Transcript rhegmatogenous retinal detachment

Retina and Vitreous Diseases
vitreous
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Clear, avascular, gelatinous body
Normally in contact with the posterior
lens capsule, the zoular fibers, the pars
plana epithelium anteriorly, retina, and
optic disk posteriorly
99% water, the remaining 1% include
collagen and hyaluronic acid
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eye movements induce incessant stress
forces, and with age, its composition
and structure change
Its role in the physiology and
pathobiology of the eye is being
increasingly appreciated, but its study is
complicated due to its invisible nature.
Retina
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The retina is the most complex of the
ocular tissues.
The macular is used primarily for central
and color vision while the remaining
retina, is utilized primarily for peripheral
and night vision.
Retina layer
Sensory retina
etinal pigment epithelium
Examination
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direct or indirect ophthalmoscope
slitlamp (biomicroscope) and contact or
handheld biconvex lens
Fundus photography and Fundus
fluorescein angiography (FFA)
B-Scan ultrasonography
visual electrophysiologic
Optical Coherence Tomography (OCT)
OCT
OCT is increasingly replace FFA as it is
fast, non-invasive test that produces
high resolution cross-sections and
contour maps of the central retina
Vitreous diseases
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Firm vitreoretinal attachments are
observed in areas at the vitreous base,
optic disk, fovea, and over the major
retinal blood vessels .
Vitreous age change
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The aging vitreous both liquefies and
aggregates.
Liquefies (synchysis), the process of vitreous
gel liquefaction, first appears at around 4
years of age. The process begins in midlife
and in most cases progresses slowly into late
age
Aggregation (syneresis) is a consequence of
increased fibril concentration in the gel,
associated with a decreased concentration
and ultimate absence of fibrils in adjacent
areas resulting in liquefaction
Vitreous collapsed
syneretic cavity
Intravitreal cavity filled with liquid breakdown
products of syneresis
Vitreous floaters
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muscae volitantes
They are usually seen against bright
lights or a uniform light background,
they might like spots or threads floaters
Floaters maybe degeneration of the
vitreous (syneresis) or caused by
hemorrhage , inflammation or retinal
detachment.
Flashing lights
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photopsia
A common symptom of an abnormal
relationship between the retina and the
vitreous
Happened on moving eye
Vitreous syneresis with focal vitreous
traction on vitreoretinal lesions such as
lattice degeneration
Require no treatment, however, it can
induce retinal tears
Vitreous collapse
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Syneresis affects at least 65% of persons
over 60 years.
Myopies are especially
With age, the center of vireous may undergo
syneresis and become filled with liquid
It should be assumed that patients with new
floaters or photopsia have retinal tears or
detachment until proved otherwise by
thorough examination.
Vitreous collapses downward and foreward to
create a posterior vitreous detachment
Posterior VitreousDetachment
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PVD refers to the separation of the
posterior vitreous cortex from the ILM
of the retina.
Once liquefied, premacular vitreous can
find its way to the retrohyaloid space
through a break in the thinned posterior
vitreous cortex overlying the macula.
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Floaters and photopsias are the most
common symptoms reported with the
abrupt onset of a PVD
Floaters are caused by aggregations of
collagen fibrils
Photopsias caused by vitreoretinal
traction are an ominous sign of a retinal
tear, particularly when associated with
the appearance of multiple floaters
Anomalous adhesions between the posterior
vitreous face and the retinal surface are the
cause of numerous vitreoretinal complications,
while the presence of an intact posterior
hyaloid provides a scaffold for vascular
growth and anteroposterior traction.
The Vitreous, the Retinal Interface in Ocular
Health and Disease - ResearchGate. Available
from: [accessed Mar 27, 2015].
Vitreous collapse causing the retina to tear and
detach
Vitreous Condensation and
Detachment
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posterior vitreous
detachment, PVD
PVD B-Scan
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Weiss circle
PVD from the disk margin, a ring-shaped
opacity on the back of the vitreouscan be seen.
Vitreomacular interface (VMI) disease
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vitreomacular traction (VMT)
macular holes
epiretinal membrane (ERM)
VMT defination
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The progression of PVD can lead to
periods of excessive traction on the
macula. Such traction can result in
anatomic changes in the contour of the
foveal surface, intraretinal pseudocyst
formation, elevation of the fovea from
theRPE, or a combination that typically
results in reduced or distorted vision.
