Ophthalmology Notes: RETINA

R E T I N A

ANATOMY

Thickness-
Peri-papillary-0.56mm
Equator-0.18-0.2mm
Ora serrata-0.1mm
surface area-266mm2
Optic disc-pale pink
-1.5mm
Disc appears white due to lamina cribrosa & medullated n fib behind it & absence of vascular choroids.
Grey spots in lamina are d/t non-medullated n fib reflecting less light than white fib

MACULA LUTEA
5.5mm
Fovea centralis-1.85mm dia
-5 deg. Of visual field
-most sensitive part
-no rods, only cones
Foveola-0.35mm
-situated 2DD away from temporal edge of disc & 1mm
below the horizontal meridian
Umbo-correspond to foveolar reflex o’scopically

Foveal avascular zone-500µm
-inside the fovea but outside foveola

Parafovea-0.5mm
Perifovea-1.5mm

LAYERS OF RETINA
1.RPE
2.Rods & cones
3.External limiting membrane
4.Outer nuclear layer
5.Outer plexiform layer RREOOIIGNI
6.Inner nuclear layer
7.Inner plexiform layer
8.Ganglion cell layer
9.nerve fibre layer
10.Internal limiting membrane

Retinal pigment epithelium-
outermost layer
RPE is firmly adherent to the underlying Bruch’ memb & loosely attached to layer of rods & cones
Potential space bet RPE and sensory ret- subretinal space.
Adjacent RPE cells are connected with each other by tight junctions-zonula occludens & zonula adherens & constitute the outer blood retinal barrier
RPE cells at the fovea are taller, thinner,& contain more & larger pigment granules,thereby a dark colour
Functions-
photoreceptor renewal & recycling of vit A
Outer BRB actively pumps ion & water out of SR space
Transport of nutrients & metabolites
Phagocytic action
Mechanical support photoreceptor processes

2.Layer of Rods & Cones-
* Photoreceptors transform light energy into visual impulse
* Rods contain photosensitive visual purple-Rhodopsin subserve peripheral & scotopic vision [low illumination]
* Cones concerned with central vision [photopic vision] & colour vision
Rods- 120 million
Conec-6.5million
Highest density of cones- at fovea
No of cones falls off rapidly outside the fovea
Cone density is greater on nasal side & inferior retina
Rods are absent at the fovea,present in a ring shaped zone 5-6mm from the fovea.
Rods are max below the disc & number reduces towards periphery
ROD CELL-
40-60µm long
Outer seg is cylindrical,transversel striated & contains visual purple
Outer seg is attached to inner seg by a cilium.
Inner seg is thicker-2 regions-ellipsoid & myoid
Outer rod fibre arises from the inner end of rod,passes thru ELM swells into a densely staining nucleus- rod granule & then terminates as inner rod fibre.
Inner rod fibre at its end has an end bulb-Rod spherule which is in contact with the cone plate
CONE CELL-
40-80µm long
Largest at the fovea & smallest at the periohery
Outer segment is conical & contains iodopsin
Inner seg cotains Ellipsoid & Myoid
Ellipsoid is very plump
Inner seg becomes continuous directly with its nucleus & lies in outer nuclear layer
A stout cone inner fibre runs from the nucleus & is provided at its end with lateral processes called Cone foot or cone pedicle
Diag from notes
3. External Limiting Membrane-
* Fenestrated memb extending from ora serrata to optic disc,thru which pass processes of rods & cones
* Formed by zonulae adherenns bet cell memb of photoreceptors & muller cells.

4. Outer nuclear layer-
* formed by nuclei of rods & cones,cone nuclei are larger

5. Outer plexiform layer
* Contiains synapses bet the rod spherules & cone pedicles with the dendrites of bipolar cells & horizontal cells
* thickest at the macula-Henle’s layer

6. Inner Nuclear layer-
* Resembles ONL but is very thin
* It disappears at the fovea
* Contains foll –Bipolar cells
-Horizontal cells
-Amacrine cells
-Soma of Muller’s cells
-Capillaries of central retinal A

7. Innerplexiform layer-
* Contains synapses bet axons of bipolar cells [1st order neuron] & dendrites of ganglion cells [2nd order neuron]
* this layer is absent at the fovea

8. Ganglion cell layer
* 2nd order neuron
* Throughout the ret ,ganglion cell layer contains single row of cells except in macula where it is multilayered
* It is absent at the foveola

9. Nerve fibre layer-
* Contains unmyelinated axons of the ganglion cells whih converge at the ONH, pass thru lamina crib & become ensheathed by myelin post to lamina
* Retinal Vs lie here.

