RETINAL DETACHMENT (RD)

&
AGE RELATED MACULAR
DEGENERATION (ARMD)

Dr. Jyotsna Pandey

ANATOMY
DEVELOPMENT OF RETINA:
from optic cup

1. Neurosensory part (NSR): inner walls

2. Retinal pigment epithelium (RPE): outer
wall

• Between these 2 layers: Subretinal space

RETINAL DETACHMENT
• Separation of inner neurosensory
retina (NSR) from retinal pigment
epithelium (RPE)
Types
1. Rhegmatogenous RD (Fig A.)
2. Tractional RD (Fig. B)
3. Serous/Exudative RD (Fig. C)
4. Combined tractional-rhegmatogenous
RHEGMATOGENOUS RETINAL
DETACHMENT
Predisposing Factors
• Age : 40-60 years
• Sex : M:F = 3:2
• Myopia/ Aphakia
• RD in fellow eye (Fellow eye becomes involved within 6 months to 1 year )
• H/O Cataract surgery with vitreous loss
• Positive family history
• History of injury or trauma to the eye
• Retinal degenerations :
• Lattice degeneration
• Snail track degeneration
• Degenerative retinoschisis
• Posterior Vitreous Detachment
Symptoms
• Floaters (Dark spots): sudden onset, one eye
• Photopsia: flashes of light
• Blurred vision – Sudden painless LOV
• Visual field defect
• Black curtain like defect

Signs
• RAPD in affected eye
• IOP lower by 5mm of Hg compared to normal
eye
• Mild iritis
• Tobacco Dust Sign / Shaffer Sign- pigment cells
in anterior vitreous
• Retinal Breaks:
• Reddish color
• Round, horse-shoe shaped, slit-like or in the form
of a large anterior dialysis, found in the periphery
(commonest in the upper temporal quadrant)
• Epiretinal membrane
• Detached retina is thrown into folds which oscillate with the movements
of the eye
• Convex configuration, opaque, corrugated appearance due to retinal
oedema with presence of subretinal fluid
 Diagnosis
• History & clinical findings
• Fundoscopy:
• Dilated eye exam a MUST
• Detachments start in periphery, difficult to visualize
• Indirect ophthalmoscopy with scleral indentation

• B-scan USG

• Visual field Test:

• Scotomas corresponding to the area of detached
retina
• Late sign
• Patients less aware of superior field defects
• Most common defect is inferiorly
Location
• Superior field defect indicates an inferior retinal detachment
• Detachments of the superior retina are far more serious
• May rapidly extend inferiorly to involve the macula and thereby cause
the loss of central vision
Fresh Rhegmatogenous RD - Signs

• Convex, deep mobile elevation • Loss of choroidal pattern

extending to ora serrata • Retinal breaks
• Slightly opaque with dark blood vessels
Old RD:
• Retinal thinning
• Subretinal demarcation line
• Intraretinal cyst
PRINCIPLE OF TREATMENT
A. Sealing of retinal breaks – Cryotherapy / Photocoagulation
B. Reducing the vitreous traction on the retina – PPV
C. Flattening of retina by draping of subretinal fluid and external or
internal tamponade – Scleral Buckling / Pneumatic Retinoplexy
TREATMENT
• Prophylaxis: Localization of retinal breaks and treating them with
cryotherapy and laser

Treatment:
• Drainage of subretinal fluid : Inserting a fine needle into subretinal
space and drain away the fluid (Not in all cases)
• Create chorioretinal adhesion by:
• Scleral buckling
• Pneumatic retinopexy (After cryotherapy / laser)
• Pars plana Vitrectomy + Endolaser Photocoagulation + Internal Tamponade
 Localization Of Breaks and Sealing
SEALING
• Cryotherapy:

• Laser photocoagulation:
While viewing with indirect ophthalmoscope
check position of indentation in relation to
break
CRYOTHERAPY LASER
PHOTOCOAULATION
• Surround the lesion with a single • Treatment of choice for
row of application, and prophylaxis except in very
terminate freezing as soon as peripheral retinal break
retina whitens • Surround the lesion with two
rows of confluent burns of
moderate intensity
SCLERAL BUCKLING
• It is a procedure in which material
sutured on sclera create an inward
indentation
• Closes retinal break by apposing RPE to
sensory retina and reduces vitreoretinal
traction
• Explants made up of hard or soft
silicone
 PNEUMATIC RETINOPEXY
• Quick, minimally invasive, office based
procedure
• Small retinal break, breaks extending over an
area of < 2 clock hours in upper 2/3rds of
peripheral retina
• Done after sealing the break
• Intravitreal expanding gas bubble used to
seal a retinal break & reattach retinal
without scleral buckling
• Commonly used gases:
• Sulphur hexafluoride(SF6)
• Perfluoropropane(C3F8)
• Perfluoroethane(C2F6)
Pars Plana Vitrectomy + Endolaser
Photocoagulation + Internal Tamponade
INDICATIONS:
• All complicated primary RD
• All Tractional RD
• In Uncomplicated primary RD – better result
 PARS PLANA VITRECTOMY
• Removal of the vitreous by way of cutting the vitreous
strands with a vitrectomy machine/handpiece
• To remove the membrane over the RD