VMT OCT scan
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(1) evidence of perifoveal vitreous cortex
detachment from the retinal surface;
(2) macular attachment of the vitreous cortex
within a 3-mm radius of the fovea;
(3) association of attachment with distortion
of the foveal surface, intraretinal structural
changes, elevation of the fovea above the
RPE, or a combination thereof, but no
fullthickness interruption of all retinal layers.
epiretinal membrane (ERM)
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nearly half of all eyes with PVD remains
residal vitreous on the surface of the
retina. This residual vitreous may
proliferate to form an epiretinal
membrane (ERM)
Epiretinal membrane contracture causes
macular traction.
ERM
Macular Hole (MH)
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macular hole is an anatomic defect in
the fovea featuring interruption of all
neural retinal layers from the ILM to the
RPE.
The edge of the hole usually is rounded
and may contain intraretinal
pseudocysts
MH
The Gass classified MH into 4 stages.
Stage
Stage
Stage
Stage
1
2
3
4
impending hole.
occult hole
hole with pseudo-operculum
hole after PVD
MH statge
Vitreous hemorrhage
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Vitreous hemorrhage cause
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Retinal tear
Retinal neovasularization
Hypertension
Eales’ disease
Retinal disorders
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Diseases of the macula
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Diseases of the peripheral retina
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Retinal vascular disease
Diseases of the macula
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Age-related macular degeneration
Central serous chorioretinopathy
Macular edema
Inflammatory disorders involveing the macular
Myopic macular degeneration
Macular hole
Epiretinal macular membrane
Macular dystrophies
Age-related macular
degeneration (AMD)
AMD Definition
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AMD is the leading cause of permanent
blindness in the elderly. The incidence
increases with each decade over age 50.
It is usually bilateral, but may not be
symmetrical
AMD is classified into two
categories
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Non-exudative (dry or atrophic )
Exudative (wet or neovascular)
Exudative AMD has a prevalence rate
of 1.2% and dry AMD has a
prevalence of 15.6% among adults
aged 43 and older.
Nonexudative macular
degeneration
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Signs discrete, round, yellow-white deposits
of variable size beneath the pigment
epithelium and scattered throughout the
macula and posterior pole
With time, drusen can enlage, coalesce and
increase
Histopathologically eosinophilic material lying
between the pigment epithelium and Bruch’s
membrane
Visual impairment may be minimal
But the exudative stage may develop
suddenly at any time
Nonexudative AMD
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macular drusen, clumps of pigments
in the outer retina and eventually
progress to geographic atrophy of
RPE and choriocapillaris which is the
main cause of severe loss of central
vision.
Typical clinic
representation
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hard drusen
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Commonly present in all ages on fundus photograph.
The incidence and prevalence of hard drusen is not age related.
Their presence alone is not sufficient to diagnose early age
related maculopathy.
Hard drusen is not associated with increased risk for the
development of choroidal neovascularization.
Histologically are globular deposits of hyaline material.
Clinical features:
Symptoms: typically asymptomatic
Signs:
Small, hard drusen has been defined as being < 64 µm in diameter
Discrete, yellow-white deposits that are external to RPE
Almost always have distinct and well-defined border
Fluorescein angiogram usually demonstrates pin-point window
defect.
Fundus photograph demonstrates
multiple hard drusen
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Soft drusen
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Considered to be a feature of AMD.
Their presence is associated with increased risk of the
development of RPE abnormalities, geographic atrophy and
choroidal neovascularization.
Clinical features:
Symptoms: may have decreased vision or metamorphopsia
Signs:
Defined as greater than 63µm in diameter
Vary in size and shape
Occasionally seen as confluent structures with indistinct margins
Fluorescein angiogram demonstrates:
Early hyperfluorescence
Either fading of fluorescence or staining of diffuse drusen in the
late phase depending on the phospholipid content
Pooling of dye within focal detachments of Bruch's membrane
Multiple soft, confluent
drusen.
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exudative or neovascular
AMD (wAMD)
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subretinal choroidal neovascular
membrane
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Symtomps: blurred vision, distortion,
scotoma
Signs: subretinal hemorrhage, exudate,
greyish-green choroidal lesion in macula
Fluorescein or indocyanine green
angiogram
OCT
Central scotoma
Macula of an eye with exudative age-related macular degeneration.
The brownish-colored membrane in the center of the macula is
subretinal neovascularization.
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AMD demonstrating pigment epithelial detachment
associated with soft drusen. Note also some hard drusen and
areas of pigment clumping
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Retinal Hemorrhages Secondary To "Age
Related" Disciform Macular Degeneration
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CNVM causing a macular scar
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Development Of A Hard
Disciform Type Scar
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Treatment
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Anti-VEGF theraphy: intravitreal
iniection 3 times+prn
Retinal Detachment
Denotes separation of the sensory retina
from the underlying retinal pigment
epithelium.