BLOOD SUPPLY OF RETINA-
Outer 4 layers are supplied by choriocapillaries
-RPE
-rods & cones
-ELM
-ONL
2. Inner 6 layers – CRA
-OPL,INL,IPL,GCL,NFL,ILM
3. Fovea is avascular supplied by choriocapillaris
4.Macula- superior & inferior branches of CRA.Sometimes cilioretinal A runs towards the macula-Hockey stick
5.Retinal Vs are end arteriesi.e they do not anastomose with each other.

CENTRAL RETINAL A-diag from diary
Arises from the ophthalmic a near the optic foramina .
Courses forwards as-
Outside the ON-
runs a wavy course below the ON.
10-15mm behind the eyeball,along the inferomedial aspect of the ON,it bends upwards to pierce the dura & arachnoid.
In the subarachnoid space-
-Bends forward & after a short course it bends upwards at right angles & invaginates the pia to reach the centre of the ON
* In the cenyre of the ON
-The A bends forwards & along with the vein which lies on the temporal aspect,it passes anteriorly & pierces the LC
* In the ONH
-Lies superficially in the nasal part of physiological cup,covered by layer of glial tiss[ connective tiss meniscus of Kuhnt] which closes the phy cup
-CRA divides into superior & inferior division,each of which divides into a temporal & nasal br at the disc margin
* In the retina
-The 4 terminal br of CRA divide dichotomously as they proceed towards the ora serrata where they end without anastomosis

RODS- 125 million
-Scotopic vision [dimlight]

CONES- 7 million
-colour vision
-Photopic vision [daylight]

FLUORESCEIN ANGIOGRAPHY-PHASES
Arterial phase Early venous phase

Venous phase Late phase

DIABETIC RETINOPATHY-case
-New name for IDDM-Immune mediated DM
-prevalence of DR- 4-28%
-Incidence of DR is more in IDDM
-Severity of maculopathy is more with NIDDM

INTERNATIONAL CLASSIFICATION
A] Non-proliferative DR
B] Proliferative DR

NPDR-Confined to retina & do not extend beyond the ILM
1] MILD NPDR→ atleast one Microaneurysm +one > more ret haem,HE or CWS
FU – 12 mo
No need of FFA

2]MOD. NPDR→ Haem or ma or both greater than those in std photo 2A of modified airlie House of DR classn in atleast one quad + one / > of the foll-
* CWS
* Venous beading
* IRMA
FU- 6-12 mo
No need of FFA

3] SEV NPDR→ 4:2;1 rule
-Haem or ma or both greater than those in std photo 2A of modified Airlie House of of DR classn in all 4 quad
-Venous beading in 2 /> quad
-IRMA ( > than in std photo 8A) in one quad
FU 3-6 mo
Need FFA
PRP can be done if poor pt FU

4] VERY SEVERE NPDR-presence of any 2 of the above 3 features
FFA is a must

According to ETDRS, sev NPDR has 15 % chance of prog to high risk PDR in 1 year & very sev NPDR has 45% risk

PDR-
1] Early
2]high risk PDR-
1. NVD > 1/4TH – 1/3RD disc area
2. NVD < 1/4th -1/2disc area + VH/ pre retinal haem
3. NVE > / = ½ disc area + VH / pre-retinal haem
3] advanced-asstd with cardiovas dis risk factors
-persistent new Vs-VH
-TRD
-NVG
-Burnt out DR ( ↑ fibrous component and ↓ vascular component )

Patients with PDR are at risk of-
Heart attack
Stroke
Diab nephropathy
Amputation
death

RISK FACTORS FOR DR- [VIVA]
Age- rare before puberty
75 %- after 10 yrs duration
Poorly controlled DM
Renal dis with proteinuria
HT
Hyperlipidemia
Pregnancy

