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 Retina

Inner Most coat of eyeball

Extent : from orra serrata to optic disc margin

Origin Uneven Thinnest area of retina

Ciliary body Ciliary processes

Choroid
Limbus

Sclera
Cornea
Retina ( 10 layers )

Optic disc margin

Lens

Vitreous cavity
Optic nerve ( 1 layer )

Lamina cribrosa

Ciliary zonules

Parts of retina

Central Periphery

Optic disc Macula lutea

( nasal side ) ( temporal side )
Temporal visual field

Optic nerve Head Yellow spot Physiological Blind spot

Negative

or
Blind spot of mariotte Due to Xanthophyll & urochrome

Optic disc
Macula
Optic nerve
Macula: 5.5 mm 2 DD = 2 x 1.5 = 3 mm

Temporal Nasal

Optic disc 1.5 mm

Fovea centralis
1.5 mm
Blind spot on temporal side

Foveola
0.35 mm

Sharpest image is formed Which side of eye is this ?

Ans : If macula is present on right side then it is right eye
If macula is present in left side then it is left eye
Densely packed with cones no rods
So it is right eye
Floor Thinnest part of Retina
Fovea centralis
Rim Thickest part of Retina

Overall thinnest part - Orra serrata

 Foveola - foveolar reflex ( Shinning reflex )

FAZ (Foveal avascular zone) - inside foveola centralise and outside foveola
0.4 - 0.6 mm in diameter

No vascular supply

Laser photo coagulation is contraindicated

Ophthalmoscopy

Distant direct ophthalmoscopy Direct ophthalmoscopy Indirect ophthalmoscopy

Done by direct ophthalmoscope Done by indirect ophthalmoscope

Used when
Hazy media, uveitis, cataract

Direct ophthalmoscope Indirect ophthalmoscope

Used to see central fundus Used to see periphery
Area seen : 2 DD Area seen : 8 DD
Image formed : Virtual, Erect, Magnified Image formed: Real, inverted, magnified
Magnification : 15 times Magnification : 5 times

Distant direct ophthalmoscopy : Direct ophthalmoscopy form distance

25/33/40 cm

Left eye
Nasal, Right side Temporal, Left side

Red glow - due to chorio capillaries

Physiological cup

Macula
Vein
 Blood supply

Outer 4 layers + macula Inner 6 layers

By choriocapillaries Central retinal artery

Layers of retina

1. RPE - Retinal Pigment Epithelium

Melanin
Bruch’s membrane of choroid

Sub retinal space Contains sub retinal fluid

2. Layers of rod and cones ( Photoreceptors ) First order neurons Contains outer segment and inner segment

3. External limiting membrane Outer segment

Layer of rods and cones

Inner segment
4. Outer Nuclear layer - Nuclei of rod and cones
External limiting membrane
Outer Nuclear layer

5. Outer plexiform layer - synaptic cleft and Rods and cones Outer plexiform layer

Synaptic cleft

6. Inner nuclear layer - Contains nuclei of bipolar cells ( II order ) > amacrine, horizontal, muller cells

7. Inner plexiform layer - Synapse between ganglionic cells ( III order ) and bipolar cells

8. Ganglion cell layer - contains dendrites of Ganglionic cells

9. Nerve fibre layer - contains axons of Ganglion cells

Continues to form optic nerve
In optic neuropathy - Ganglion cell death

10. Internal limiting membrane

Choroid
RPE
Retina Sub retinal space Neurosensory retina
Neurosensory retina ( 9 layers )
RPE
Vitreous
Transparent/ colourless
Sub retinal space
Red glow from choroid

1. The layer Most resistant to radiation : RPE > GCL

2. The layer Most sensitive to radiation : Layer of rods and cones
3. Optic nerve : NFL
4. Layer Most prone to pathology : OPL & INL
5. Macula- contains all 10 layers

Fovea Foveola centralis

5 layers 6 layers

1. RPE 1. RPE
2. Layer of cones 2. Layer of cones
3. OLM ( ELM ) 3. OLM ( ELM )
4. ONL 4. ONL
5. ILM 5. OPL ( Henle’s layer )
6. ILM
 Histology of retina
Internal