Three main types
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Rhegmatogenous detachment
Tractional detachment
Exudative detachment
Symptoms:
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Blurry or various degree of
decreased visual acuity
“dark curtain” that obscures
peripheral vision
Photopsia (subjective visualization of
flashing lights)
Risk factors:
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Myopic eyes
Family history of retinal detachment
Vitreoretinal syndrome
Aphakia
Rhegmatogenous retinal
detachment
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The most commonly seen retinal
detachment.
Usually there is/are retinal break(s)
induced by posterior vitreous detachment.
Fluid from liquefied vitreous can pass
through the break(s), enter the potential
subretinal space and undermine the retina
from the RPE.
Signs:
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Retinal break(s)
Undulating bulla, retinal tear flap, or
corrugated folds
Pigment in vitreous (tobacco dusts)
Low intraocular pressure
Rhegmatogenous Retinal Detachment
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Anterior circumferential tear (retinal dialysis)
rhegmatogenous retinal
detachment
Elevation of the transparent detached sensory retina
Management:
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Scleral buckling, cryotherapy or laser
to promote firm chorioretinal
adhesion.
Pneumatic retinopexy for selected
superior detachment.
Vitrectomy.
治疗
(1) Careful localizatin of retinal break
and treatment with cryotherapy or laser
in order to create an adhesion between
the pigment epithelium and the sensory
Retina.
(3) Sclera buckling
(2) Sclerotomy & drainage
of subretinal fluid
(4) Pneumatic retinopexy
Protocol of rhegmatogenous retinal detachment surgery
Traction retinal detachment
May be caused by proliferative diabetic
retinopathy, proliferative vitreoretipathy,
retinopathy of prematurity, or ocular
trauma
Tractional retinal detachment from
proliferative diabetic retinopathy.
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Commonly associated with:
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Proliferative diabetic retinopathy
Proliferative sickle-cell retinopathy
Retinopathy of prematurity
Proliferative vitreoretinopahy (PVR)
Signs:
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Proliferative fibrous membrane
Smooth, concave detachment toward
the anterior segment
Vitreoretinal traction
Normal intraocular pressure
Tractional retinal detachment caused by proliferative
vitreoretinopathy (PVR) demonstrating a single starfold
associated with diffuse retinal contraction.
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Management:
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release of vitreoretinal traction by
vitrectomy and membrane dissection.
Serous & hemorrhagic retinal
detachment
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Absence of either retinal break or
vitreoretinal traction.
Be the result of a collection of fluid
beneath the sensory retina and are
caused by diseases of the retinal
pigment epithelium and choroid.
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Diabetic Retinopathy
DR
How are the eyes affected? Basically,
diabetes is a disease of blood vessels.
With large amounts of glucose coursing
through the circulatory system
DR
the most accurate predictor of
retinopathy is duration of diabetes.
After 10 years, more than half of
patients will show signs of retinopathy,
and after 15 years this number
increases to nearly 90%.
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FIGURE 1 Stages of diabetic retinopathy: (a) R1 (background retinopathy: multiple microaneurysms and
occasional haemorrhages); (b) R2 (preproliferative retinopathy: multiple blot haemorrhages, intraretinal
microvascular abnormalities (IRMAs); (c) R3a (proliferative retinopathy): new vessels on disc and
elsewhere (NVD and NVE); (d) M1 (maculopathy): hard exudates within the macula
Colour fundus photograph, retinal thickness map and optical coherence tomography scan
of patient with diabetic macular oedema. (b) Images from the same patient as (a),
showing near resolution of macular oedema following repeated ranibizumab therapy for
12 months. There has been a reduction in the number of haemorrhages in the macula
Two Types of Retinopathy
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A. Nonproliferative diabetic retinopathy
(NPDR)
Proliferative Retinopathy
NPDR
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“background retinopathy.” The earliest
signs of retinal damage arise from
capillary wall breakdown, seen on the
fundus exam as vessel microaneurysms.
Injured capillaries can leak fluid into the
retina and the aneurysms themselves
can burst, forming “dot-and-blot
hemorrhages.”
NPDR
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With worsening retinopathy and vessel
damage, the retina begins to show early
signs of ischemia.
Cotton-wool spots, seen with hypertension
and stasis, are gray spots with soft edges
that indicate ischemia/infarction of the
superficial retinal nerve fibers.
As vessel damage progresses, you can also
see beading of the larger retinal veins and
other vascular anomalies.
