Retinal diseases

Anatomy - retina
A thin semitransparent sheet of
neural tissue that lines the inner
aspect of the posterior two-thirds of
the wall of the globe.
10 Layers
The inner surface opposes the
vitreous humour.
The outer surface opposes the
Choroid
 Layers of the retina

Retina consists of two primary layers: an inner

neurosensory retina and an outer retinal
pigment epithelium (RPE).
The RPE is formed from a single layer of cells. It
facilitates the passage of nutrients and
metabolites between the retina and the
choroid. It takes part in the regeneration of the
photoreceptor visual pigments.
 Optic disk

Consists of optic nerve fibers formed by axons.

Is located nasal (or medial) to the fovea.
Has no photoreceptor cells, and, thus, is
insensitive to light.
Has a depression in its center termed the
physiologic cup 𪆵
The central artery of the retina, which is a
branch of the ophthalmic artery, enters the eye
through the optic disc to nourish the retina.
Macula

Oval-shaped yellowish area near the center of

the retina, on the temporal side of the optic
disk.
Contains the Fovea.
High-resolution, color vision.
Both the macula and the fovea are essential for
normal vision
Fovea

Is a central depression in the macula.

Is avascular and is nourished by the choriocapillary lamina of the choroid.
Has a high density of cones (no rods), each of which is connected with only one
ganglion cell, and thus provides the highest visual acuity.
The fovea is responsible for sharp central vision (also called foveal vision), which
is necessary in humans for any activity where visual detail is of primary
importance.
 rods
� Most numerous in the
periphery of the retina.
� Specialized for vision in dim
light (night vision).
� They are sensitive to light and
do not signal wavelength
information (color).
� They form the large majority of
photoreceptors in the
remaining retina.
cones
Most numerous in the �
foveal region.
Contain photopsins. �
� Require more light than
rods for activation and are
associated with visual
acuity and color vision.
� Subgroups of cones are
responsive to different
short, medium and long
wavelengths (blue, green,
red).
 Retinal blood supply

The retina receives its blood supply from two sources:

1. The choriocapillaris which supplies the
outer third of the retina, including the photoreceptors,
and the retinal pigment epithelium. The foveola is
supplied entirely by the choriocapillaris and is
susceptible to irreparable damage when the retina is
detached.
2. Branches of the central retinal artery,
which supply the inner two-thirds.

Both receive blood from the ophthalmic artery.

Blood-retinal barrier

The blood-retina barrier (BRB) is composed of both an

inner and an outer barrier.
The outer BRB refers to the barrier formed at the
retinal pigment epithelial cell layer and functions to
regulate the movement of solutes and nutrients from
the choroid to the sub-retinal space.
The inner BRB is located in the inner retinal
microvasculature and comprises the microvascular
endothelium which line these vessels. The tight
junctions located between these cells mediate highly
selective diffusion of molecules from the blood to the
retina and the barrier is essential in maintaining
retinal homeostasis.
viterous

The vitreous humor is a transparent, colorless,

gel-like substance that fills the space between
the lens and the retina within the eye. The
vitreous humor is composed mostly of water.
The vitreous humor’s main role is to maintain
the round shape of the eye. The size and shape
of the vitreous humor also ensures that it
remains attached to the retina. Supports the
lens.
Clinical tests for retina, macular and optic
nerve disease:
Imaging and
Functional tests
Fluorescein Angiography:
- Inject fluorescein dye into the arm
and trace it through the blood vessels in the
retina, where the appearance of fluorescent
patches can reveal leakage.
 Imaging and
Functional tests

� Ocular Coherence Tomography

OCT:
� - A non-invasive technique to image the
retina. OCT produces cross-sectional
images of the retina so that the
different layers and their thicknesses
can be measured.
 Imaging and
Functional tests

ICG “Indocyanine Green” Angiography:

- A special dye test to evaluate the
circulation of the choroid.
Tonometry:-
This test measures the pressure inside the
eye
• Ultrasound:-
• This test uses high-
frequency sound waves
(ultrasonography) to help
view the retina and other
structures in the eye.
Retinal detachment
and retinal tear
Worood Almomani
Definition
• Retinal detachment refers to the detachment of the
inner layer of the retina (neurosensory retina) from
the retinal pigment epithelium.
●A retinal detachment is an ophthalmic emergency
requiring urgent diagnosis and treatment
.●The longer retinal detachment goes untreated, the
greater your risk of permanent vision loss in affected
eye.