This is on internal side — Internal Nuclear layer

Dark layers are nuclear layer

This is on external side — External nuclear layer

External

Blood retinal barrier

Outer Inner

By tight junction of RPE Retinal vascular endothelium

Broken in CSR ( Central serous retinopathy ) Broken in Diabetic retinopathy

CME ( Cystoid Macular Edema ) Hypertension retinopathy
 Pathologies of retina

1. Roth spots : Present in the SABE ( Sub acute bacterial endocarditis )

Roth spot Multiple superficial hemorrhages

ith
W

White dot Fibrin clot

Etiology : Retinal Hypoxia

2. Vitreous haemorrhage

Blood in vitreous cavity

Clinical features: Sudden painless diminition of vision Mostly posterior segment pathology

Floaters due to climbing in vitreous gel

Absence of the fundal glow ( no red glow )

Etiology : mc cause of vitreous haemorrhage- spontaneous > trauma

mc cause of recurrent vitreous hemorrhages

Young Elderly

Eale’s disease PDR ( proliferative diabetic retinopathy )

Due to hyper sensitivity reaction to TB patients

TOC : Steroids + ATT

3. CRAO ( Central Retinal Arteriolar Occlusion )

Ophthalmic emergency
Due to

Central Retinal artery - 4 end arteries - No collaterals

More common in males of >50 years

MC cause : Thrombosis (80%) > Embolism (20%)

Occur due to Cholesterol crystals known as

Hollen Horst plaques
Retinal hypoxia time 60-90 mins
MC site : Lamina cribrosa

Clinical features : Sudden painless loss of vision

RAPD present ( due to optic nerve disease )

Signs Cherry red spot

Cattle track appearance Segmentation of blood column in veins

CRAO — pale retina

Milky white in colour due to exudate collection in ganglionic cell layer

Absent in fovea centralis

Fovea centralis Ganglionic cell layer absent

Supplied by choriocapillaries

Cherry red spot : only area through which choroid continues to shine
 D/D of cherry red spot

Niemann pick disease Sand hoff disease

Cherry Trees Never Grows Tall in Sand and Mud

Metachromatic leucodystrophy
CRAO Tay Sach disease
Blunt trauma
Gangliosidosis and Gucher disease
Macular edema
( Berlin’s edema )
Pseudo cherry red spot

Treatment 1. Immediate lowering of Intra ocular pressure to dislodge the the thrombus

IV Mannitol
Acetazolamide
Ocular massage
Paracentesis ( aspiration of anterior chamber )

2. Carbol mixture : 95% O2 + 5% CO2 = for vasodilation

To maintain respiratory drive

( if 100% O2 given : Respiratory depression )

3. IV Steroids
Anti coagulants Streptokinase, urokinase, tPA
Embolysis

4. CRVO ( Central retinal venous Occlusion )

Less severe but more common than CRAO

Types

Non ischemic Ischemic

Mild changes Severe changes Edema

Hemorrhages
Hemorrhages Tortuosity
Edema
Tortuosity Ischemia

No treatment required
VEGF release

Neovascularisation Newly formed vessles are fragile

Neovascular glaucoma ( 100 day glaucoma )

It is complication of CRVO Vitreous hemorrhage

Splashed tomato appearance

Treatment : Laser photo-coagulation

 5. Hypertension retinopathy

1. Earliest sign : Nasal angiospasm : thinning of blood vessels in nasal quadrant

Directly proportional to severity of hypertension

2. Arteriosclerosis : increase in total peripheral resistance

Increase in diastolic B.P.

