VITREOUS

Anatomy
-

Clear, avascular, gelatinous body

Comprises 2/3 of volume and weight of the eye
Volume and weight: 3.9 ml or g
Composition
o Collagen
o Sodium Hyaluronate
o Vitrosin (fibrous protein)
o Water (95-99%)
In contact with the following:
o Posterior lens capsule
o Zonular fibers
o Pars plana epithelium
o Retina
o Optic nerve head

Primary Vitreous
Formed from the
protoplasmic process of
the lens vesicle and
inner layer of the optic
cup

Embryology
Secondary Vitreous
th
9 week of fetal life
Formed by vitreal and retinal
cells
Bulk if the post-natal
vitreous

Tertiary Vitreous
Produced by the margin of
growing optic cup
Becomes the suspensory
ligaments of lens

Vitreous base (pars plana and retinal periphery)

- Firmest attachment of vitreous
Hyaloidocapsular Ligament of Weiger
- Attachment to posterior lens surface
Firm attachment on early life but soon disappears
COMMON SYMPTOMS OF VITREOUS PROBLEMS

FLOATERS
o Black, shadowy floating objects in field of vision
o strings, spider webs, small saucer-like objects, or a
transparent ring
o Posterior vitreous detachment : causes the
majority of floater complaints

PHOTOPSIA
o Flashes of light like the stars flashing
when cartoon characters hit their
heads

Persistent Hyperplastic Primary Vitreous

Vitreous Liquefaction/Detachment
o Partial or complete failure of the embryonic hyaloid
o Syneresis; loss of gel-like consistency
vascular system (tunica vasculosalentis) to regress
o Usually occur in the aged, myope,
trauma or in intraocular
o White to pinkish retrolental mass containing blood vessels
inflammation
is seen with small deformed or cataractous lens
o
Causes dehiscence of the posterior
o With dilated pupil: (+) elongated, stretched ciliary
hyaloid from the retina resulting to
processes dragged into the pupillary space
vitreous detachment
o Results to collapse of the vitreous
toward the vitreous base away from
the macula and optic disc

Vitreous Opacities
o Opaque particles which may get
suspended in the vitreous and
interfere with its clarity
a. inflammatory cells- posterior
uveitis, endophthalmitis
b. RBCs- vitreous hemorrhage
c. saponified calcium soaps-asteroid
hyalosis
d. cholesterol crystals-synchesis
scintillans
e. tumor cells-retinoblastoma
f. foreign bodies

VISION IMPAIRMENT
Worst complication or
symptoms

Vitreous Bands and Membranes

o Dense opaque or semi-opaque
structures in the vitreous
o Due to condensation of the
fibrillar structure of the vitreous
or actual fibroblastic or glial
proliferation from vascular
elements
o Pigmented epithelial cells also a
source of bands/membranes
o Seen after:
A perforating injury to the
vitreous

Musca Volitantes
o caused by fine aggregates of
vitreous protein due to age or
myopia
o floating spots especially
pronounced when gaze is

Signs and Symptoms:

o Decreased vision
o Leukocoria cats eye reflex
o Strabismus
o Nystagmus
o Microphthalmos
o Shallow anterior chamber
o Large radial vessels that often cover the iris
o Angle closure
o Vitreous hemorrhage
o Retinal detachment worst cases

Signs and Symptoms

o Acute onset of floaters and
photopsias
o Circular vitreous condensation
(Weiss ring)
o Anterior displacement of the
posterior hyaloids
o Vitreous opacities
o Vitreous pigment cells
o Focal intraretinal, preretinal or
vitreous hemorrhage
Liquefaction of the vitreous results to
lacuna formation. Normally, vitreous is
homogenous and gel-like
Vitreous no longer homogenous and
there is presence of lacunae

Signs and Symptoms

o Floaters or spots in the field of
vision
o Decreased visual acuity

Foreign bodies
Inflammation
Hemorrhage
Trauma
Any loss of formed vitreous in
cataract surgery
Common complications:
o Retinal traction
o Retinal edema, hemorrhage,
tear or retinal detachment.
Therapy
Intravitreal injection of certain
substances (steroids, antibiotics,
hyaluronidase)
breaks down hyaluronic acid
Vitrectomy
Removal of pathologic vitreous
Eating up of the pathologic
vitreous
Pars plana (closed) - more
commonly used; Utilizes gauge 16
needle, light source, a special type
of lens and a microscope

How pathologic vitreous is removed?