21
Pathophysiology
Detachment of the neurosensory retina, which contains -
the photoreceptor layer, from the retinal pigment
epithelium.

Disturbed metabolism of the photoreceptor layer leads -

to loss of retinal function (i.e., vision impairment)

Separation of the retina from the choroid for more than -

12 hours leads to retinal ischemia and retinal
.degeneration

22
Types of retinal detachment

Rhegmatogenous Non-rhegmatoge nous

the most common • Tractional(concave) •
Convex shape • Exudative (fluid accumulation) •
From Greek : “ Rhegma” = Tear •

23
Presentation Title 24
 Rhegmatogenous retinal
detachment Mechanism
retinal fluid,
which is
formed by
vitreous
Retinal degeneration retinal
tears/holes , seeps into detachment
the
subretinal
space

Presentation Title 25
Rhegmatogenous retinal detachment Risk
factors
High axial myopia (associated with a thinning of the retina and RPE density •
in the equatorial region)
Previous intraocular surgery •
Posterior vitreous detachment (increased risk with advanced age, high •
myopia)
Retinal detachment of the other eye •
Family history of retinal detachment •
Increased age (over age 50) •
CMV retinitis •
Lattice degeneration •

26
Rhegmatogenous retinal detachment
27
 Tractional retinal
detachment Mechanism
traction on the
vitreoretinal
band during
eye
Formation of movements or
as a result of retinal
vitreoretinal
sudden detachment
bands
decrease in
intraocular
pressure

Presentation Title 28
Tractional retinal detachment Risk factors
Proliferative diabetic retinopathy •
Retinopathy of prematurity •
Sickle cell retinopathy •
Inflammatory effusions (tractional or exudative?) •
Plastic cyclitis •
Post-hemorrhagic retinitis proliferans •
Eales disease •
Scar tissue following penetrating injury •

29
Tractional retinal detachment in proliferative
diabetic retinopathy

30
 Exudative retinal
detachment Mechanism
Subretin
Tumor
al fluid
growth
accumul
ation
without
retinal
retinal
detachm
tears
ent

Presentation Title 31
Exudative retinal detachment Risk factors
Systemic diseases : Pre-eclampsia , Hypertension , Bleeding •
disorders , Polyarteritis nodosa....
Ocular diseases •
Infections : Syphilis , TB , Toxoplasmosis •
Retinoblastoma •
Malignant melanoma of the choroid •
Other risk factors : Sarcoidosis , Corticosteroid use •

32
tumor-
associated
exudative
retinal
detachment

Presentation Title 33
34
Clinical Features
Prodromal symptoms:• Floaters• Flashes of light ( Photopsia) •
<symptoms of posterior vitreous detachment>

Localized retinal detachment: scotoma (visual field defect) • •

Typically unilateral gradually reduced side (peripheral) vision

Extensiveretinal detachment and/or macular involvement• •

Sudden, painless loss of vision in the affected eye (often described by
patients as a curtain descending over their field of vision

Relative afferent pupillary defect •

35
 The unaffected eye
should always be
examined, as in ∼
15% of cases of
rhegmatogenous

Diagnosis retinal detachment,

there is a .bilateral
tear

Both direct and indirect ophthalmoscopy

should be performed after dilating the pupil. Indirect
retinoscopy is useful to visualize the peripheral retina.
Ocular ultrasound: if the retina cannot be viewed
during fundoscopy (e.g., in the case of vitreous
hemorrhage or an advanced cataract)
Perimetry: to assess visual field defects
Electroretinography: decreased or absent impulse
in the region of the retinal detachment

36
Funduscopy

Opacification and wrinkling of detached retina •

37
Treatment For rhegmatogenous
retinal detachment
extensive retinal detachment

- Scleral buckling •
(external retinal holes/retinal tears with little or no retinal detachment
tamponade)-
laser photocoagulation or •
Pneumatic •
cryoretinopexy in the direct
retinopexy (internal
vicinity of the retinal defect
tamponade)