Vicious cycle More angiospasm

Directly proportional to duration of hypertension

3. Increased vascular permeability

Flame shaped hemorrhages

Flame shaped hemorrhages Cotton wool spots Retinal edema

Superficial hemorrhages Soft exudates

Present in nerve fibre layer of retina

Keith, Wagner, Barker — Stages of hypertension retinopathy

I — Mild angiospasm ( A:V from 2:3 to 1:3 )

II — Moderate angiospasm + Salu’s sign
III —Copper writing of f arterioles + grade II changes + Gunn sign and bonnet sign
IV — Silver wiring of arterioles + grade III changes + papilloedema ( marker of stage IV hypertension )

Spasm Change in colour in blood vessles

Bright red

Dark red

Copper coloured Grade III

No blood Silver wiring Grade IV

Tapering/ deflection of f veins W.R.T. AV crossings

1. At AV crossing : Salu’s sign
2. Distal to AV crossing : Bonnet sign
3. Perpendicular to AV crossing : Gunn sign

Mc cause of diminition of vision in hypertension retinopathy — Maculopathy ( Not papilloedema )

6. Diabetic retinopathy
Risk factors : 1. IDDM ( Type I )
2. Females
3. Hypertension
4. Anemia
5. Pregnancy
 Most important factor for pathogenesis of diabetic retinopathy — Duration of Diabetes Mallitus ( >10 years )
Diabetic retinopathy is micro angiopathy
Small

Arterioles Capillaries Venules

Maximum ischemia

Maximum VEGF

Maximum neovascularisation MC - Recurrent vitreous haemorrhage in elderly

MC cause of neovascular glaucoma

ETDRS — Early Treatment Diabetic Retinopathy Study

Stage of Diabetic Retinopathy — 4

1. NPDR ( Non Proliferative Diabetic Retinopathy ) or Background DR — Earliest stage

Earliest sign — Micro aneurysms Pin point hemorrhages

Due to loss of pericytes from the capillary walls

Present in Inner Nuclear layer of retina
Deep hemorrhages — called as Dot- blot hemorrhages

Hard exudates are present in Outer Plexiform Layer

Lipids and lipoprotein deposits
Micro aneurysms

Circinate retinopathy

AV shunt
IRMA : Intra Retinal Micro Vascular Abnormality
Eg : venous changes Bleeding
Loops
Eg : AV shunts ( Arterio- Venous shunts )
Retinal edema

Severity of NPDR : 4-2-1 Rule

Criteria 1. All 4 quadrants have micro aneurysms

2. Venous changes in at least 2 quadrants
3. IRMA ( AV shunts ) in at least 1 quadrant

If any 1 criteria present : Severe NPDR

If any 2 criteria present : very severe NPDR

Neovascularisation Micro aneurysms

2. PDR ( Proliferative Diabetic Retinopathy ) — Always occurs after NODR

Neovascularisation ( Hallmark )

NVE NVD

Elsewhere Disc

Along major blood vessles Optic Disc

 3. Diabetic Maculopathy — Macular involvement

CSME - Clinically Significant Macular Edema

1. At macula Edema
Exudates

or, 2. Within 500um from centre of macula

with 3. Increased retinal thickening atleast 1 DD ( due to edema )

Maculopathy can occur after NPDR

PDR

4. Advanced Diabetic Eye Disease — Complications

Neovascular glaucoma (NVG), Tractional Retinal Detachment (TRD),

Screening of Diabetic Retinopathy

IDDM/ Type I NIDDM / Type II

Start within 5 years of diagnosis Immediately/ ASAP

Early onset so duration is less Adult onset so duration is less

Follow up

NPDR — Mild : Yearly

Moderate : 6 monthly
Severely : 3 monthly

PDR — 2 monthly

Diminition of vision in Diabetic Retinopathy

Sudden Gradual Cataract

Tractional Retinal Detachment (TRD)
NPDR PDR Diabetic retinopathy

MCC : Maculopathy MCC: Recurrent vitreous haemorrhage

Most important test to see changes in Diabetic Retinopathy

Breakdown of Inner Blood Renal Barrier

Fluorescein Angiography

Fluorescein dye is injected in Anti cubital vein

 Treatment of Diabetic Retinopathy

1. Control of Blood Sugar because chances of Diabetic Retinopathy are due to glycemic end products
2. PRP ( Pan Retinal Photo coagulation ) — Laser
Whole Retina : 2000-3000 Laser spots
Each laser spot : 500 um foot 0.1 second
Distance between 2 spots : 500 um
Started from periphery to centre leaving macular area (FAZ = Foveal Avascular Zone)