PATHOGENESIS- [pathophysiology-d-05]
Hypoxia plays the major role
2,3, Di-phosphoglycerate influences the O2 dissociation curve
2,3 DPG decrease → decrease O2 release to the tiss→Hypoxia
Raised glycosylated Hb[10-15%] ,[Nml-5-8%]→ greater O2 binding capacity→ Less O2 release→ Hypoxia
Polyol pathway gets activated d/t raised glucose→increased intracellular sorbitol & fructose→Increased osmotic press within cells→cellular edema→.impedance of O2 diffusion into cell→hypoxia
Impaired glucose metab→GH→liver→Fibrinogen}
→α2globulin } →Hyperaggregation of RBCs & platelets→sludging of bld flow
Raised von willebrandt factor viii & antihemophilic factor→platelet adhesion & aggregation
Cell membrane phospholipids acted upon by phospholipase-A2 forms Arachidonic acid
Cyclooxegenase pathway→ Prostacyclin→+platelet aggregtn
[vasodilator]
→Thromboxane-A2→[-] platelet aggregtn
[vasoconstrictor]
Lipoxygenase pathway→Leukotrienes→[-]PGI-2
→[+]TXA-2

Hematological & biochem abnmlt-VIVA
Increased platelet adhesiveness
Increased RBC aggregation
abnml ser lipids
Defective fibrinolysis
Abnml levels of GH
Upregulation of VEGF
abnml ser & whole bld viscosity

PATHOLOGY
DR is a microangiopathy affecting pre-capillary arterioles,capillaries &post-capillary venules.
*DR →Microvascular occlusion
→Microvascular leakage

MICROVASCULAR OCCLUSION-
1] Due to Capillary changes→
-loss of pericytes
[earliest microscopical lesion.Results from sorbitol accumn]
-BM thickening[nml- 0.5µ,becomes 5 times thick]
-endothelial cell proliferation

2] Due to Haematological changes→
-Rouleaux formn
-RBC deformt
-Platelet stickiness
-Platelet aggregatn
Microvascular occlusion→Retinal ischaemia→A-V shunts
→vasoformative
Subst→NV→Iris→ Rubeosis iridis
→retina→proliferative RP

MICROVASCULAR LEAKAGE-
Breakdown of inner BRB→leakage of plasma constituents
Physical weakening of capillary walls→localized saccular outpouchings→microaneurysms [ SN-NOTES]
Increased vascular permeability→Intraretinal h’age
→Retinal edema
Retinal edema→Diffuse→d/t extensive capillary dilatation &
Leakage
Localized→-Focal leakage from microaneurysm & dilated capillary segment
-Chronic localized edema→ hard
Exud

VIVA- Hypoxia suggested by-
CW spots
IRMA
Venous beading
Extensive ret h’age
Iris NV

Potential visual loss in DR-viva
Macular edema ( capillary leakage)
Macular ischaemia ( capillary non-perfusion)
Sequelae from ischaemia induced NV
Visual loss in IDDM-PDR
Visual loss in NIDDM- Macular edema

CW SPOTS-[SN]
-Accumulation of cytoid bodies
-Result from functional obliteration of capillaries
-Focal infarction in inner retinal layers
-Whitish grey,fluffy with feathery edges
-Lie in superficial NFL
-present within few disc dia from the OD
-Appear suddenly & disappear within 4-12 weeks leaving no trace
-Recurrences are never at the same site
-Ischaemia→ axonal obstruction→axonal distension
-Occur where NFL is thick-around the disc & temporal arcade
-Obscure underlying BVs
- seen in-
HTR
Toxaemia of preg
DR
CRVO
BRVO
Anaemia
Leukemia
Collagen dis
Dysproteinemia
Hodgekin’s dis
Pneumonia
SABE
HIV

MICROANEURYSMS-
CRVO
HTR
DR
Coat’s dis
anaemia
Dysproteinemia
Eale’s
-In DR ,microaneurysms arise from the venous side of capillaries whereas in other dis they arise from arterial side
-20-200 µ size
-Present at the level of INL
-not seen with DO .Visible ON FA

DOT-BLOT H’AGES-
-arise from venous end
-level- INL

HARD EXUD-
Level- IPL & INL

IRMAs-Intraretinal microvascular abnormalities-
-Shunt Vs
-Intra-retinal location
-No leakage on FFA
-Do not cross the main retinal Vs