●A vitrectomy may be required, which is carried out using fine

microsurgical cutting instruments inserted into the eye ،This may
be combined with the use of special intraocular gases (for
example, sulphur hexafluoride) or silicone oil to keep the retina flat,
38
And go back to its original place.
Treatment For non-rhegmatogenous retinal
detachment
Exudative (serous) retinal detachment Tractional retinal detachment
spontaneous reabsorption of • Vitrectomy followed by internal •
fluid; no treatment is required tamponade and
Enucleation? • laserphotocoagulation/cryoretin
opexy

39
Prognosis
Non-rhegmatogenous retinal
Rhegmatogenous retinal detachment : detachment:
The smaller the area of • significantly poorer prognosis •
detachment, the better the The exception is exudative •
prognosis retinal detachment
The prognosis is good if surgery •
is performed at an early stage
and if there is no macular
involvement.
Complications
●• Without treatment, progressive retinal detachment causes •
blindness, especially if the macula is involved
.●• Proliferative vitreoretinopathy. •
●• Toxic uveitis (due to endocular toxins) in the case of long- standing •
retinal detachment.
●• Retinal detachment in the other eye. •

Presentation Title 41
 macular disorders

age related macular degeneration

retinitis pigmentosa

by: rand fraij

The macula is the •
round area at the
center of your retina,
at the back of your
eyeball.
Responsible for •
focusing central vision
in the eye, and it
controls our ability to
read, drive a car,
recognize faces or
colors, and see objects
in fine detail.
The macula has a high •
concentration of
cones, which help you
process the details in
your vision.
Age related macular degeneration
• An aqciured degeneration of the macula that causes significant central visual
impairment.
• The most common cause of blindness in individuals>65 in developed countries
Age of onset usually > 55 years old •
Females > males •
It has two major forms : dry AMD and wet AMD . •
Risk factors include : advanced age, family history, gender, •
cardiovascular diseases, smoking, obesity, race (more common in
white).
Age related
macular
degeneration
Pathophysiology: •
The retinal pigmented epithelium (RPE) removes and processes the •
used discs of the photoreceptors. Over time, undigested lipid
products, as age pigment lipofuscin, accumulate in the RPE and the
excess material is transferred to Bruch’s membrane, impairing its
diffusional properties.
Extracellular deposits form between the RPE and Bruch’s •
membrane which can be seen with the ophthalmoscope as
discrete, sub-retinal yellow or white lesions called drüsen.
Dry AMD (~90%) : the accumulated drusen on RPE will later on cause •
slowly progressive central retinal atrophy and retinal degeneration .
This type is also known as non-exudative or non-neovascular. Slowly
(years).
Wet AMD (~10%): choroidal neovascularization between RPE and •
bruch’s membrane , causes leakage of intavascular fluid and proteins
which causes edema which will lead to localized elevation of the
macula and/or RPE detachment and hemorrhage. This type is also
known as exudative or neovascular. Rapidly (over weeks to months) .
Clinical presentation:
Blurred central vision. •
Difficulty performing tasks that require focusing ( reading , driving ) •
Metamorphopsia : type of visual distortion in which straight lines •
appear wavy, can be tested by amsler grid .
Scotoma : areas of loss of visual field. •
A reduction (micropsia) or enlargement (macropsia) of object size may •
also occur
amsler grid test for metamorphopsia
Investigations :
1-Fundoscopy: dry AMD: drusen RPE atrophy.
wet AMD: Grayish-green discoloration under the macula, retinal edema and
elevation
• 2- Fluorescence angiography:
Gold standard in confirming wet AMD
Dry AMD: well-defined hyperfluorescence of the altered retinal pigment epithelium

Wet AMD: neovascularization and exudation (diffuse hyperfluorescence) in the macular region