Open-sky (open) via cornea, to remove the vitreous. Remove the lens and use artificial lens after. Used in trauma where there is avulsion of
cornea.- More invasive, less common
In cases in which there is damage to the cornea, e.g. massive corneal laceration and avulsion, we just go through what we call the open sky surgery
in which you have to remove the entire cornea first in order to get access to the vitreous. However, this is rarely used unless there is already
avulsion or large laceration through the cornea. Otherwise, we still use the pars plana (closed type).

o
o

RETINA
ANATOMY
Thin, semitransparent, multilayered sheet of neural tissue that lines the inner aspect of the posterior 2/3 of
the wall of the globe
Extends as far anteriorly as the ciliary body, ending at that point in a ragged edge, the oraserrata

o
o

FUNCTIONS
Transduce information from an optical image into electrical signals (rods and
cones)
Process certain features of the visual world from the photoreceptor signals and
relay this information to the brain via the optic nerve (neural circuits)

Layers of Retina
Common Symptoms
Bruchs membrane: actually the basement membrane of the
retinal pigment epithelium
Outer plexiform layer: contains the connections of the bipolar
and horizontal cells with the photoreceptors
Inner plexiform later: contains the connections of the ganglion
cells with the amacrine and bipolar cells
Nerve fiber layer: contains the ganglion cell axons passing to the
optic nerve

o
o
o
o

Blurring of vision
Photopsia flashes of light due to disturbance in retina
Visual field defects
Disturbance of image shape or size
Metamorphopsiadistortion of image
Macropsia enlargement than normal
Micropsia- decrease size than normal
o Nyctalopia night blindness
VASCULAR DISTUBANCES IN THE RETINA

CENTRAL RETINAL ARTERY OCCLUSION

o
o
o

Commonly caused by embolization (from heart or carotid artery)

e.g. Cholesterol, fibrinoplatelet, calicific, septic emboli
May also be caused by vaso-obliteration by atheroma or arteritis
Rarely caused by raised IOP(needs to be very severe ~70 mmHg)

Symptom
o Sudden, unilateral, painless loss of vision

Signs
o Decreased visual acuity
o (+) RAPD due to massive loss of blood supply to the retina aka Marcus Gunn Pupil
o Diffuse retinal whitening and arteriole constriction with segmentation (boxscarring) of blood flow
o Visible emboli
o Cherry-red spot in the macula (pathognomonic)- retina becomes very pale

Rarely caused by increased IOP, if ever, increased IOP must be severe to cause CRAO.
(+)RAPD since there is massive retinal pathology. In the case presented, diffuse retinal whitening and arterial
constriction with segmentation known as Buchs scarring of blood flow, visible emboli, and cherry red spot.

CENTRAL RETINAL VEIN OCCLUSION

o
o

Usually caused by thrombus

Associated with:
Increasing age
Hypertension
Coronary artery disease
Diabetes mellitus
Peripheral vascular disease
Hypercoagulable states
Systemic lupus erythematosus
Syphilis
Sarcoid
Homocystinuria,
Malignancies (e.g. Multiple myeloma, leukemia),
Open angle glaucoma
AIDS
Oral contraceptive pills intake
Collagen vascular disease

What causes the cherry red spot?

Since the retina is already devoid of blood supply, what you see actually is
the vasculature of the choroid. Remember: the macula is the thinnest part
of the retina.

Symptoms
o sudden unilateral painless loss of vision (moderate to severe)

Signs
o Decreased visual acuity ranging from 20/100 to hand movement
o +)RAPD massive damage
o Dilated, tortuous retinal veins with superficial retinal hemorrhages
o Cotton-wool spots are infarctions of the nerve fiber layer; aka soft exudates but
are not true exudates
o Optic disc hyperemia
o Disc edema
o Macular edema
o Rubeosis (neovascularization at the
iris)
o Disc/retinal neovascularization
o NVG (neovascular glaucoma)
o Vitreous hemorrhages

Cherry red spot is pathognomonic of central retinal artery occlusion.