NVD are more dangerous than NVE as they have a more propensity to bleed

NV is common at the OD d/ t absence of ILM

Burnt –out PDR-
Fibrous component of fv proliferation is more evident & vascular component decreases.Bld becomes non-perfused & no proliferation occurs

VENOUS CHANGES-
Beading
Omega looping
reduplication
sausaging
dilatation

EVOLUTION OF NV-3 stages-
Fine new VS with min fibrous tiss extend across the ILM
new Vs increase in size & extent with an increase in fibrous component
new Vs regress,leaving residual fv proliferation along the
post hyaloid

PDR-shows NV,cws,ma,irma

proliferative diabetic retinopathy
proliferative diabetic retinopathy

FA-PDR-shows nvd & MA

DIABETIC MACULOPATHY
DEF- Accumulation of interstitial fluid within the macula with/without hard exud & with/without cystoid changes.

Clinically Macular edema is retinal thickening within 2DD of centre of macula

Most freq cause of visual loss .

PATHOGENESIS
Breakdown of inner BRB at the level of capillary endothelium→leakage of fld & plasma constituents
Source of this fld includes abnormally permeable MA,IRMA,retinal capillaries

CLASSIFICATION-
Recent class-
1. CSME with sponge like thickening
2.CSME with Cystoid macular edema
3. CSME with serous RD
4. CSME with taut post hyaloid membrane
5. CSME with Foveo-vitreal traction

1] FOCAL EXUDATIVE-
Well-circumscribed retinal thickening asstd wih complete/incomplete rings of perifoveal hard exud
FA-focal hyperfluorescence d/t leakage
-good macular perfusion

2]DIFFUSE EXUDATIVE-
-Diffuse retinal thickening with cystoid changes
-FA-widespread spotty hyperfluor.-Flower petal pattern

3]ISCHAEMIC-
-D/t non-perfusion of para-foveal capillaries
-decreased v/a
-nml appear. Of fovea
-FA-capillary non-perfusion at fovea & also at post.pole & periphery
-enlargement of FAZ > 1000µm dia means visual loss

4]MIXED-ischaemic + exud

Diagnosis best made by SL biomicro-
Location of Retinal thickening relative to fovea
Presence & location of exud
Presence of CME

CLINICALLY SIGNIFICANT MACULAR EDEMA-
Retinal edema within 500µm of centre of fovea.
Hard exud within 500µm of fovea with adjacent retinal thickening [ which may be outside this limit]
Retinal edema one disc area [1500µm] or larger, any part of which is within 1DD of the centre of fovea.

Moderate Visual loss –
Def by ETDRS as doubling of visual angle ( decrease from 20/20 to 20/40),a drop of 15 letters or more on ETDRS v/a charts or a drop of 3 or more lines of Snellen

TREATMENT-
1] PHOTOCOAGULATION-

INDICATIONS-
1] Eyes with CSME with centre involved→ consider for immediate t/t
2]Eyes with CSME without centre involved & even good vision should also be considered for immediate t/t.
3]Eye with macular edema which is not clinically significant shud be watched without t/t.

TECHNIQUE-
*Once CSME is detected clinically, do a FA to identify treatable lesions.
*According to ETDRS protocol, these treatable lesions are-
1 ] DISCRETE points of hyperfluorescence/leakage
[ most of these are MA]
2]Areas of DIFFUSE leakage
,i.eMA,IRMA,diffusely leaking capillary zones

* Eyes with sev. Macular ischaemia/ only CME are NOT advised laser therapy as this cud worsen vision.
* Both Argon green & Krypton red are equally effective.

Photocoagulation→ Focal
→Grid

FOCAL PHOTOCOAGULATION-
Goal-TO obtain closure/ obliteration of leakage
Spot size- 100-200µm
Duration-0.1sec
Directly treat all the focal fluorescein leaks which wud include MA,IRMA, or short capillary seg
End-point is whitening/ darkening of the lesion.