ENDOLASER
• Apply around the area of tear and hole to create
chorioretinal adhesion
• 2-3 rows of nearly confluent laser burns around
• Firm chorioretinal scar forms in 7-10 days
INTERNAL TAMPONADE
• Gas
• Silicon Oil: Highly viscous, transparent
liquid with high surface tension, lighter
than water
TRACTIONAL RETINAL DETACHMENT
Pathogenesis Etiology
• Progressive contraction of • Proliferative retinopathy due to
fibrovascular membrane over Diabetic retinopathy,
large areas of vitreoretinal Retinopathy of prematurity,
adhesions – leading to Sickel Cell Retinopathy
separation of RPE with NSR • Penetrating posterior segment
trauma
• Retinal dysplasia
• Toxocariasis
Symptoms
- Flashes & floaters usually absent
- Slowly progressive visual field defect

Signs
- Smooth Concave configuration
- Retinal breaks absent
- Immobile retina
Tractional retinal detachment along the superotemporal
- Shifting fluid absent vascular arcade extending temporal to the macula
- Epiretinal membrane
TREATMENT
• Tractional elements (usually
epiretinal or subretinal
membranes) must be relieved -
Pars plana vitrectomy
• Internal tamponade: Gas / silicon
oil
• Can be combined with scleral
buckling
SEROUS RETINAL DETACHMENT
• Characterized by accumulation of SRF (Subretinal fluid) in the
absence of retinal breaks or traction

• Any pathological process that affects choroidal vascular permeability

can potentially cause an exudative retinal detachment.
• Alternatively, damage to the RPE prevents the pumping action of fluid
and can lead to fluid accumulation in the subretinal space
 Causes
• Neoplastic causes- Choroidal tumours: Choroidal melanomas,
hemangiomas
• Inflammatory – Vogt Koyanagi Harada disease, posterior Scleritis
• Central serous chorioretinopathy
• Vascular- subretinal neovascularization, hypertensive choroidopathy in
toxemia of pregnancy
• Iatrogenic- RD surgery & PRP
Symptoms
• Floaters may be present if vitritis
• No photopsia
• Visual field defect

Signs
• Convex, smooth configuration
• Detached mobile retina
• No holes / tear
• Shifting fluid – Changing position of the detached
retina with gravity
Treatment
• Management is usually nonsurgical. Treatment of the cause.
• Any inflammatory disease or underlying mass should be identified
and treated if possible.
• Systemic corticosteroids
• Argon laser photocoagulation: Central serous chorioretinopathy
• Enucleation: Intraocular tumors
AGE RELATED MACULAR DEGENERATION
INTRODUCTION
• K/a senile macular degeneration
• Bilateral disease
• Age: > 60 years
• It is a leading cause of blindness in developed countries

• Acquired degeneration of the retina that causes significant central

visual impairment through a combination of non-neovascular (drusen
and retinal pigment epithelium abnormalities) and neovascular
derangement (choroidal neovascular membrane formation)
RISK FACTORS
• Old age: More after 75 years
• Female
• Hereditary
• Smoking
• Alcohol
• Obesity
• Sun exposure
• Hypertension
• Cardiovascular Disease
• Hypercholesterolemia
 PATHOGENESIS Drusen: Extracellular deposit of
lipid, protein and cellular debris
Hallmark of ARMD
Aging
Light exposure Drusen accumulation (between
Oxidative stress Photoreceptor atrophy
Bruch membrane and RPE)
Genetic predisposition

No exchange between retina

Ischemia of RPE and and choroid (Nutrient from Reduces blood flow from
Photoreceptor choroid to retina / Waste choroid to retina
product from retina to choroid)
 Ischemia of RPE and Photoreceptor

Breaks in Bruch Membrane leads

to blood vessels grows from
choroidal circulation to retina DRY ARMD – 90%
cases
Drusen deposition
WET ARMD Geographic atrophy of RPE

Detachment of RPE
Choroidal neovascularization

New abnormal blood vessels leaks Loss of photoreceptor

serous fluid and blood under retina
CLINICAL FEATURES
SYMPTOMS:
• Asymptomatic for a long period
• Blurred vision – mild to moderate (Dry ARMD), Marked progressive
loss of vision (Wet ARMD)
• Distorted vision - especially the central vision
• Decreased reading ability, especially in dim light
• Difficulty with dark adaptation
Amsler Grid
SIGNS
• Gray-green or pinkish-yellow, slightly elevated,
sub-RPE lesion of variable size: Drusen
• Patchy (geographic) atrophy of the retinal
pigment epithelium
• Subretinal fibrosis
• RPE changes
• Detachment of RPE
• Subretinal fluid or hemorrhage/hard exudate
• Choroidal Neovascularization
DIAGNOSIS
• Clinical diagnosed - Fundoscopy

• Fundus fluorescein angiography and indocyanine

green angiography
• For detecting choroidal neovascularization (CNV) in
relation to foveal avascular zone
• OCT
TREATMENT – DRY ARMD
• NO SPECIFIC TREATMENT
• Modification of Risk factors
• Nutrition supplementation
• Dietary supplements and antioxidants:
• Antioxidants, vitamins and minerals (vitamin C and E, beta carotene, zinc and
copper) could possibly prevent or delay the progression of ARMD
TREATMENT: WET ARMD
• Argon green-laser Photocoagulation : For extrafoveal CNV
• Photodynamic therapy (PDT) : For subfoveal CNV
• Antiangiogenic Agent: Intravitreal Anti – VEGF Therapy ( Bevacizumab,
Ranibizumab) and Intravitreal steroid:
• Transpupillary Thermotherapy
• Radiotherapy
• Surgery:
• Submacular surgery: Vitrectomy, posterior retinotomy and removal of the
subfoveal CNV.
• Macular translocation: Surgically moving the fovea over to an area of healthier RPE
THANK YOU