Central retinal artery occlusion causes painless catastrophic visual loss
occurring over a period of seconds; antecedent transient visual loss (amaurosis fugas) may be reported
In a fluorescein angiography of a patient with CRAO. You could see that the ones with the black dye are actually
already the vein. But you could no longer see any artery in this case because the arteries are already blocked.

Treatment
(Immediate treatment needed if patient presents within 24 hours of visual loss) if >24h, chances of regaining
vision is nil
o Digital ocular massage to dislodge emboli, could reverse if done within 24 hours
o Systemic Carbonic Anhydrase Inhibitor
o Topical B-blocker
o Anterior chamber paracentesis (CA-I, BB, paracentesis: decrease IOP)
o Carbogen treatment
95% O2 prevent hypoxia
5% CO2 promote vasodilation
for 10mins q2h for 24-48 hrs)
o Hyperbaric oxygen, antibibrinolytic drugs, retrobulbarvasodilators (unproven treatments)

All treatments are aimed at oxygenation of retina and vasodilation of the artery. If all of these fail to work, the patient
would be permanently blind.

The clinical appearance varies from a few small

scattered retinal haemorrhages and cotton-wool spots to a marked hemorrhagic
appearance with both deep and superficial retinal haemorrhage which rarely may break
through into the vitreous cavity

Treatment
o Panretinal laser photocoagulation
Kills the new blood vessels since they are fragile and they increase risk of
bleeding
o Consider aspirin
o Treat underlying medical conditions

Why do you do PRP? (Pan retinal Laser Photocoagulation)

In patients with CRVO, they easily grow new vessels. These new blood vessels are very
fragile and they easily bleed so we dont want them. We do PRP to prevent further
bleeding

RETINOPATHY

Hypertensive Retinopathy

Hypertensive Retinopathy
Arteriosclerotic Retinopathy
Diabetic Retinopathy
Central Serous Retinopathy
Retinitis Pigmentosa
Retinal Detachment
o Retinal vascular changes secondary to chronic or acutely (malignant) elevated systemic blood pressure
o Fundus picture of hypertensive retinopathy: vasoconstriction, leakage and arteriosclerosis
Symptom: asymptomatic; rarely decreased vision
Signs
o Retinal arteriole narrowing/straightening
o Copper/silver-wire arteriole changes (arteriosclerosis)
o AV crossing changes (nicking)
o Cotton-wool spots(soft exudates infarct of nerve fiber layer) vs DM retinopathy which are hard exudates lipoprotein deposits
o Microaneurysms
o Flame-shaped hemorrhages
o Hard exudates
Arterial macroaneurysm (Disc hyperemia or edema with dilated tortuous vessels)
What are cotton wool spots?
Soft exudates which are Infarcts of the nerve fiber layer. Cotton wool spots are not true exudates. The hard exudates on the other hand are lipoproteins which
have leaked out of the blood vessels. These are true exudates.
Treatment
o Treat underlying hypertension!because there is no treatment directed to the hypertensive retinopathy itself
Normal AV Ratio = 2:3
Picture
Features
A
1
Mild to moderate narrowing and sclerosis of
arteries
AV Ratio: 1:2
B
2
Moderate to marked sclerosis of retinal
arterioles
Exaggeration of light reflex
AV compression changes
Generalized compression of arterioles
AV Ratio: 1:3
C
3
Retinal arteriolar narrowing, retinal edema,
hard exudates, cotton-wool spots,
haemorrhage
D
4
Grade 3 + papilledema

Arteriosclerotic Retinopathy
(may be part of systemic arteriosclerosis)

ATHEROSCLEROSIS
o Whitish plaques of lipid deposits
seen in the wall of the retinal
artery
o Lipoidal infiltration may make the
vascular wall visible and is seen as
a white streak at the side of the
blood column called vascular
sheathing or pipestream
sheathing

ARTERIOLAR SCLEROSIS
o Various changes in the pathology of the vascular wall can manifest in the fundus:
Changes in the median arteriolar light reflex
Arteriolar light reflex - median streak produced by the light
reflected from the cylindrical blood column of the artery
As the wall thickens from continuous vasoconstriction(due to
decreased blood vessel caliber), the light reflex becomes more
diffuse and partially obscures the blood column copper
wiring or silver wiring
Copper wiring-blood column still visible(appears
gold/yellowish)
Silver wiring extremely constricted (appears white)