GRID PHOTOCOAGULATION-( crimping tech)
* Main aim-To tickle the RPE cells & stimulate the retino-choroidal pump to hasten the absorption of fluid & not to destroy the region.
* Applied to areas of thickened retina showing diffuse fluorescein leakage &/ or capillary dropout.
* Spot size- 100-200 µm
* Duration-0.1 to 0.05sec
* Grid is not placed
- within 500µm of centre of macula
or within 500µm of disk margin
,but can be placed
- in the papillomacular bundle.Peripherally it can be placed in all dir. Upto 2DD from centre of macula or to the border of PRPt/t

FOLLOW-UP-
Review the patient after 4 wks & do FA
If some obvious treatable lesions are missed at the initial session,they are then are treated 4mo later.
Since it may take 4mo for the edema to resolve, retreatment shud not be considered before that.
Follow-up shud be 4mo
Explain to the pt that laser t/t is effective in preventing further visual loss rather than restoring the vision already lost.

COMPLICATIONS-viva
Choroidal neovascular membrane
Choroidal effusion
Ciliary body & choroidal detachment
Transient myopia
Impaired accommodation
Transient increase of aqueous flare
Angle closure glaucoma
Paracentral Scotoma [ d/t direct inv of macula ]
Subretinal fibrosis
10.Inadvertent foveolar burns

Medical Rx of DME-
1) Posterior subtenon inj of triamcinolone acetonide
2) Intra-vitreal steroids
3) Intra-vit anti-VEGF
Avastin (bevacizumab)- 1.25mg/ 0.05ml
Lucentis ( Ranibizumab)- 0.5mg/o.o5ml
Macugen ( Pegaptanib) – 0.3mg/ 90 µl

Surgical Rx of DME-
PPV + detachment of posterior hyaloid ,particularly for posterior hyaloid traction & diffuse DME

2] VITRECTOMY-
Indicated wen macular edema is asstd with tangential traction from a thickened & taut post. Hyaloid membrane

TREATMENT- DR
MEDICAL T/T-
Bld sugar level control
Diet
Exercise
Bld glucose monitoring
Antioxidants-B-carotene,vit E,Zn,se,vitc
Aldose reductase inhibitors→reduce sorbitol→reduce cellular edema & capillary permeability
Eg- sulindac,indomethacin,sorbinil,cyclooxygenase inhibitor
* aspirin 325mg BD for 8 weeks→
Inhibits cyclooxygenase + prostacyclin+ arachidonic acid mediated aggregation
Thus aspirin prevents platelet aggregation
2.LASER PHOTOCOAGULATION
2 major clinical trials-1.diabetic retinopathy study [DRS]
-2.Early treatment DR study [ETDRS]

They recommend –
CSME- Focal photo
-Grid photo
Sev NPDR & PDR – PRP

PAN-RETINAL PHOTOCOAGULATION/ FULL-SCATTER

INDICATIONS
1.PDR with high risk characteristics-
- NVD >1/4th -1/3rd DA
- NVD < 1/4th-1/2 disc area) + VH/pre ret h’age
- NVE > /= 1/2 disc area + VH

2.Presence of fibrous proliferation + TRD +HRC
T/T shud be mild – mod & these areas shud be avoided to prevent extension of TRD into macula

3.Iris & angle NV

4.Very sev NPDR or PDR without HRC

5.Sev ischaemia-i.e –extensive retinal h’age
-capillary- non-perfusion
-multiple & prominent soft exud
All these increase the risk of ant. Segment NV

6.Burnt out RP & regression of RP shud not be t/ted

7.PDR + maculopathy→ Treat maculopathy first→ 2-4wks → PRP
If delay in PRP is undesirable, focal macular Rx + nasal half PRP→ 2-4wks→ completion of PRP.Always treat MP first bcos PRP aggravates mac edema

.Factors known to worsen RP-
1. Pregnancy
2.Nephropathy
3. Cardiac failure
4. Coronary artey dis
5. Cataract
6. YAG laser capsulotomy
7. Uncontrolled bld sugar
*Recent institution of insulin in a pt with longstanding uncontrolled DM
8. Poor pt foll. Up

TECHNIQUE
Laser- argon green/blue green
-hazy media-Krypton red / diode
Mode of delivery-slit lamp/ IO
Parameters-
Spot size-500µ
Duration-0.1sec
Power 250-270mW
Total -1600-2000 burns,one burn width apart.