Blind spot
Total area = Ring scotoma

Diminition of vision in Diabetic Retinopathy is irreversible

PRP is done to prevent complications

3. Maculopathy Focal laser Photo coagulation ( lesser energy )

or
Intra vitreal Injection of Triamcinolone (Steroid)

4. Intra Vitreal Injection of anti VEGF agents Severe / very severe NPDR
PDR
Ranibizumab or Lucentis
Bevacizumab or avastin
Pegaptamib or macugen

5. PPV : Pars Plana Vitrectomy — Aspiration of fibro vascular tissue from vitreous cavity through Pars Plana to prevent TRD

7. ROP ( Retinopathy of Prematurity )

<28 weeks - Period of gestation

<1.7 kg - Birth weight

Exposed to high [O2]

Prone to obliteration because of immature retinal vasculature

Due to release of VEGF

Intense fibrovascular proliferation especially behind the lens

Hence called Retrolental fibroplasia

Leucocoria d/d
1.PHPV
Leucocoria
2. Congenital cataract
3. Retinoblastoma

Stages of ROP - 5
TRD
1. Dermarcation of line : Between the vascular and avascular retina
2. Ridge : permanent line
3. Ridge with fibro vascular proliferation
4. Subtotal RD ( TRD )
5. Total RD
 Zones and Extent

3 Clock hours

Zone I : Concentric circle centered on optic nerve

Radius = 2 x distance from nerve to fovea
= 2 x 2 DD = 6 mm

Zone II : concentric annular area from outer border of zone I

2DD
to the Orra serrata nasally and just beyond equator temporally

Zone III : Temporal crescent from outer border of zone II to temporal orra serrata

ROP — Plus Disease

TAVE Tortuous arteries

Engorged veins

Treatment of ROP

Threshold Disease

5 contiguous areas or 8 non contiguous areas in stage 3 + Zone I/II with plus Disease

Pre threshold Disease

1. Zone I + any stage + plus disease

2. Zone I + stage 3
3. Zone II + plus disease + stage 2

Treatment : Photo coagulation upto the orra serrata ( to burn fibro vascular proliferation )

Screening

<28 weeks >28 weeks

Examined within 2 weeks <1.7 kg >1.7 kg

Examined within 3 weeks Examined Within 4 weeks

2-4 weeks from birth/ 32-36 weeks from periods of gestation

8. Retinitis pigmentosa

MC hereditary pigmentory dystrophy of Retina affecting Photo receptors ( rods >> cones )

Involve RPE Degenerative

More common in males

Bilateral
Symmetrical

Inheritance : MC - sporadic (35%) > familial

Most common
AR>AD>XR
Best prognosis Worst prognosis

Symptoms : 1. Rods >Cones Earliest sign Night blindness

2. Delay in dark adaptation
3. Tunnel vision or Tubular vision

Signs : Triad
1. Pale yellow wavy optic disc
2. Pigmentory spicules
3. Attenuation of retinal arterioles

Ring scotoma

Tests : EOG ( Electroculography ) & ERG ( Electroretinography )

EOG done in sitting position and ERG done in supine position

Eye Retina

Resting potential between cornea ( + ve charged ) and macula ( - ve charged )

Resting potential
+ —

Light adapted state

Spikes Maximum spike
X 100 = Arden’s Ratio
Dark adapted state Minimum spike

Normal : >185 %
Borderline : 180-150%
Sub normal : < 150
Flat : <125
ERG ( Electroretinography )

Change in the potential induced by flash of light

3 waves a - negative wave

b
Positive wave
c

a - from Rods and cones ( I order neurons ) Rods are affected a wave affected

b - From muller cells s to

II o
rder
g oe
tial
ot e n
- shows activity of bipolar cells ( II order neurons ) Affe
c te d
p

c - RPE activity (pigmentory dystrophy) - abnormal Wave

Hence all waves are affected

Therefore best test for retinitis pigmentosa = ERG
 Systemic associations of Retinitis pigmentosa