AV crossing changes
Concealment of the vein Gunns sign(Due to loss of
transparency of the arteriolar vascular wall)
Tapering of the vein- Due to extension of the arteriosclerotic
changes from the artery to the vein
Depression of the vein into the substance of the retina- due
to pressure of the hardened arterial wall(artery presses hard
on the vein because wall of artery is already hardened which
in turn, depresses the retina)
Humping of the vein- Salus arch (with the pressure on the
vein, the proximal side becomes humped)
Venous banking- Dilatation of the vein proximal to the AV
crossing
Deflection of the vein as S-shaped or Z-shaped as it crosses
the artery
Tortuosity of the vessels
Attenuation of the arteries

Median arteriolar light reflex

Its a median streak produced by the light reflected from the cylindrical blood column of the artery. As the
wall thickens from contiguous vasoconstriction, the light reflex becomes more diffused and partially
obscures the blood column thus resulting to copper wiring. In severe cases, it becomes silver wiring in
which you could no longer see the blood column (only a whitish streak)

Diabetic Retinopathy
Grading and Classification for NPDR
1

Mild

Moderate

Severe

Features measured against size

of optic disk
(+) microaneurysms
Fluorescein angiography

(+) retinal hemorrhages and

microaneurysms
- and/or soft exudates
- and/or venous
beading(abnormal dilatation of
thevenules)in 1 quadrant
- and/or IRMA < 1 quadrant
IF Artery: Known as aneurysm
White spots are areas of
microaneurysms seen in
fluorescein angiography
4:2:1 Rule based on the (EDTRSearly diabetes treatment
retinopathy study); any of the
following:
Diffuse intraretinal
hemorrhages and
microanuerysms in 4 quadrants
Venous beading in 2
quadrants
IRMA in 1 quadrant

o
o

Retinal vascular complication of diabetes mellitus classified into:

- Nonproliferative (NPDR) and
- Proliferative (PDR) forms
A microangiopathy affecting retinal precapillary arterioles, capillaries and venules.
Characterized by both microvascular occlusion and leakage

What separates non proliferative from proliferative? The presence of neovascularization.

i. Microvascular Occlusion:
o Due to thickening of capillary basement membraneCapillary endothelial cell damage and proliferationChanges in RBC leading to
defective O2 transport
o And increased stickiness and aggregation of platelets
Arteriovenous Shunts- Intraretinalmicrovascular abnormalities (IRMA)
Neovascularization- due to hypoxia
ii. Microvascular Leakage:
o Due to loss of integrity of vessel wall brought about by reduction in the number of pericytesdistension of the capillary walls and breakdown
of the blood-retinal barrier leakage of plasma constituents
Diffuse retinal edema- due to extensive capillary dilatation and leakage
Localized retinal edema- due to local leakage from microaneurysms and dilated capillary segments
o chronic leakage lead to deposition of hard exudates (lipoprotein and lipid-filled macrophages) at the junction of healthy and edematous retina

NONPROLIFERATIVE DIABETIC RETINOPATHY

PROLIFERATIVE DIABETIC RETINOPATHY

The most severe ocular complications of diabetes mellitus are due to
proliferative diabetic retinopathy.
Proliferative retinopathy develops in 50% of type I diabetics within 15 years of
onset of their systemic disease. It is less prevalent in type II diabetics, but as
there are more patients with type II diabetes, more patients with proliferative
retinopathy have type II than type I diabetes.

Features
o Microaneurysms
o Dot and blot hemorrhages
o Hard exudates
o Retinal edema
o Dilatation and beading of retinal veins
o IRMA(intraretinalmicrovascular abnormalities)
o Nerve fiber layer infarcts

o Arteriolar abnormalities and

o Areas of capillary nonperfusion
What is ETDRS?
Early Treatment Diabetic Retinopathy Study. Group which classified
DR and grading.
Fluorescein angiography. You could see here that there are already
haemorrhages. You could see little dots which are areas of IRMA.
Those are areas of leakage. Supposedly, they should not be there.