STEPS OF PRP-
Close to disc & below inferotemporal arcade
Protective barrier around macula to prevent inadvertent t/t of fovea & around superotemporal arcade
Nasal to disc & completion of post.pole
Peripheral t/t until completion

Avoid PRP over-major Vs
-pre-retinal h’ages
-chorioretinal scars
-1DD of centre of macula to avoid risk of h’age/large scotomas
-prominent fv memb
-vr traction
-TRD

COMPLICATIONS-
Reduced night vision, colour v, & peripheral v
Loss of one / 2 lines of V/A
Glare
Temporary loss of accommodation
Macular edema if present prior to PRP gets aggravated

FOLLOW-UP GUIDELINES AFTER PRP-
Change in new Vs since last t/t
Appearance of new Vs[ caliber,degree of network formn,extent of fibrous tiss]
Frequency & extent of VH
Status of vit. Detachment
Extent of photocoagulation Scars
Extent of TRD & fib. Proliferation

ADDITIONAL PHOTOCOAGULATION REQD IF-
1.Lack of regression 6-8 wks after last t/t.
2.Active new Vs [tight Vs,little fibrous tiss,rapid growth in size]
3.Recurring VH
4.Extensive intraretinal lesions [ IRMA,venous beading,blot h’age,retinal edema]
5.Skip areas & room for more burns in betn previous scars

CRYOABLATION
INDICATIONS-
Hazy media
Recurrent VH

C/I- TRD

TECH-
Transconjunctival approach-2 rows of 3-4 applications in each quad,12mm &16mm from limbus
Limbal approach-20 spots in 4 rows in each quad

2 sessions ,1 wk apart
Temp→-60deg cel
Time 10-15sec
BENEFITS-
Accelerated absorption of longstanding VH
Regression of NV

COMPLICATIONS- TRD

4] VITRECTOMY- [J-07]
INDICATIONS- V V V IMP
Non- clearing VH > 3mo
TRD inv macula
TRD + Rheg RD
Sev prog fibrovascular proliferation
Ant seg NV with post seg opacity
Pre-macular h’age
Macular edema with pre-macular traction
Ghost cell glaucoma
Cataract

AIMS/ GENERAL PRINCIPLES OF VITRECTOMY-
To remove visually significant media opacity
To excise & remove entire post vit surf
To remove retinal & pre-retinal fibrovas. Tiss
To treat all retinal breaks
To obtain haemostasis
To flatten retina by internal tamponade with air, gas, or oil
TO prevent further fibrovas. Proliferation & recurrent VH by endophotocoag.

TECHNIQUE-
3 or 4 port v’tomy
Lens removal avoided or done sev wks prior to have more physiological optical system & reduce risk of rubeosis iridis
All ant-post & tangential tractional bands & vit adhesions removed
Circumferential belt buckling -2 or 2.5mm silicone band
Bipolar diathermy / endolaser→ stop bleeding
Retinal breaks t/ted by SRF drainage, retinopexy around the holes with endolaser.

RISKS-
Rubeosis iridis
Cataract
Glaucoma
Recurrent VH
RD

CATARACT Sx & DR-
Pts with CSME, sev NPDR or PDR should undergo photo prior to cat Sx if media is clear enough.otherwise ret should be evaluated after cat Sx.
FOLLOW UP– time table-
0-30 yrs- within 5 yrs of diagnosis→ annually
31 & > -upon diag→annually
Pregnancy-Before conception or 1st trim→every 1-3 mo
Microaneurysms- annually
Mild NPDR- EVERY 9 MO
Mod NPDR-Every 6 mo
Sev NPDR,CSME,PDR-every 2-4mo

DDs-
CRVO-
Sudden UL LOV
Marked tortuousity
Hard exud usually not found
NFL h’ages mostly

BRVO-
h’ages distributed along a vein & do not cross the horizontal raphe.

Ocular ischaemic syn-
Pain
Cor edema
AC reactn
Episcleral congestion
Mid-dilated poorly reactive pupil
NVI
H’ages mostly in mid periphery
Exud absent

HTR-
A:V crossing changes
Fewer h’ages & typically flame-shaped
5. Radiation RP

OTHER OCULAR SIGNS IN DR
1.Visual defects-
Hyperglycemia→ myopia
Hypoglycemia→HM
2.decreased accommodation
3.3rd N palsy
4.painful O’plegia
5. Lids-stye
-xanthelesma
6.Conjunctiva- tortuous Vs + sludging
7. Cornea- Delayed epith healing
-Punctate KP
-Infective keratitis
8. Iris-rubeosis iridis
9.lens-nuclear sclerosis
-snow-flake cat
-early onset –senile cat
10 Vit- VH
11. Retina-DR,CRVO
12. IOP- NVG

OCULAR ISCHAEMIC SYNDROME

DEF-
Results from chronic ocular perfusion sec to sev IL atherosclerotic carotid stenosis.