3- Optical coherence tomography (OCT) : Detection of intraretinal or subretinal fluid retention Helps confirm the
diagnosis of wet AMD and to monitor progress under treatment.
Treatment:
Dry AMD : no casual treatment is available •
Supportive treatment:
1- patient education
2- avoid risk factors (e.g; smoking)
3-Antioxidants therapy: vitamins A, C, and E, beta-carotene, zinc
4-Visual and reading aid ( magnifying glass).
For wet AMD:
• First-line:anti-VEGF injection (ranibizumab,bevacizumab) into the vitreous cavity, They reduce
visual loss and restore the normal anatomical appearance of the macula.
• Second line: Photodynamic therapy, intravenous dye activated by laser , local toxic effect,
thrombosis of subretinal neovascularization .Needs to be repeated every few months
 Retinitis pigmentosa

A group of Inherited disorder of photoreceptors which has several

genotypic and phenotypic varieties.
It may occur in isolation or in association with a number of other •
systemic diseases, like:Usher’s syndrome (a recessive disorder
characterized by deafness and retinitis pigmentosa).
 phathophysiology
The disease affects both types of photoreceptors but the rods are particularly •
affected.
- Inheritence could be: •
autosomal dominant; later onset and milder degree •
autosomal recessive (sporadic cases are often in this category) •
X-linked recessive. •
- X-linked recessive and autosomal recessive disease produce the most severe •
visual symptoms and may present in infancy or childhood.
• Several forms of retinitis pigmentosa have been shown to be due to mutations in the gene for rhodopsin.
Clinical presentation
diagnosis
Usually made clinically through careful •
family history to determine the mode
of inheritance.
Fundoscopy: •
1- peripheral clumps of retinal •
pigmentation (termed bone spicule’
pigmentation);
2 -attenuation of the retinal arterioles; •
3 -disc pallor – optic atrophy. •
diagnosis

Electrophysiological •
tests are also useful
in diagnosis. The
electroretinogram
(ERG) response may
be lost early in the
disease, where there
may be few clinical
signs.
complications
1-macular edema: treated with acetazolamide.

2-Post subcapsular cataract: treatedwith surgery.

management
Unfortunately, nothing can be done to prevent the progression of the disease. •
Associated ocular problems can be treated. Cataracts can be removed, and
macular oedema may respond to treatment with acetazolamide
The possibility of genetic counselling should be discussed with the patient. •
Prognosis •
X-linked recessive and autosomal recessive disease produce the most severe •
visual symptoms. About 50% of all patients with retinitis pigmentosa will have
an acuity of less than 6/60 by the time they reach 50.
Often leads to blindness •
Vascular occlusions:
-Arterial occlusions.
-Venous occlusions.
 Retinal Arterial occlusions

Central retinal artery occlusion (CRAO)

Branch retinal artery occlusion (BRAO)

Etiology : • Risk factors •

-carotid artery HTN
stenosis DM
-Vasculitis AGE
-arrhythmia
 Clinical presentation :

-Sudden, painless loss of vision • -Scotomas •

in one eye.
-Amaurosis fugax : transient •
episode of complete / partial
monocular blindness that lasts
from seconds to minutes ( due to
decrease blood flow to retina)
 Ophthalmoscopic findings :

- Cherry-red spot at the fovea centralis

-Retinal emboli:
◦ Hollenhorst plaque: cholesterol
embolus that presents as a refractive,
iridescent lesion (∼ 20% of cases)
◦ Whitish-gray platelet thrombi
◦ White calcific plaques
Cherry red spot
 No Treatment

IV acetazolamide ( to decrease -
IOP ) ● Patients may also benefit from •
Eyeball massage - Surgery ( paracentesis of the
Vasodilators ( Calcium channel - anterior chamber ) to decrease
blockers ) intraocular pressure
 VENOUS OCCLUSION
Definition: Occlusion of one of the four branches of the central retinal vein
• Central retinal vein occlusion (CRVO) :

Non-ischemic CRVO (venous stasis retinopathy) ◦ .1

Ischemic CRVO (hemorrhagic retinopathy) .2

• Branch retinal vein occlusion (BRVO)

The exact cause is unknown

Risk factors :
Systemic diseases: •
Atherosclerosis .1
HTN .2
DM .3
Thrombophilic disorder .4
age .5
 Presentation :
-Patient complains of a sudden partial or complete loss of vision in the
affected eye.
Ophthalmoscopy findings :