Features
o Neovascualrization differentiating factor vs non proliferative type
o Vitreous detachment,
o Hemorrhage ( vitreous, preretinal)
Treatment
o Control blood sugar
o Laser photocoagulation burn the fragile blood vessels because they
cause bleeding
o Pars plana vitrectomy
If bleeding has already occurred and if there is formation of fibrous
membrane as well as traction of retina (esp. in proliferative type), do
Pars Plana Vitrectomy to remove the pathologic vitreous. Then do
endolaser and remove all fibrovascular complexes because these
complexes may pull on to the retina and further cause retinal
detachment.

Patients with proliferative diabetic retinopathy may bleed into the vitreous from
retinal neovascularization.
These patients must be managed aggressively with laser panretinal
photocoagulation, often combined with anti-VEGF therapy using
intravitreal injections of bevacizumab (Avastin) or similar agents.
If the blood prevents visualization of the retina, ultrasound
examination must be performed to rule out traction retinal
detachment. Vitrectomy can be done to improve vision and apply
endolaser panretinal photocoagulation.

Grading/ Classification
Features measured
against size of optic
disk
1

Early
NVE < disc area
NVD < 1/3 disc area

High Risk
NVE > disc area
NVD >/= 1/3 disc area
NVD < 1/3 disc area but with preretinal or vitreous hemorrhage
(+) fibrous proliferation
(+) pre-retinal or vitreous hge
(+)traction retinal detachment

*NVE- neovascularisation elsewhere

NVD- neovascularisation in the disc

Central Serous Retinopathy

Description
o Idiopathic leakage of fluid from the
choroid into the subretinal space due to
retinal pigment epithelium dysfunction
o Usually occurs in males age 20-59 years
old
o Associated with type a personality,
stress, OCD, hypochondriasis, pregnancy,
steroid use and organ transplantation

Signs and Symptoms

Symptoms
o Blurring of central vision,
o Micropsia
o Metamorphopsia
o Mild dyschromatopsia
o May be asympotmatic
Signs
o Entral/paracentralscotomas (blind spot)
o Metamorphopsia
o Induced hyperopia
o Single or multiple, round or oval-shaped shallow,
serous retinal detachment or pigment epithelial
detachment

Treatment
o
o

No treatment required usually

resolves spontaneously
Treatment considered for:
Patients who require quicker
visual recovery
Poor vision in fellow eye
No resolution after 4-6
months
Recurrent episodes with poor
vision low intensity
direct laser photocoagulation
to leakage site

Retinitis Pigmentosa

Description
o Characterized by premature death of
photoreceptor cells with subsequent changes
in retinal pigment epithelium (RPE).
o Can be transmitted as a dominant, recessive
or even as a sex-linked trait
o Rod-cone dystrophies
o Night blindness is the most common initial
symptom due to early involvement of the
rods

Retinal Detachment
o separation of the neurosensory retina from the RPE
Retinal detachment is the separation of the sensory retina,
ie, the photoreceptors and inner retinal layers, from the
underlying retinal pigment epithelium. There are three main
types: rhegmatogenous, traction, and serous or
hemorrhagic detachment.

Symptoms
Nyctalopia
Dark adaptation problem
Photophobia
Constriction of visual fields (tunnel vision)
Dyschromatopsia
Photopsias
Slowly progressive decreased

Signs
o Decreased visual acuity
o Fundus with dark pigmentary clumps in the
midperiphery and perivenous areas (bony spicules)
o Attenuated retinal vessels
o CME (Cystoid macular edema)
o Fine pigmented vitreous cells
o Waxy disc pallor
o
o
o
o
o
o
o

Rhegmatogenous RD
o

o
o

The most common type of retinal detachment,

rhegmatogenous retinal detachment is characterized by a
full-thickness break (a rhegma) in the sensory retina,
variable degrees of vitreous traction, and
Due to full thickness retinal break (tear/hole/dialysis) that
allows vitreous fluid access to the subretinal space
Common Etiology:
Lattice degeneration- thining of peripheral retina esp. in
myope patients
Posterior vitreous detachment
Myopia
Trauma
Previous ocular surgery (esp. with vitreous loss)
Retinal dialysis and Giant retinal tears

Why is RD common in myopia?