EPID-
7th decade
UL
Asstd with- DM

-HT
-IHD
-CV disease
Patient gives H/O amaurosis fugax d/t retinal embolism
SYMPTOMS-
Gradual LOV over wks to mo
SIGNS-
ANTERIOR SEGMENT-
Diffuse episcleral injection
Corneal edema & striae
Aq cells
Pupil- mid-dilated & poorly dilated
Iris atrophy
Rubeosis iridis→ NVG
Cataract
FUNDUS-
Venous dilatation + /- mild tortuosity & arteriolar narrowing
Microaneurysms
Dot-blot h’ages
Proliferative RP & PVD
Macular edema
Spontaneous arterial pulsation near OD

INV-
FFA-
delayed & patchy choroidal filling
Prolonged arteriovenous transit time
Retinal capillary non-perfusion
Prominent arterial staining
ERG- Reduced b & a wave amplitude
Rx-
Topical steroids
Topical mydriatics
Rx for NVG
PRP for proliferative RP
Most definitive t/t –Carotid endarterectomy

RADIATION RETINOPATHY

DEF –Devlops foll t/t of IO tum by plaque radiotherapy or external beam radiotherapy
Rare below 3000rads

Presents bet 6mo-3yrs
SIGNS-
discrete capillary occlusion
collateral channels
microaneurysms
macular edema
HE
Flame-shaped h’ges
CW spots
Papillopathy
Prolifrative RP
TRD
Rx-
Laser photo
Steroids-syst for papillopathy
RETINAL ARTERY OCCLUSION case

CLASSIFICATION-
Branch retinal artery occlusion
Central retinal artey occlusion
Cilioretinal artery occlusion

CAUSES-
Atherosclerosis related thrombosis- at the level of lamina
Cribrosa
-MCC of CRAO
2. Carotid embolism
- originates from the bifurcation of common carotid A
-Retinal emboli may be of the foll types-
a. CHOLESTEROL EMBOLI-
Hollenhorst plaques
Located at arteriolar bifurcation

b.FIBRINOPLATELET EMBOLI-
-May cause transient ischaemic attack

c.CALCIFIC EMBOLI-
Originate from –atheromatous plaques in ascending aorta / carotid As & calcified heart valves
-Often located close to the disc
-Very dangerous→ permanent occlusion of CRA

3.Giant cell arteritis
4. Cardiac embolism-
* Since the ophthalm. A is the 1st br .of ICA embolic material from the heart & carotid A hav a direct access to the eye.
* emboli from heart-
1. Calcific from aortic/mitral valve
2.Vegetn from cardiac valves in endocarditis
3.Thrombus from left side of the heart consequent to MI ,MS asstd with AF or MVP
4.Myxomatous material from atrial myxoma

5.Periarteritis asstd with
-Dermatomyositis
-SLE
-PAN
-Weg. Granulom
-Behcet’s dis

6.Thrombophilic disorders-
-Hyperhomocystenemia
-Antiphospholipid antibody syn

[ Cholestrol emboli→ carotid]
[Calcific emboli→ cardiac]

CLINICAL FEATURES
sudden & profound LOV
APD
No direct pupillary reaction
NO PL
Fundus-arteries are reduced to threads
-veins are little altered except on the disc where they
Are contracted
-retina -loses its transparency
-opaque
-milky-white
-cherry red spot-at the fovea where the retina is extremely thin d/t absence of NFL ,the red reflex from the choroids is visible & appears as a round cherry red spot, presenting a strong contrast to the cloudy white background of the surrounding NFL
-cattle truck appearance [boxcarring]-wen obstrn to the bld flow is not complete,the flow may be partially restored.wen gentle pressure is applied upon the globe the venous bld column breaks up into red beads separated by clear interspaces which move in a jerky fashion.
* FA- delay in arterial filling
-masking of choroidal fluorescence
-filling of a patent cilioretinal A during the early phase
*ERG-dimunition of b-wave d/t inner retinal layer ischaemia.