-Flame-shaped hemorrhages
CRVO : all segments •
BRVO : one segment •
-Cotton wool spots
-Macular edema
 Treatment :
Ischemic CRVO must be treated BRVO and non-ischemic CRVO
with: usually do not require treatment.
PRP : • - If macular edema is present:
-Corrects ischemic hypoxia and intravitreal injection of steroid Or
thereby minimizes anti-VEGF
neovascularization.
A technique that uses a laser to
cause thermal burns to retinal
tissue.
 DIABETIC
RETINOPATHY
1)Type I : is due to loss of insulin
secretion, mostly in young people .
2)Type II : is due to high insulin
resistance , mostly in older people .
Diabetes is associated with the following ocular event :

 retinopathy
 cataract: a rare, acute ‘snowflake’ cataract in youth related to
extreme fluctuation in glucose levels, and a greater frequency and
earlier onset of age-related cataract
 glaucoma (certainly, rubeotic glaucoma, but an association with
chronic open-angle glaucoma is disputed)
 extraocular muscle palsy due to microvascular dis ease of the
third, fourth or sixth cranial nerves.
■ Duration of diabetes:{80% with DR after 20 years)
■ Poor diabetic control( high glucose levels)
■ Coexisting Disease especially HTN
■ Smoking
■ Pregnancy: can accelerate retinopathy and need careful
screening (eye test at 28 wks)
■ Diabetic retinopathy is a microvasculopathy disease that cause :

1. Retinal capillary occlusion by : capillary basement membrane

thickening , abnormal proliferation of capillary endothelium ,
increased platelets adhesion , increase blood viscosity , defective
fibrinolysis .
2. Retinal capillary leakage by : loss of pericytes , weakening of capillary
wall , which will result in (edema , hard exudate , retinal hemorrhage).
- Diabetic retinopathy is asymptomaticin early stages of the disease

- As the disease progresses symptoms mayinclude :

■ Blurred vision
■ Floaters (small dark shapes that float across your vision)
■ Fluctuating vision
■ Distorted vision
■ Dark areas in the vision
■ Poor night vision
■ Impaired color vision
■ Partial or total loss of vision
 Proliferative Diabetic Retinopathy (PDR)

■ There are three types depend on the anatomical location :

1. Neovascularization on the disk (NVD) .

2. Neovascularizatin on iris (NVI) .

3. Neovascularization elsewhere .
 Diabetic Macular Edema

■ The macula is responsible for central vision.

■ Diabetic macular edema may be Asymptomatic at first , As the edema
moves in to the fovea (the center of the macula) the patient will notice
blurry central vision, the ability to read and recognize faces will be
compromised.
Investigations

1) Visual acuity

2) Fundus exam : looking for abnormal blood vessels,

scars , bleeding or retinal detachment .

3) Fluorescent angiography: inject a dye into arm vein , to

reach blood vessels and detect leaky or closed blood
vessels .

4) Slit lamp examination: will be able to detect

hemorrhage,new vessels ,exudates, and retinal
thickening due to edema .
5) Optic coherence tomography (OCT) :cross sectional
image of the retina that show the thickness of the
retina, so we can detect macular edema or cysts .
Complications

 Vitreous hemorrhage : new abnormal blood

vessels bleed into retina, may causes acute
vision loss if it is severe.
 Retinal detachment : new blood vessels
stimulates growth of scar tissue, which
can pull the retina away from the back
of the eye.
 Glaucoma : new blood vessels grow in the front
part of the eye thus block fluid from draining
out of the eye.
 Primary open angle glaucoma is the most
common type.
 Blindness
Treatments
■ Controlling diabetes and maintaining the HbA1c level in the 6-7% range are the goals in the
optimal management of diabetes and diabetic retinopathy.
■ Rx depends on the type of DR:
■ Maculopathy : first line (Anti-VGEF)\second line Laser and (Steroids) to reduce macular edema
and risk of blindness
■ NPDR: Follow up
TREATMENTS AND
PROCEDURES
Hawra Jalab
Retinal laser treatment
Retina Laser works by creating photocoagulative reaction at site of application, in simple
language it creates a scar which is a toughened area at site of application

two main type of lasers used in treatment of Retina diseases according to their spectral
wavelength i.e. Green and Yellow / there is also red laser used for certain situations ( retinal
hemorrhage and retinopathy of prematurity. Most commonly used is called ARGON GREEN
LASER.