Acanthocytes /
spurr cells

Ocular associations of Retinitis Pigmentosa

POAG
Myopia
Keratoconus
VKC
CME
9. CSR ( Central Serous Retinopathy )

Macula SRF Collection

Spontaneous detachment of neurosensory retina from RPE in macular area = collection of SRF

Foveal depression

Neurosensory retina
CSR Sub Retinal space
RPE

More common in males

20-50 years
Type A personality Hurry
Worry
Curry
Stress, Smoking, Steroids

Clinical features : Sudden painless diminition of vision (6/9 to 6/24)

Metamorphopsia ( Distorted images ) Metamorphopsia ( Distorted images )

Acquired hypermetropia Correctable with plus lenses

Due
t o

Decrease in effective axial length

Tests : 1. Slit lamp Bio-microscopy or Direct ophthalmoscopy

Better
Circular ring sign

Normal
2. OCT (Optical coherence tomography)

Neurons sensory retina Foveal depression

OCT findings in CSR patient

SRF

RPE

3. Confirm by FFA ( Fundus Fluoroscein Angiography )

Mushroom pattern/ Ink Blot pattern/

Umbrella pattern/ Enlarging dot sign
Smoke stack pattern

Treatment : Just wait and watch for spontaneous resolution ( usually self limiting : 4-12 weeks )
10. CME ( Cystoid macular edema )

Cyst like spaces in macula due to collection of fluid in outer flexiform ( Henle’s layer ) and INL

Etiology : Mc inflammation after cataract surgery known s as Irvine-Gass syndrome

Retinitis pigmentosa
Posterior uveitis
Niacin toxicity
Prostaglandin analogues
Diabetic Retinopathy
Epinephrine (CME in aphakia )
CRVO /BRVO

Clinical features : Sudden painless diminition of vision

Metamorphopsia

Tests : 1. Slit lamp Bio-microscopy or Direct ophthalmoscopy Honey comb appearance

2. OCT (Optical coherence tomography)

3. FFA : confirmation : Flower petal appearance

Due to radial/ petalloid arrangement of the fibres in the Henle’s layer

Treatment: Steroids + Causative treatment

 11. ARMD (Age Related Macular Degeneration)
>60 years
Males = Females
Bilateral
Symmetrical

MC cause of irreversible diminition of vision in developed countries

ARMD

Dry/ Geographic (90%) Wet (10%)

Main lesson : Drusens Choroidal neovascularisation After thickening of Bruch’s membrane

Extra cellular eosinophilic deposition between the Bruch’s membrane and RPE Dysfunctional Bruch’s membrane
+
Atrophic areas in retina
+
Irregular pigmentation RPE
Choroid

Mild or no diminition of vision

Treatment: No treatment
Multivitamins + anti oxidants RPE PED
Choroid

Pigment epithelial detachment

CNVM
Drusens ( Choroidal Neovascular Membrane )

Clinical feature : Severe diminition of vision

Treatment

Extra Foveal area Foveal / sub Foveal area

Laser photo coagulation 1. TOC : Anti VEGF agents

2. Previously TOC : PDT ( Photo Dynamic Therapy )

Using a light activated compound

Known as Verteporfin

Followed by Diode laser

3. Transpapillary thermotherapy

RPE

PED

Choroid
 12. Angiod Steaks

Pigmented Steaks due to changes in elastic fibres of Bruch’s membrane of choroid

Etiology : P - pseudoxanthoma Elasticum - MC

E - Ehler Danlos Syndrome
P - Paget’s disease
S - sickle cell Retinopathy
I - Idiopathic

13. Salt and Pepper Retinopathy

Yellow and black flecks in retina

Congenital Rubella
Congenital Syphillis
Fungus flavimaculatus
Atypical Retinitis Pigmentosa
Phenothiazine toxicity ( Thioridazine )
Cerebro Maculo facial Degeneration

14. Photo Retinitis

Retinopathy by light IR Emitted by Sun during solar eclipse known as Solar/ Eclipse Retinopathy
UV
Visible blue