NPDR
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Signs
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Microaneurysm, intraretinal hemorrhages,
cotton wool spots and hard exudates
Venous tortuosity or beading, capillary
dropout and intraretinal microvascular
abnormalities (IRMA)
Increasing formation of microaneurysm
leads to increased vascular permeability
of the retinal capillaries and result in
retinal edema particularly in the macular
area
Fluorescein angiography
demonstrates
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Scattered hyperfluorescence dots of
microaneurysms which can be
associated with minimal dye leakage
Spots of hypofluorescense in the
area of hemorrhages and exudates
Areas of irregular capillary pattern or
capillary closure
Management
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Improve patients education and understanding
about the disease process.
Control of blood glucose, cholesterol and blood
pressure.
Photocoagulation in severe nonproliferative
retinopathy.
Annual check-up 5 years after onset for patient
aged less than 30 years old, and at time of
diagnosis for patients aged 30 and older.
Frequency of scheduled check-up depends on
the status of the retinopathy
Proliferative Diabetic
Retinopathy (PDR)
PDR
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With ongoing injury to the retinal vasculature,
the vessels occlude entirely, shutting down all
blood supply to areas of the retina. In
response, the ischemic retina sends out
chemicals that stimulate growth of new
vessels. This new vessel growth is called
neovascularization, and is the defining
characteristic of proliferative retinopathy.
PDR demonstrating dot and blot hemorrhages, hard exudates and
network of new vessels (NVE) with early fibrovascular proliferation
tissue extend over the surface of the retina.
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Advanced proliferative
diabetic retinopathy.
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Characterized by growth of new
vessels on the surface of the retina.
Symptoms: progressive loss of
vision, particularly in those who are
not properly followed or treated.
Signs
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new vessels grow on the optic disc, neovascularization of
the disc (NVD) or elsewhere (NVE)
These new vessels may leak and resulting in retinal edema.
They are also fragile and prone to bleed
Opaque fibrovascular proliferation tissue often appears on
the internal limiting membrane (adjacent to the new vessels)
and becomes adherent to the vitreous. Contraction of this
fibrovascular tissue may lead to: Distortion or dragging of
the macula , Mild to extensive retinal detachment, avulsion
of retinal vessels and vitreous hemorrhages
Neovascularization of the
disc (NVD)
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Neovascularization of the
disc (NVD)
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Neovascularization of the retina elsewhere
(NVE)
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Managements
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Strict blood glucose, blood pressure and cholesterol
control.
Photocoagulation for clinically significant macular edema
prior to scatter (panretinal) photocoagulation.
Consider PRP in severe proliferative diabetic retinopathy.
the extent of vitreous hemorrhage or worsening of overall
vitreoretinal condition need vitrectomy.
Anti-VEGF
PRP
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Diabetic Grading Classification
None no diabetic retinopathy
Background
microaneurysms or hemorrhage
venous loop
any exudate
any cotton wool spot
Pre-proliferative
venous beading
venous reduplicaton
multiple blot hemorrhage
IRMA (intraretinal microvascula abnormality)
Proliferative
new vessles on disc
new vessles elsewhere
preretinal hemorrhage or vitreous blood
preretinal fibrosis tractional retinal detachment
DR conclusion
As you can see, diabetic retinopathy is a big
problem as a large percentage of our patients
have diabetes. Retinal vessel damage leads to
edema, and vessel occlusion stimulates
neovascularization that can lead to trouble.
Fortunately, better glucose control and
surgical treatments have significantly
decreased the incidence of visual loss in these
patients.
Central serous chorioretinopathy
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serous detachment of the sensory
retina as a consequence of focal
leakage of fluid from the choriocapillaris
through a defect in the retinal pigment
epithelium.
young to middle-aged men and may be
related to life stress events.
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Symtomps: sudden onset of blurred
vision, micropsia, metamorphopsia, and
central scotoma
Signs: VA moderately decreased, serous
detachment of the sensory retina
FFA: dye leaking accumulate below the
pigment epithelium or sensory retina
Treatment
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80% spontaneous resorption with 6
months
Argon laser photocoagulation directed
to the active leak significantly shortens
the duration of the sensory detachment
and hastens the recovery of central
vision.
Central retinal artery
occlusion
Central retinal artery occlusion
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Typically unilateral.
More commonly affect older people in their midsixties, but can also occur in younger patients.
Most common cause: systemic hypertension.
Other etiologies: diabetes mellitus, emboli from
valvular heart diseases, carotid atherosclerosis
and circulatory compromise, coagulopathies,
collagen vascular diseases, other vasculitides
and trauma.