Indications for retinal lasers:

- Diabetic Macular oedema
- Peripheral retinal degenerations/holes/tears
- Proliferative diabetic retinopathy
- Eales disease and other retinal vasculitis
- Macular oedema due to retinal vein occlusions
- Central serous retinopathy
-Neovascularization secondary to retinal
- Retinopathy of prematurity
vein occlusions
-Extrafoveal polyps of polypoidal choroidal
vasculopathy (PCV)
 It is an in clinic procedure lasting about 15
Procedure minutes :

- First the patient is prepared by dilating the

-
pupil and giving anesthetic
- Using the slit lamp to visualise the retina
- Using a special lens to direct the laser
during procedure
Proliferative diabetic
retinopathy (PDR) - Optic disc and retinal new vessels are
treated with scattered laser burns to the
entire retina (pan-retinal laser or PRP),
- leaving an untreated area around the optic
disc and around the central region of the
macula, to preserve vision.
- The laser treatment ablates are as of
ischaemic retina
- thus reducing the release of
vasoproliferative factors from the retina as
a whole.

- This results in the regression of the new

vessels and prevents the development of
advanced retinopathy.
 - Here laser is directed at special areas
Macular edema - Identified points of leakage
- This promotes destruction and closure
of the vessels stopping leakage and
preventing the edema from
progressing
- If treatment is effective the edema and
exudate will resorb but may take few
months
- Sometimes combined with anti-VEGF
injections
 More uses

Retinal tear: Retinal Vein Occlusions:

Laser treatment can be used on area of tear Is some situations is used to suppress
sealing it off and preventing fluid from edema formation and growth of new vessels
accumulating under the tear
Risk and side effects

● Temporary pain or ache of the eye during or after treatment

● Bleeding in the eye
● Decreased peripheral or night vision
● Retinal scarring
● Reduction in contrast sensitivity
● Need for retreatment
Anti - V EGF treatment

Currently anti-VEGF treatment is used for the

following conditions:

wet age-related macular degeneration (wet AMD)

diabetic macular oedema (DMO)

macular oedema caused by retinal vein occlusion

myopic choroidal neovascularisation (myopic CNV).

Pathophysiology

The most important factor in retinal New vessels are sight threatening because
neovascularization appears to be vascular they are fragile and tend to bleed to obscure
endothelial growth factor (VEGF)
the media.
which targets mainly vascular endothelial They are also associated with fibrosis and
cells but can also act on retinal pigment
membrane formation which leads to traction
epithelium (RPE) cells.
retinal detachment.
Leading to the formation of new blood
vessels in the retina
 Bevacizumab is a full-length recombinant
Pegaptanib humanized anti-VEGF monoclonal antibody
a 28 nucleotide RNA aptamer that binds to the (IgG)
VEGF-A165 isomer initially FDA approved for treatment of
metastatic colorectal cancers.
used predominantly in the treatment of DME It has twice the half-life of ranibizumab.
its use has declined in favor of antibody-based
treatments.
Ophthalmic uses of bevacizumab are not
FDA approved however many studies prove
its efficacy
Ranibizumab
is a recombinant antibody fragment of the humanized anti-VEGF monoclonal antibody. Based on bevacizumab,
ranibizumab underwent affinity maturation to increase binding affinity to all isoforms of VEGF.
Its half-life is shorter (administered once a month) than other anti-VEGF molecules due to the lack of the
antibody Fc domain making it also smaller
The smaller size is thought to facilitate easier penetration into the the retina and faster clearance systemically;
however, this may also expedite clearance from the vitreous.