Causing foveolar defect

RPE defect surrounded by mottled pigment

Rarely cause FTMH ( Full Thickness Macular Hole )

Latent period : 4-6 hours

Fundus is normal

15. Macular dystrophy

MC - Stargardt’s disease ( Fundus flavimaculatus )

Autosomal recessive
Diffuse deposition of lipofuschin ( Golden brown pigment ) in RPE of macula — Beaten bronze appearance

FFA - fluoroscein dye — Auto fluorescence

Lipofuschin covers fluorescence

Silent choroid or Dark choroid

EOG Subnormal / Normal ERG

Age : young
Best Vitelliform macular dystrophy/ Best disease
2nd mc macular dystrophy
Autosomal dominant
Mutation of Bestrophin gene
Localised deposition of lipofuschin in RPE of macula — Egg yolk appearance
Age : Children and young

Best test for Best disease : EOG

Abnormal EOG with relatively Normal ERG

EOG : measures resting potential ERG : a wave : Rods and cones : Normal
Macular dystrophy : affects -ve charge of macula b wave : Bipolar cells : Normal
Hence abnormal EOG is obtained c wave : RPE : Abnormal
Only decreased c wave

Bull’s eye Maculopathy / Annular Benign Concentric Macular Dystrophy

Patients present with Fundus and FFA findings

Patients taking 500 mg/ day Hydroxychloroqine

Chloroquine derivatives
- Drugs used in treatment of malaria, rheumatological and dermatological disorders
- Toxicity : CQ - 3 mg/ kg/ day, HCQ - 6.5 mg/ kg/ day for 5 years
Cumulative dose: > 460 g for CQ and > 1000 g for HCQ
- MOA : Drug + Melanie in RPE > prolonged effect
- The primary damage is to the Photo receptors and as the ONL degenerates, there is secondary disruption of the RPE

Screening of Chloroquine toxicity

- Aim - Early detection and minimisation of toxicity
- Baseline examination within 6 months of prescription
- Routine ocular follies up every 6-12 months
- Amsler grid once a week
- If abnormality suspected: Automated VF, SD-OCT and mfERG

Rule of 5 ( screening purposes ) Visual acuity and Fundus examination

Fields ( perimetry ) : central/ paracentral
Multifocal ERG : potential
Spectral OCT : layers of Retina seen
Auto fluorescence : lesions

Risk factors : Rule of 5

1. Daily dose : > 3 g/kg/day for CQ and >6.5 g/kg/day for HCQ

2. Cumulative dose : > 460 g for CQ and >1000 g for HCQ

3. Liver/ Renal disease

4. Duration : > 5 years

5. Also using Tamoxifen

 Retinal detachment

Misnomer : It is actually separation of RPE from neurosensory retina

Retinal Detachment

Rhegmatogenous (MC) Exudative Tractional

RRD ERD TRD
Retinal hole : most imp risk factor
Due to pushing of retina towards vitreous cavity Occurs due to pulling of retina towards vitreous cavity
MC Shape — Horse shoe shaped by collection of exudates/ fluids / tumor cells due to dense fibro vascular tissue in vitreous cavity
Site — Superotemporal quadrant
Old vitreous hemorrhages
Other risk factors
Smooth convex RD
Males, old age, trauma, High myopia, Etiology : PDR - mc
lattice Degeneration, pseudophakia Sclera Eale’s disease
Choroid
Aphakia RPE Trauma
Neurosensory retina
Sickle cell Retinopathy
Clinical features
Sudden painless diminition of vision Sudden painless diminition of vision Only RD which causes Gradual painless DOV
Photopsia + floaters : Unique to RRD No photopsia or floaters
Flashes of light Dark spots B scan USG
Curtain like effect Greyish reflex present
TRD
Shifting fluid levels - Pathognomic
Ophthalmoscopy : Greyish reflex Movement Concave / tent shaped

N : Red reflex

Sheffer’s or Tobacco dusting sign : pigment

Dispersal in anterior vitreous Change in the levels of the fluid due to
movement of patients due to gravity Treatment :
Lincoff rule : to locate retinal hole 1. Laser photo coagulation
On Indirect Ophthalmoscopy Etiology : Renal hypertension
In 99.9% cases Eclampsic Retinopathy to stop vitreous hemorrhages
( Gestational HTN + proteinuria + seizures )

