Far Eastern University – Nicanor Reyes Medical Foundation

OPHTHALMOLOGY: DISORDERS OF THE RETINA, CHOROID, AND VITREOUS – FEBRUARY 2022

OBJECTIVES DEVELOPMENT
• Be familiar with vitreous and vitreoretinal diseases In its inception, the organelle starts as a
• Know the etiology, risk factors, clinical presentation, and treatment vascularized gel (primary vitreous). As Remnants of the vascular
it develops the hyalocytes secretes the system can be seen in
for the following retinal diseases: secondary amorphous gel which premature babies and if it
o Hypertensive Retinopathy progressively compresses the persist, it is called the
o Diabetic Retinopathy fibrovascular primary core till they Persistent Hyperplastic
o Age-related Macular Retinopathy become a nearly indistinct canal in the
Primary Vitreous.
o Retinal Vein Occlusions adult (Cloquet’s canal) with minor
o Retinal Artery Occlusions attachments to the lens (Weiger’s
ligament and Mittendorf’s dot) and the papilla (Bergmeister’s papilla).

NOTE � The tertiary stage of development contributes in the formation of the

lenticular zonules, which together with the ciliary body, enables the
USE AT YOUR OWN RISK � You can email me at
accommodative visual capability. The latter provides the stabilizing
[email protected] for corrections/questions. Happy aral! parallel-antiparallel forces in between the collagen fibers that maintain
the gel matrix. Maintenance of this regular matrix is essential to the
REFERENCES: function of the organelle that keeps it acellular, avascular and, clear as
• 2022 PPT, Dr. Santiago’s uploaded lecture it functions primarily as a transmission media for light.
• Manual
SAMPLE QUESTION
VITREOUS AND VITREORETINAL INTERFACE DISEASES The ADULT vitreous is primarily composed of? Secondary vitreous
PHYSIO-ANATOMY
VITREOUS ATTACHMENTS
The vitreous is normally attached in its outer core to certain underlying
structures of the posterior pole. It plays a role in the pathology in the retina.
• Vitreous base – firmest attachment; a circumferential 4 mm band
spanning the outer 2 mm of the peripheral retina, ora serrata, and the
first few millimeters of the pars plana.
• Lens
• Papilla
• Macula
• Vessels
• Areas of vitreoretinal degeneration

EXAMINATION OF THE VITREOUS AND ITS INTERFACE

Vitreous is clear and microscopic making its examination difficult.
• Pupillary dilation addresses the limitations imposed by the pupil.
• Slit-lamp biomicroscopy with special aspheric condensing
lenses (60-90 diopters)
• Principles of retroillumination – highlight axial lesions with the red-
orange reflex serving as a contrasting background.
• Ocular sonology – evaluation of the gel in media opacity

VITREOUS BODY
- Amorphous gel occupying the inner eye
- From retro-lenticular space (behind the lens) to pre-papillary bursa [LEFT PICTURE] Vitreous
(pre-optic nerve) examination with the slit lamp and
o Approximately 4.5 ml in volume specialized lenses produces a virtual
o Accounts for 75% of total ocular volume inverted image between instrument
- Components and lens.
o 98% water
o Collagen
o Hyaluronic Acid
- Primary function: Transmission media for light PATHOLOGY
POSTERIOR VITREOUS DETACHMENT (PVD)
- Aging precipitates the critical dissociation of hyaluronic acid and
collagen (Note: physiologically normal & part of aging process)
- The matrix stability is compromised resulting in the liquefaction and
pooling of the hyaluronic acid (synchysis and syneresis) (Fig 3)
- While the collagen fibers coalesce to form odd-shaped opacities or
floaters whose shadows are imaged onto the retina (floaters).
Eventually, the gel collapses, tugging on its peripheral interface
attachments (producing photopsia).

Patient often described it as “May nakikita

akong itim na lumilipad” “Parang may nagflaflah
na ilaw”.