Symptoms
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Sudden, painless loss of vision
May have a history of amaurosis
fugax ( antecedent transient visual
loss)
Signs
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Normal anterior segment in acute cases
Pale, whitening, swelling retina especially in the posterior pole
Cherry red spot as a presentation of orange reflex from the intact
choroidal vasculature beneath the foveola surrounded by the retinal
pallor
Afferent pupillary defect is usually present
Emboli may be seen
After 4-6 weeks, the cloudy swelling retinal commonly resolves,
leaving a pale optic disc, attenuated retinal vessels, segmentation or
"boxcarring" of the blood column
Final visual acuity is most often worse than 20/400
Visual acuity of better than 20/40 may be achieved with patent
cilioretinal artery
Fluorescein angiography
demonstrates
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Delay in retinal arterial filling and
arteriovenous transit time
Segmentation of the blood column
Choroidal vascular filling is usually
normal
Management
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Thorough evaluation of systemic etiology.
May consider the following treatment to
lower the intraocular pressure: ocular
massage, anterior chamber paracenthesis.
Inhaled Oxyen-carbon dioxide mixture
Other treatments may include: oral
vasodilator and systemic anticoagulants.
Direct infusion of a thrombolytic agent
into the ophthalmic artery
Central retinal artery obstruction with diffuse superficial retinal
whitening in the posterior pole. Note also the marked delay in
arterial filling and incomplete venous laminar filling in the
later phase of the study.
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Central retinal vein
occlusion
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CRVO is the second most common retinal vascular disorder.
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Patients are usually 50 years or older, but it can occur in
younger patients.
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Two clinical types: perfused (nonischemic) - 75%, and
nonperfused (ischemic) - 25%.
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The second eye can develop vein occlusion in 6-17% of
cases.
Central retinal vein
occlusion
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Symptoms: sudden, unilateral,
painless visual loss that can range
from better than 20/400 in nonischemic eyes to 20/400 or worse in
ischemic eyes
Fundoscopic findings
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Widespread retinal hemorrhages in all four quadrants,
which vary in appearance from a small-scattered retinal
hemorrhages to marked confluent hemorrhages
Marked dilated and tortuous retinal vessels
Cotton-wool spots
Optic disc edema, macular edema, and retinal thickening
Vitreous hemorrhages may be present
A relative afferent pupillary defect (RAPD) can be present in
ischemic CRVO
Collateral optociliary shunt vessels can develop
The fundoscopic findings in nonischemic CRVO are
relatively milder than the changes seen in ischemic CRVO
Branch retinal vein occlusion is involving the
superior temporal quadrant
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Ischemic Central Retinal Vein Occlusion
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Associated conditions include
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open-angle glaucoma or various
systemic diseases such as diabetes
mellitus, systemic hypertension or
atherosclerotic cardiovascular
diseases.
Prognosis:
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Poor visual prognosis especially if involves a total area of at least
10 disc areas of retinal capillary nonperfusion and poor visual
acuity at presentation.
Prognosis is better in the nonischemic CRVO especially when
initial visual acuity is 20/40 or better or at least better than 20/200.
Two-thirds of eyes with ischemic CRVO may develop iris
neovascularization or angle neovascularization and subsequent
neovascular glaucoma. Retinal neovascularization is uncommon.
Nonischemic type may progress to ischemic CRVO in 5-22% of
cases.
Permanent loss of central vision due to persistent macular edema.
Management:
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Ocular work-up: best-corrected visual
acuity, intraocular pressure, slit lamp
biomicroscopy, gonioscopy and dilated
fundus examination.
Monthly visits.
Treatment of associated systemic medical
condition.
Panretinal laser photocoagulation is
indicated if neovascularization develops.
Retinal degeneration and
dystrophy
retinitis pigmentosa
Retinitis pigmentosa is a group of
hereditary retinal degenerations
characterized by progressive dysfuncion
of the photoreceptors and eventual
atrophy of several retinal layers
signs
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Night blindness (nyctalopia) and gradually progressive peripheral visual
field loss are the hallmark symptoms
In early stage, there are scattered accumulations of pigment shaped as
spider or bone-spicule formationon equatorial retina which may, cover
a part of blood vessels.
waxy-yellowish disc may be seen, with the developing of illness it
becomes pale, atrophy with clear margin.
Retinal blood vessels are markedly narrowed.
In late stage, pigment expands to periphery and posterior pole, if the
macula is involved, the central vision decreases obviously
ERG is extinguished
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leukocoria
Retinoblastoma
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Retinoblastoma is a rare but lifeendangering tumor of childhood.
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For small tumors within the eye,
treatment consists of external beam
radiation, photocoagulation (laser), or
cryotherapy (precise freezing). When
tumors are large or if there is little
expectation that vision can be
preserved, the eye is removed