VITREORETINA

dr.Reinne Natali Christine, SpM

Dept. Ilmu Penyakit Mata
FK UKI / RSU FK UKI
RETINA

• The innermost layer of the eyeball.

• It is extremely thin and transparent

(0.5mm)

• It contains visual receptors of the eye

• The retinal neurons transmit the picture

through the optic nerve fibers to brain for
perception
 STRUCTURE OF THE RETINA

• There are 10 layers in the retina

• Retinal pigment epithelium

• Layer of rods and cones
• External limiting membrane
• Outer nuclear layer
• Outer plexiform layer
• Inner nuclear layer
• Inner plexiform layer
• Ganglion cell layer
• Nerve fibre layer
• Internal limiting membrane
RETINAL RECEPTORS
THE RETINAL RECEPTORS ARE DIVIDED INTO TWO MAIN POPULATIONS

Rods Cones

• Function best in dim light • Function best in daylight

• There are 125million rods in the
retina
• Rods are relatively poor in visual
details
• There 6 million cones in the
retina
• Cones enable us to see small
visual details
• Helps to visualize the colors
FOVEA AND ORA SERRATA

• The cones form a concentrated area in the retina known as fovea (no rods)
• It lies in the center of the macula lutea
• The junction of the periphery of the retina and ciliary body is called ora
serrata
VITREOUS

• The Vitreous humour is a transparent gel that provides a clear optical medium.
• It is helps to keep the three layers apposed to each other
• It occupies approximately 80% of the volume of the globe.
• The vitreous consist of water, collagen fibrils, molecules of hyaluronic acid, peripheral
cells and mucopolysacharides forming a gel like material.
• It nourishes lens, ciliary body and the retina.
RETINAL DIAGNOSTIC TESTS

• Fundus Photography
• Fluorescein Angiography (FA)
• Optical Coherence Tomography (OCT)
• Ocular Ultrasonography
• Electroretinography (ERG)
DISORDER OF RETINA AND VITREOUS

Hereditary retinal Vascular (arteri or

Diabetic retinopathy
disorder vein ) occlusion

Age related macular

degeneration and
Retinal detachment
choroidal
neovascularization
HEREDITARY CONGENITAL RETINAL DYSTROPHIES

1. RETINITIS PIGMENTOSA
2. LEBER CONGENITAL AMOUROSIS
3. CONE-ROD DYSTROPHIES
4. MACULA DYSTROPHIES
DIABETIC RETINOPATHY

Year No of adults with People with DR

diabetes in
Indonesia*
2010 (9th) 6,964,000 2,409,544

2030 (6th) 11,980,000 4,145,080

*J.E.Shaw, R. A. Sicree, Global estimates of the prevalence of diabetes for

2010 and 2030, Diabetes Research and Clinical Practice 87 (2010) 4-14

According to IDF (2014), Indonesia already in the 6th rank worldwide with no.
DM case was 9,116,030

10
PATHOPHYSIOLOGY

• The exact cause of diabetic microvascular disease is unknown.

• Exposure to hyperglycemia over an extended period results in biochemical and
physiologic changes that ultimately cause endothelial damage.
• Specific retinal capillary changes :
- selective loss of pericytes
- basement membrane thickening
- changes that favor capillary occlusion and retinal nonperfusion
CLASIFICATION
NPDR
(Non Proliverative Diabetic Retinopathy)
•Loss of retinal capillary pericytes
• Weakens capillary walls
• Causes non-perfusion in capillary beds
and hypoxia
• Divided into mild, moderate, and severe
(and very severe)
PDR
(Proliferative Diabetic Retinopathy)
• Hallmark is retinal neovascularization
– response to ischemia from capillary
closure grow onto lattice of vitreous
– new vessels are fragile and easily
rupture
• Divided into 2 : High risk and advance
MECHANISMS OF VISION LOSS

• Retinal ischemia
• Macular edema
• Vitreous hemorrhage
• Epiretinal membrane formation
• Retinal detachment
• Neovascular glaucoma
NPDR
NPDR OCT
PDR
VITREOUS HEMORRHAGE (VH)
VH ULTRASOUND
TRD ULTRASOUND
EPIRETINAL MEMBRANE
TREATMENT

• NPDR without macular edema :

• Observe

• Macular edema :
• 1. Focal/Grid laser photocoagulation
• 2.Vitrectomy with membrane peeling
• 3. Intraocular Steroid*
• 4. Intraocular VEGF inhibitor*
* Off-label use, contraversial
TREATMENT

• Vitreous Hemorrhage:
• 1. Pan-retinal photocoagulation
• 2.Vitrectomy with laser photocoagulation
• 3. Intraocular VEGF inhibitor*

• Traction Retinal Detachment :

• 1. Observation if not involving the macula
• 2.Vitrectomy with membrane dissection

* Off-label use, contraversial

RETINAL VASCULAR OCCLUSION

• Arteri :
Central Retinal Arteri Occlusion ( CRAO)
Branch Retinal Arteri Occlusion ( BRAO)
• Vein
Central Retinal Vein Occlusion ( CRVO)
Branch Retinal Vein Occlusion ( BRVO)
CENTRAL RETINA ARTERY OCCLUSION
(CRAO)

• Unilateral, painless, acute vision loss (counting fingers to light perception in 94% of eyes)
• Occuring over seconds, may have a history of amaurosis fugax.
• Signs:
- A marked afferent pupillary defect
- Narrowed retinal arterioles; box-carring or segmentation of the blood column in
the arterioles.
Clinical finding in CRAO

• VA < 6/60
• APD - marked
• Retinal whitening
• ‘Cherry-red spot’ at macula
• Arteriolar and venular narrowing
• Sludging and segmentation of
blood column (cattle-trucking)
• Very poor prognosis
MANAGEMENT