Ranibizumab binds to the receptor-binding site on VEGF-A, which inhibits the binding of VEGF molecules to their
receptors on the surface of endothelial cells
Aflibercept
a recombinant fusion protein of the binding domains of human VEGF-R1 and VEGF-R2, fused with the Fc
domain of human IgG1 (so longer half life).
It binds endogenous VEGF molecules to prevent their activation of VEGF-R, and it has been shown to bind
VEGF with greater affinity than other anti-VEGF agents. Additionally, it can bind placental growth factor
(PIGF). FDA-approved for the treatment of neovascular age-related macular degeneration (AMD)

Comparisons
Aflibercept successfully inhibits VEGF for an entire 7 day period, but ranibizumab only 72 hour/
bevacizumab displayed inhibition for just 48 hours.
In terms of prolonged VEGF inhibition, aflibercept is the most effective, followed by ranibizumab,
and bevacizumab as the least effective
 Vitreoretinal surgery
Uses and indications

● Diabetic retinopathy
● Floaters and flashes: Flashes occur when vitreous moves around in the eye and pulls on the retina,
creating a flash of light. Floaters occur when small substances form in the vitreous or from a retinal
tear or a hemorrhage.
● Macular holes: Age-related condition in which the vitreous shrinks and pulls the retina, tearing a hole
in a section called the macula (center of the retina where most focus occurs), affecting vision.
● Macular pucker: A wrinkle in the very small area of the retina that’s responsible for focus, causing
distorted vision.
● Retinal detachments or tears:
● Retinitis pigmentosa:
● Retinopathy of prematurity: Eye disorder of the retina that primarily affects premature babies.
Because the retina is not fully developed, abnormal blood vessels can grow into it, leading to
distortion and detachment of the retina.
● Retinoblastoma: A form of eye cancer that is almost always diagnosed in infancy or early childhood.
Vitreoretinal surgery

2 main types : posterior and anterior

1Anterior : Sometimes vitreous gel comes out through the pupil in the anterior segment of the eye. This may occur
due to eye trauma or injury, lens problems or during cataract or glaucoma surgery. This vitreous is therefore removed
via the anterior approach to prevent problems later on like retinal detachment and glaucoma and to promote recovery.

2Posterior : Pars plana vitrectomy (PPV) is a more commonly employed technique in vitreoretinal surgery that
enables access to the posterior segment for treating conditions such as retinal detachments, vitreous hemorrhage,
endophthalmitis, and macular holes in a controlled, closed system. The procedure derives its name from the fact
that vitreous is removed (i.e. vitreous + ectomy = removal of vitreous) and the instruments are introduced into the
eye through the pars plana.
Retrobulbar Anesthesia
to obtain akinesia of the globe, as well as sensitivity block.
The types of regional anesthesia are specific nerve branch blocks
(e.g. supratrochlear, infraorbital), retrobulbar, peribulbar, and
subtenon.
located behind the globe of the eye.
Complications
Retrobulbar hemorrhage
Ocular perforation
Subarachnoid or intradural injection
Diplopia secondary to myotoxicity
Cardiorespiratory distress
Contusion and atrophy of the optic nerve
Vascular retinal occlusion
Seizure
Corneal abrasion
Chemosis
Ptosis
 Components
Vitreoretinal ● Vitrectomy machine (e.g., Alcon
surgery Constellation, DORC EVA, Bausch + Lomb
Stellaris PC)
● Surgical microscope and wide-angle viewing
system (e.g., Zeiss RESIGHT, Oculus BIOM,
AVI)
● Infusion cannula: to maintain intraocular
pressure set by the vitrectomy machine
● Endoillumination light source: for
visualization of the posterior segment
including vitreous and retina
● Vitrectomy cutter (or vitrector): for vitreous
removal, aspiration, and peeling and cutting
membranes among other functions
Complications
Vitreoretinal
Vitreoretinal surgery employs inert gases and
silicone oil to flatten the detached retina and

surgery endoscopic probes which allow manipulations in the

vitreous space and the dissection of microscopic
membranes from the retinal surface.

Example : Vitreoretinal surgery for traction retinal

detachment, requiring excision of the contracting
bands, is required to repair these detachments. In
these cases, it may be necessary to inject silicone oil
into the vitreous cavity, temporarily ,to hold the
retina in place.
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