Hole is 1-2 clock hours on most Coat’s disease 2. PPV : pars plana vitrectomy
( idiopathic vascular telengiectasia )
convex side of RD
12 1
11
VKH syndrome Vitreous aspiration of fibro vascular tissue
Intra ocular tumors :
1. Retinoblastoma 3. RD surgery
2. Malignant melanoma of choroid
Test : RAPD present in large RD
Indirect ophthalmoscopy Treatment of ERD : Causative treatment
Confirm : B scan USG
Brightness/ 2D USG Coat’s disease
Unilateral, idiopathic vascular telengiectasia
Total funnel Shepard RD
more common in boys, <10 years

TRD : B scan

Posterior vitreous detachment

Vascular malformation
Confuse with: CD /PVD / RR
Choroid detachment
Inflammation
Combine A and B scan
High spike
rn
ea
RD Exudates
Co
Sclera

Complicated cataract
Inflammatory glaucoma
Leucocoria
ERD
M spike : CD
No spike : PVD
Treatment
1. Sealing of retinal hole by lesser Photo coagulation
2. Scleral buckling/ encirclage operation Most imp step

Silicon patch Convex

Encircling sclera
Fix the retina

ERD : B scan
Suturing

3. Internal temponade:

Reverse hypopyon
Silicon oil
or
Heavy gases : SF6 gas

Remove within 3 months

because of ADR
Eg: Oil granuloma

Inverse hypopyon
4. Drainage of SRF especially in long standing cases

Horse shoe shaped

Funnel shaped Optic nerve shadow

B scan
 Tumors of eye

Primary Secondary ( metastasis )- mc

Intra orbital Intra ocular

Adult Children Adult Children

Cavernous hemangioma Rhabdomyosarcoma Malignant melanoma of choroid Retinoblastoma

Benign Malignant

Malignant: NHL Benign : dermis cyst

NON HODGKINS LYMPHOMA

Retinoblastoma

Arises from blast cells of Retina

Gene mutation 13q14
Knudson’s 2 hit hypothesis
MC age of diagnosis : <3 years ( 1.5 years )

Types

Sporadic (90%) Familial (10%)

Unilateral Mostly : Bilateral

Somatic Germ line

Non hereditary Hereditary
(2/3) (1/3)
Unilateral Bilateral

Total no of bilateral cases : 25-40%

MC tumor associated with Retinoblastoma : Pinealoblastoma

MC secondary tumor ( patient is disease free ) : Osteosarcoma

Unilateral
Retinoblastoma Bilateral
Trilateral = Bilateral Retinoblastoma + Pinealoblastoma

Microscopy Mc : Flexner–Wintersteiner rosettes

Homer wright rosettes
Pseudorosettes
Fleurettes

4 stages
1. Quiescent/ Asymptomatic : Signs >> symptoms
Earliest sign : Leucocoria ( 1st MC )
2nd MC : Squint ( convergent )
Nystagmus, poor vision, ERD

1.5 year baby with leucocoria

1st d/d should be Retinoblastoma

2. Glaucomatous ( 3rd MC sign )
Buphthalmos ( IOP )

3. Local spread - MC Optic nerve

4. Distant metastasis Direct route

Lymphatic
Blood route ( most severe )

Liver
Most common cause of death

Tests : B - scan
CT - scan - calcification, not preferred in children
MRI - better to see calcification
It will also show optic nerve involvement

Plasma LDH levels : Not diagnostic, only prognostic value

Treatment :1. Unilateral, <10 mm — tumor destruction by laser photo coagulation or cryotherapy
2. Unilateral, >10 mm — TOC : Enucleation
3. Bilateral, metastasis present : TOC — chemo

VEC regimen

Vincristine, Etoposide, Carboplatin + life long surveillance

Rb can mimic inflammatory condition Pseudo uveitis or Masquerade syndrome