[LEFT PICTURE] Vitreous matrix degeneration

results in the clumping of collagen (C) and pooling
of liquid hyaluronic acid (H) in the vitreous cavity

[FIGURE 3] From normal gel

coalesced protein aggregates are
suspended in the gel and
shadowed onto the retina as
floaters [FIGURE 4]
Source: American Academy of
Ophthalmology
Topic: DISORDERS OF THE RETINA, CHOROID, AND VITREOUS

At the same time, the pool of liquefied gel accesses the subhyaloidal space ADDITIONAL INFOR FROM THE MANUAL
and begins the postero-anterior detachment of the gel in a process known Metamorphopsia and central field loss may eventually require
as posterior vitreous detachment. membrane stripping surgery to restore functionality and vision.

“Okay lang yung vitreous ang mag-detach but it becomes a problem VASOPROLIFERATIVE DISORDERS
kapag retina yung nag-detach” As a result of vitreous degeneration and barrier function loss, it creates
neovascular (abnormal new vessels) membranes which pervade the
RETINAL DETACHMENT vitreoretinal interface and result in complex forms of traction retinal
- PVD may generate critical traction produce breaks of the retina detachment.
o Fluid thus accesses the subretinal space and overwhelms the • Diabetic Retinopathy
retinal pigment epithelium (RPE) pump to detach the retina. • Retinopathy of Prematurity
- Treatment: Scleral buckling and/or Pars Vitrectomy • Proliferative Vitreoretinopathy
o It is best treated before the macula becomes involved, hence • Retinitis Proliferans
becomes urgent when threat to this section is noted
o Reattachment is achieved by identifying and closing all retinal
breaks, relieving traction and creating a chorioretinal seal
around the breaks

[PICTURES ABOVE by Shanti Saroj Netralay]

Surgical management of Proliferative Diabetic Retinopathy with Traction
Membranes (Left photo) entails advanced vitreoretinal surgery (Middle
figure) to restore anatomy and function as well as stabilize the proliferative
pocess (Right photo)

RETINAL DISEASES
• Hypertensive Retinopathy
• Diabetic Retinopathy
• Age-related Macular Degeneration (ARMD)
• Central retinal vein occlusion (CRVO)
• Branch retinal vein occlusion (BRVO)
• Central retinal artery occlusion (CRAO)
• Branch retinal artery occlusion
[PICTURE ABOVE: Illustration showing progressive vitreous
degeneration with subsequent liquefaction and matrix collapse HYPERTENSIVE RETINOPATHY
resulting in a variety of breaks in the underlying retina] - A manifestation of systemic disease; can be observed in direct
ophthalmoscopy
OTHER PATHOLGIES OF THE VITREOUS AND ITS INTERFACE - Two disease processes:
Aside from the gel collapse, the loss of the matrix nullifies its primary and o Acute effects: vasospasm to autoregulate perfusion
secondary functions. Clarity is lost as macromolecules, cells and even o Chronic effects: arteriosclerosis (and predispose patients to
blood vessels begin to invade the vitreous body. visual loss from vascular occlusions or macroaneurysms)
• Synchisis Scintillans – amyloid - Treatment: primarily focused upon reducing blood pressure.
and calcium entry; obscuring
vision due to the suspended RISK FACTORS
particulates within the gel ADDITIONAL INFO FROM THE MANUAL
• High salt diet
• Obesity • Major risk for arteriosclerotic hypertensive
• Tobacco use retinopathy is the duration of elevated
• Epiretinal Membrane/Macular • Alcohol blood pressure
Pucker – loss in barrier function • Major risk factor for malignant
• Family history
which allows cells to enter the hypertension is the amount of blood
• Stress
fray and settle on the retinal pressure elevation over normal
surface, transforming into • Ethnic background
• HR is diagnosed based upon its clinical
membranes that lead to
appearance on dilated fundoscopic exam
anatomic and visual distortion
and coexistent hypertension

