMPPPE)
 Serpiginous (Geographic Helicoid Peripapillary)
Choroidopathy
 Birdshot Retinochoroidopathy (Vitiliginous Chorioretinitis)
 Acute Macular Neuroretinopathy
 Multiple Evanescent White Dot Syndrome (MEWDS)
PRIMARY BENIGN INTRA-OCULAR TUMOR
 Retinal Angioma
occur as isolated tumors or associated with
cerebellar hemangioblastomas, pancreatic cysts
and carcinomas, renal cysts and carcinomas, and
If you really want to know if someone cares and loves you, Page 10 of 10
just see if they take you towards sin or if they protect you from it.
pheochromocytomas in von Hippel-Lindau
syndrome
The retinal tumors are pink or red, endophytic, and
usually supplied by a large feeder vessel.
Juxtapapillary tumors are usually exophytic.
Vision is affected by bleeding or exudation from
the tumor vessels. Photocoagulation, diathermy,
and cryotherapy are used to treat the retinal
lesions.
 Astrocytic (Glial) Hamartomas
Astrocytic hamartomas are translucent to whitish
retinal and optic nerve head tumors most
frequently associated with tuberous sclerosis
(Bourneville's disease)
They may also be associated with
neurofibromatosis-1 and -2 or may occur as
isolated findings.
These tumors are congenital.
They may grow slowly and, as they mature,
become calcified, acquiring a mulberry
configuration
PRIMARY MALIGNANT TUMORS
 Retinoblastoma
a rare but life-endangering tumor of childhood.
Two-thirds of cases appear before the end of the
third year; rare cases have been reported at almost
every age.
Bilateral disease occurs in about 30% of cases.
This is generally a sign of heritable disease, but up
to one-third of heritable cases have purely
unilateral disease.
An allele within chromosomal band 13q14 controls
both the heritable and nonheritable forms of the
tumor.
Enucleation is the treatment of choice for large
retinoblastomas
 LYMPHOMA
Intraocular lymphomas may occur in association
with systemic lymphomas or as primary tumors,
most often involving the retina and vitreous.
Most are large B cell lymphomas, though T cell
lymphomas have been reported.
They often mimic retinitis, vitritis, or uveitis;
therefore, it is important to consider this tumor in
the differential diagnosis of unexplained
intraocular inflammation in an older patient.
Vitreous tap or retinal biopsy may be required to
establish the diagnosis.
Death may occur as a result of central nervous
system involvement.
Treatment with radiation and chemotherapy often
prolongs survival.
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Young DS