1. Immediate ocular massage

2. Anterior – chamber paracentesis
3. Acetazolamide, 500 mg I.v. or two 250-mg tablets, p.o and/or a tropical -blocker (e.g.
timolol, or levobunolol, 0.5% b.I.d.) is used to reduce the intraocular pressure
BRANCH RETINAL ARTERI OCCLUSION

• Acute BRAO may not initially be apparent ophthalmoscopically, within hours to days
• It leads to an edematous opacification caused by infarction of the inner retina in the
distribution of the affected vessel
BRANCH RETINAL VEIN OCCLUSION

• Portion of retina involved

• Mostly temporal
- 62% Superotemporal
- 38% Inferotemporal
• Nasal – uncommon & asymptomatic
• Occurs exclusively at arterial overcrossing at
AV intersection by a thrombus
CENTRAL RETINAL VEIN OCCLUSION

Pathogenesis :

Thrombosis of the central retinal vein at and posterior to the level of the lamina cribrosa.

In some cases, a thickened central retinal artery may impinge on the central retinal vein
 turbulence  Endothelial damage  thrombosis
In CRVO vision loss is most commonly sudden:

Mild vision loss  nonischemic CRVO

Severe vision loss  ischemic CRVO

Less commonly, patients may experience premonitory symptoms

of transient visual obscuration before overt retinal manifestations

appear.
 SIGNS

Decreased visual acuity

RAPD: +
Marked venous dilation
Severe splinter and dot hemorrhage in four quadrant
Cotton-wool spots
Macular edema
MANAGEMENT

• Current treatment is directed at secondary complications of CRVO that affect vision,

including:
a. Macular edema  Laser photocoagulation
 Anti VEGF injection ( Ranibizumab,
b. Retinal neovascularization Bevazicumab)
c. Neovascularization iris  Anti glaucoma medicine (if needed)

d. Neovascular Glaucoma
e. Retinal Detachment
• Treatment also involves management of predisposing risk factors, such as diabetes,
hypertension and hyper-lipidemia
RETINAL DETACHMENT

There are three distinct types of retinal detachment (RD). All three forms
show an elevation of retina.
A.Rhegmatogenous (RRD)
B. Non Rhegmatogenous :
- Tractional (TRD)
- Exudative
 Indirect ophthalmology
Condensing lenses Technique

• The higher the power, the less the • Keep lens parallel to patient’s iris plane
magnification, the shorter the working • Avoid tendency to move towards patient
distance but the greater the field of view • Ask the patient to move eyes and head
into optimal positions for examination
RHEGMATOGENOUS (RRD)

• Symptoms
- Flashes of light
- Floaters
- a curtain or shadow moving over the field of vision
- peripheral or central visual loss or both.
• Critical Sign
Elevation of the retina with an accompanying retinal break(s)
 Pathogenesis of rhegmatogenous RD
Two components for retinal break formation
• Acute posterior vitreous detachment (PVD)
• Predisposing peripheral retinal degeneration

Possible sequelae of acute PVD

Uncomplicated PVD (85%) Retinal tear formation and Avulsion of retinal vessel and
haemorrhage (10-15%) haemorrhage (uncommon)
ANOTHER SIGNS

• Pigmented cells in the anterior vitreous

• Vitreous hemorrhage

• Posterior vitreous detachment

• Lower intraocular pressure (IOP) in the affected eye

• The detached retina is often corrugated in appearance.

• An afferent pupillary defect (APD) may be present.

EXUDATIVE RETINAL DETACHMENT

• Symptoms
Minimal – to – severe visual loss or visual – field defect
• Critical Sign :
- Serous elevation of the retina with shifting subretinal fluid (SRF)
- The area of detached retina changes when the patient changes position:
While sitting, the SRF accumulates inferiorly, detaching the retina inferiorly; while in
the supine position, the fluid accumulates in the posterior pole, detaching the macula.)
- There is no retinal break.
• Etiology
• Neoplastic (e.g,choroidal malignant melanoma, metastasis, choroidal
hemangioma, multiple myeloma, capillary retinal hemangioma )
 Fluorescein angiogram and ultrasound may be helpful in making a
differential diagnosis
• Inflamatory disease (e.g,Vogt-Koyanagi-Harada (VKH) syndrome,
posterior scleritis, other chronic inflamatory processes)
• Critical Sign :
- Serous elevation of the retina with shifting subretinal fluid (SRF)
- The area of detached retina changes when the patient changes position:
While sitting, the SRF accumulates inferiorly, detaching the retina inferiorly; while in
the supine position, the fluid accumulates in the posterior pole, detaching the macula.)
- There is no retinal break.
TRACTIONAL RETINAL DETACHMENT

• Symptoms :

Visual loss or visual – field defect; may be asymtomatic

• Critical Signs

- The detached retina appears concave with a smooth surface

- Vitreous membranes exerting traction on the retina are present.

(Detachment may become a convex RRD if a tractional retinal tear

develops.)
Other Signs
- The retina is immobile, and the detachment rarely extends to the ora serrata.
- A mild APD may be present.
Etiology
- Fibrous bands in the vitreous
(e.g. resulting from proliferative diabetic retinopathy, sickle-cell
retinopathy, retinopathy of prematurity, toxocariasis, trauma,
previous giant retinal tear)
- Contract and detach the retina.
PRINCIPLES OF RETINALDETACHMENT SURGERY

1. Scleral buckling • Configuration of buckles

• Preliminary steps
• Localization of breaks
• Cryotherapy
• Insertion of local explant
• Encircling procedure
• Drainage of subretinal fluid
• Causes of early failure
2. Pneumatic retinopexy
• Giant tears
3. Vitrectomy
• Proliferative vitreoretinopathy (PVR)
• Diabetic tractional RD
THANK YOU