- Epiretinal membrane: term used to describe the formation of

membrane
- Macular Pucker – kapag sobrang lala na; happens when
wrinkles, creases or bulges form on your macula.
- Patient complains about metamorphosia: visual defect that
causes linear objects, such as lines on a grid, to look curvy or
rounded (e.g., yung mga poste, nagiging wavy)

• Macular Hole – much worse condition; tangential

and circumferential forces from these macular
membranes causing to break open and
subsequently result in central blindness.
Signs of malignant
hypertensive retinopathy
• Endopthlamitis – inflammatory include:
condition of the intraocular • Constricted and tortuous
cavities usually caused by arterioles
infection; will require even more • Retinal hemorrhages
intensive medical and surgical • Hard exudates
therapy • Cotton wool spots
• Retinal edema
• Papilledema – inflammation
of optic nerve (blurred
margin and slightly reddish)

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Topic: DISORDERS OF THE RETINA, CHOROID, AND VITREOUS

Signs of chronic arterial hypertension in the retina include:

• Widening of the arteriole reflex
• Arteriovenous crossing signs
• Copper or silver wire arterioles (copper or silver coloredarteriole light
reflex).

Hypertension causes choroidopathy and poor perfusion of the

choriocapillaris causes:
• Elschnig spots – hyperpigmented patches in the choroid surrounded
by a ring of hypopigmentation.
• Siegrist streaks – linear hyperpigmented lesions over choroidal
arteries.
• Focal pigment epithelium detachment leading to exudative retinal
detachment
• Note: Very common in pregnant women

Hypertension may lead to optic neuropathy. The signs of optic

neuropathy include:
• Flame shaped hemorrhages at the disc margin
• Blurred disc margins
• Congested retinal veins
• Papilledema [PICTURE ABOVE: NON-PROLIFERATIVE DIABETIC NEUROPATHY]
• Secondary macular exudates. Note: Slit lamp examination and dilated fundus examination should be
performed. “Hindi pwedeng basehan na 20/20 vision pa sila. Usually kapag
MODIFIED SCHEIE CLASSIFICATION OF HYPERTENSIVE malabo na yung mata, malala yung condition.”
RETINOPATHY
FROM MANUAL
• Grade 0: No changes
One should look carefully for the presence of neovascularization of the iris
• Grade 1: Barely detectable
(NVI or rubeosis), cataract (associated with diabetes) and vitreous cells
arterial narrowing (blood in the vitreous or pigmented cells if there is a retinal detachment with
• Grade 2: Obvious arterial hole formation).
narrowing with focal • Intraocular pressure (IOP) should be checked especially when NVI is
irregularities seen.
• Grade 3: Grade 2 plus retinal • Dilated fundus examination should include a macular examination
hemorrhages, exudates, (contact lens or non-contact examination lens) to look for
cotton wool spots, or retinal microaneurysms, hemorrhage, hard exudates, cotton wool spots, retinal
edema swelling (edema)/ cystoid macular edema.
• Grade 4: Grade 3 plus • The optic disc and area surrounding it (for one disc diameter) should be
papilledema examined for presence of abnormal new blood vessels
neovascularization of the disc (NVD), optic nerve head pallor or
glaucomatous changes.
SCHEIE CLASSIFICATION OF CHRONIC ARTERIOSCLEROTIC • The remainder of the retina should also be examined for presence of
HYPERTENSION abnormal new blood vessels neovascularization elsewhere (NVE).
• Stage 1: Widening of the arteriole reflex
• Stage 2: Arteriovenous crossing sign The macular area can develop abnormal findings in diabetic retinopathy.
These findings can be present in the non-proliferative or the proliferative
• Stage 3: Copper-wire arteries (copper-colored arteriole light reflex)
forms of the disease. These changes in the macula include the presence
• Stage 4: Silver-wire arteries (silver-colored arteriole light reflex).
of abnormally dilated small vessel outpouchings (called microaneurysms),
retinal bleeding (retinal hemorrhages) and yellow lipid and protein deposits
(hard exudates).
• The macula can get thicker than normal (macular edema).
• Non-proliferative retinopathy can be classified into mild, moderate or
severe stages based upon the presence or absence of retinal bleeding,
abnormal venous beading of the vessel wall (venous beading) or
abnormal vascular findings (intraretinal microvascular anomalies or
IRMA). Treatment may not be necessary at this stage.
• Proliferative diabetic retinopathy (PDR) is progressive and requires
treatment to prevent bleeding and scar tissue formation.