Long eyeball in myopia. Retina is stretched out. It easily breaks
and vitreous fluid easily gains access to the retinal space. Myopic
esp. -5 dioptres, screen for presence of tears because they are
prone to retinal detachment.

Treatment
o No effective treatment (this is a
degenerative disease)
o Correct any refractive errors
o Low vision consultation for visual aids
and early training (train patient how to
use visual aids while he/she can see
because eventually vision will be lost)
o High dose vitamin A no proven
benefits but still given
Starts with the rods but will eventually
involve the cones.

Non-Rhegmatogenous RD
(retinal break)
Serous/Exudative
Traction RD
o Due to subretinal transudation of fluid from
tumor, inflammatory process or
degenerative lesion (may be in the form of a
central serous central retinopathy)
Etiology:
Vogt-Koyanagi-Harada syndrome
An idiopathic multi-system disorder that
affects pigmented individuals (e.g. Asians,
common in Japanese)
Characterized by skin and neurologic
changes; with high mortality
Skin changes: vitiligo, poliosis (whitening of
eyelashes), alopecia
Neurologic changes: irritation,
encephalopathy, auditory changes (tinnitus,
deafness, vertigo), CSF lymphocytosis
Eye problems: chronic granulomatous
iridocyclitis, uveitis, posterior segment
changes (exudative retinal detachment
Haradas Disease

o Due to fibrovascular proliferation

(bands and membrane changes) and
subsequent contraction pulling on
retina
o Tractional forces actively pull the
sensory retina away from the
underlying pigment epithelium
toward the vitreous base
o Traction retinal detachment has a
more concave surface and is likely to
be more localized
Etiology:
o
o
o
o
o

DM retinopathy,
Sickle cell retinopathy,
Retinopathy of Prematurity
Proliferative
vitreoretinopathy
Toxocariasis

Treatment
Pars plana vitrectomy
- allows removal of the tractional
elements followed by removal of the

 Presents with neurologic changes and

exudative retinal detachment
IF ALL SYMPTOMS ARE PRESENT, Harada
disease is clumped together with VOGTKoyanai-Harada Syndrome

General Symptoms
Symptoms (in general)
o Acute onset of photopsias
o Floaters
o Shadow across visual field, daw may nahulognakurtina
o Decreased vision
o May be asymptomatic

Signs
o Undulating, mobile, convex, corrugated folds;
o Retinal break usually seen
o tobacco dust (Shafers sign: pigment cells in the vitreous)
o Vitreous hemorrhage
o Operculum
TREATMENT
o Pneumatic retinopexy
o Scleral buckling, cryotherapy- belt is placed on the globe to
allow reattachment of neurosensory retina with RPE
o Pars planavitrectomy
o Drainage to address transudation of retinal fluid
o Endolaser used as glueto re-attach the retina to the RTE
o and/or other surgical maneuvers
Injection of silicon oil to the eye (disadvantage is patient will go
back to the OR and remove the oil after reattachment

fibrotic membranes.
Retinotomy and/or injection of
perfluorocarbons or heavy liquids
may be required to flatten the retina.

Other etiologies
o Uveal effusion syndrome
o Choroidal tumors
o CSCR central serous central retinopathy
o Hypertensive retinopathy
o Coats diseasemost severe form of retinal
cholangiectasia; presents with massive
exudative RD
o Retinal coloboma
o Toxemia of pregnancy

Gas tamponade, silicone oil, or scleral

buckling may be used

o Smooth, serous elevation;

o Subretinal fluid shifts with changing head
position

o Smooth, concave, usually localized,

does not extend to the oraserrata;
o Often with fibrovascular
proliferation and pseudo-holes
o pseudo-holes because it is only a
hole in thefibrovascular membrane
and not in the retina

TREATMENT
o Treat underlying condition; rarely requires
surgical intervention

We could use air or gases. We could

use C3F8. Thats the usual gas which is
being used to attach the retina.
However the disadvantage is that the
patient has to be in prone position at
all times. Treatment is 6 weeks to 2
months.

TREATMENT
o Retinal surgery to release
vitreoretinal traction