DIABETIC RETINOPATHY
- Occurs in patients with diabetes mellitus.
- Main types of diabetic retinopathy:
o Non-proliferative diabetic retinopathy – absence of
abnormal new blood vessels
o Proliferative diabetic retinopathy – presence of abnormal [PICTURE ABOVE: PROLIFERATIVE DIABETIC NEUROPATHY]
new blood vessels in the RETINA Take note of the fine, tortuous vessel and hemorrhages (because it
- Symptoms: decreased vision or fluctuating vision, presence of bleeds easily).
floaters (vitreous hemorrhage) or defects in the field of vision
- Take note of patient’s blood pressure & HbA1c DIAGNOSIS:
- Ophthalmologic consult – important to know when to refer: • Request for Fluorescein Angiography (FA) – looks at the blood flow
o DM Type 1: 5 years after diagnosis (common in younger to your retina and the rest of your eye; use to rule out a retinal disease
patient) - Used to determine the degree of ischemia or the presence of
o DM Type 2: at the time of diagnosis (common in adult) retinal vascular abnormalities
- Areas of microaneurysms appear as hyperfluorescent spots
Patien often complain “Doc, halos kakapalit ko pa lang ng salamin ko” and may leak on the late frames resulting in areas of retinal
= mabilis lumabo yung mata. edema clinically.
- The areas of NVD/ NVE show leakage on the FA

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Topic: DISORDERS OF THE RETINA, CHOROID, AND VITREOUS

HALLMARK FINDINGS:
• Non-exudative ARMD – drusen, RPE changes, and geographic
atrophy

• Optical coherence tomography (OCT) – noninvasive imaging

technology used to obtain high resolution cross-sectional images of
the retina. • Advanced ARMD, drusen may fade or become resorbed in areas of
- Useful to determine the retinal thickness measurements. The geographic atrophy. Large areas of geographic atrophy may show
OCT can be sequentially obtained to determine whether the prominent deep choroidal vessels with atrophy of the
macular thickening is responding (swelling/ edema is choriocapillaries.
decreasing) to therapy.
DIAGNOSIS:
• Fluorescein angiography – performed when there is suspicion for
choroidal neovascular membrane (CNVM) formation
• Optical coherence tomography

TREATMENT:
• Non-neovascular ARMD: Observation with risk factor modification
and nutritional supplementation
• Neovascular ARMD: intravitreal injections of anti-VEGF agents

CENTRAL RETINAL VEIN OCCLUSION (CRVO)

SYMPTOMS:
• Sudden onset blurring of vision or gradually over the course of
TREATMENT several days.
Systemic control of diabetes, hypertension, hyperlipidemia, • Patient often complain of scotomas (focal areas of black vision) due
hypercholesterolemia, nephropathy and other diseases are of paramount to the flameshaped hemorrhages that occur due to increased
importance. backwards pressure in the central retinal vein.
• Macular edema – treatment is needed to prevent loss of vision or to - This causes the retinal vein to become dilated and tortuous.
try to improve vision. Treatment includes: - This is often described as a “hotdog-ketchup” fundus.
o Use of lasers
o Intravitreal injection of drugs that cause the retinal CRVO is divided into the ischemic and non-ischemic type.
swelling/macular edema to resolve (e.g., anti-VEGF drugs are • Ischemic type CRVO
more effective than focal laser) - May present with 4-quadrant hemorrhages, (+) RAPD, venous
• Proliferative DR – laser photocoagulation of the peripheral dilatation or tortuosity and extensive cotton wool spots (fluffy
retina/panretinal photocoagulation (PRP) white lesions: axoplasmic transport disruption).
- Used to create scars on the peripheral retina. - Vision is generally worse and prognosis of recovery is poorer.
- If successful, vitreous bleeding may be averted. - A late complication of ischemic CRVO is neovascular
- In advanced cases and there is bleeding filling the eye (and glaucoma (90-day glaucoma).
preventing laser to be done) or scar tissue that wrinkles the • Non-ischemic CRVO has less hemorrhages and tortuosity.
retina or pulls it off the eye wall surface. In these situations, - Carries a better clinical course.
surgery is necessary.
• The goal of surgery is to remove blood and scar tissue from the retinal
surface and to place laser treatment as needed. Intraoperatively,
intraocular gas or silicone oil may be needed to reattach the retina to
the underlying layers and sclera.

AGE-RELATED MACULAR DEGENERATION (ARMD)

- Mainly affects the macula (central part of the retina)
- An acquired degeneration of the retina that causes significant central
visual impairment through a combination of non-neovascular
(drusen and retinal pigment epithelium abnormalities), and
[LEFT: CRVO of the Right Eye showing flame shaped, dot and blot
neovascular derangement (choroidal neovascular membrane
hemorrhages in all retinal quadrants]
formation).
[MIDDLE: Fluorescein Angiogram of CRVO, Right Eye showing blocked
- Advanced disease may involve focal areas of retinal pigment
fluorescence corresponding to the hemorrhages on color photo.]
epithelium (RPE) loss, subretinal or sub-RPE hemorrhage or serous
[RIGHT: Optical Coherence Tomography of the Macula showing
fluid, as well as subretinal fibrosis.
intraretinal hyporeflective cystic spaces consistent with cystoid macular
edema]
SYMPTOMS:
• Decreased visual acuity • Metamorphopsia
BRANCH RETINAL VEIN OCCLUSION (BRVO)
• Distorted near vision • Vague visual complaints - Similar to CRVO but involves less retinal quadrants.
• Scotoma - Better prognosis than CRVO.
- Occurs mostly in hypertension due to the stiffening of the arteriole
TYPES: beside the venule which shares its common adventitia. This leads
• Non-neovascular ARMD (Dry ARMD) constitutes 85-90% cases; to the point of occlusion as one of the apex of triangle of retinal
usually does not cause severe vision loss. hemorrhage. Treatment of BRVO is similar to CRVO.
• Neovascular ARMD (Wet ARMD) constitutes 10-15% of cases;
major cause of severe vision loss; abnormal blood vessel in
CHOROID
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Topic: DISORDERS OF THE RETINA, CHOROID, AND VITREOUS

[LEFT PICTURE] Branch Retinal Vein

Occlusion of the Right Eye showing cotton
wool spots and dot- blot, flame shaped
hemorrhages at the superior macula.

CENTRAL RETINAL ARTERY OCCLUSION (CRAO)

- Painless sudden blurring of vision.
- True ocular emergency.
o Prompt treatment must be instituted as soon as possible.
o These may be in the form of brown bag rebreathing, carbonic
anhydrase inhibitors, or vitreous taps.
o All try to increase retinal blood flow to areas of ischemia.

Risk factors for development of CRAO include:

• Diabetes
• Hypertension
• Arteriosclerosis
• Blood dyscrasia
• Intravenous drug use and other
coagulopathies.
• Embolus may also be the cause of
CRAO which could come from common
carotid plaques and valvular heart
disease.

It can be recognized with the presentation of a cherry red spot on

fundoscopy. There is opalescence of the involved retinal tissue. The
central vision in CRAO may be saved if a cilio-retinal artery is present.

BRANCH RETINAL ARTERY OCCLUSION

- Presents similarly to CRAO but to a lesser extent (quadrantanopsia,
sector field defect).
- Prognosis is better than CRAO.
- Treatment is similar to CRAO.
- The key is early recognition and prompt referral for treatment.

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