TREATMENT-
INITIAL T/T-
Ocular massage with a 3-mirror contact lens for 10sec to obtain CRA pulsation or cessation of flow foll. By 5 sec of release.The aim is to mechanically collapse the arterial lumen & cause prompt changes in arterial flow.
sublingual isosorbide dinitrate 10mg to dilate peripheral BVs & reduce resistance
IV. Acetazolamide500mg
IV. Mannitol 20 % ,1gm/kg→ reduce IOP

SUBSEQUENT T/T-if the above measures fail in reestablishing the cir. After 20min→
AC paracentesis-wen CRAO <24hrs
-0.1-0.4ml aqueous is aspirated thru the limbus
2. IV streptokinase 750,000u → disintegrate fibrin emboli
+
IV.methyl prednisone 500mg →reduce risk of strepto related allergy & blding
3.Amyl nitrate inhalation→ vasodilatation

SYSTEMIC ASSOCIATION-
Giant cell arteritis
ipsilateral carotid artery disease

CENTRAL RETINAL VEIN
OCCLUSION- case[j-05]

DEF-Obstrn of CRV at the lamina cribrosa.

TYPES-1.Non-ischaemic-75%
Also k/as venous stasis RP or partial CRVO
2.Ischaemic
( complete CRVO)
3.Papillophlebitis

Age-6th-7th decades
UL
CAUSES-viva
1.Vascular-HT
-DM
-atherosclerosis
2. Raised IOP- POAG
-OHT
3.Vasculitis-Sarcoidosis
-Behcet’s dis
-Syphillis
-SLE
4.hypercoagulable state-polycythemia
-Lymphoma
-Leukemia
-SC anaemia
-Multiple myeloma
-Cryoglobulinemia
-Waldenstrom’s macroglobulinemia
-Anti-phospholipid antibody syn
-Activated protein C resistance
-Hyperhomocystinemia
5. Drugs- Diuretics
-OCPs
6.Retrobulbar external compression-TED,orbital tum

3 Basic mech inv in CRVO-
1. external compression on the vein
2.Venous stasis
3. Degenerative changes of venous endothelium

NON-ISCHAEMIC CRVO- [< 10 disc areas of capillary non-perfusion]
MC type [75%]
CLINICAL FEATURES-
-Sudden UL blurring of vision
-visual impairment-mod-sev
-APD-absent/mild
-Fundus-Veins-tortuous & dilated
-Dot-blot & flame-shaped h’ges
-occasional CW spots
-optic disc edema-mild-mod
-macular edema
-FA-delayed venous return
-staining along retinal veins
-microaneurysms
-dilated optic n head capillaries
-retinal capillary non-perfusion-min/absent ( 10 disc areas)

RESIDUAL FINDINGS /longstanding cases-
-Disc collaterals
-epiretinal gliosis
-Macular pigmentary changes
-CME

RISK FACTORS- VIVA
-DM
-HT
-Glaucoma

MEDICAL & OPHTHAL WORKUP-
Slit-lamp exam – iris NV [viva-DR,CRVO,BRVO,RD,ROP,NVG]
Gonio-iris & angle NV[viva-Fuch’s uv,NVG, chr uveitis]
IOP
FA
BP ( bed-side)
Bld sugar (bed-side)
Complete bld count
Prothrombin time
Partial thromboplastin time
Antinuclear antibodies
Serum protein electrophoresis
Lipid profile
Anti-phospholipid antibodies
VDRL & RPR
ESR
ERG decreased b-wave amplitude

TREATMENT-
Foll- up for 3 years to detect conversion to ischaemic CRVO
High intensity laser-
- 50µm spot, power-1.5-2.5W
-create an anastomosis bet retinal V & choroidal V,thereby bypassing the site of obstrn to venous outflow
Risk- Fibrous proliferation at the laser site
-H,age from the ruptured vein or choroidal Vs
Chr. CMO is unresponsive to laser. (Anti –VEGF)

ISCHAEMIC CRVO [>10 disc areas of capillary non-perfusion]
CLINICAL FEATURES-
U/L ,sudden & sev visual impairment
SUDDEN DOV- viva
-CRAO
-RD
-VH
-Acute angle closure glauc
ON-Optic neuritis
-AION
Macula-CSR
-Macular h’age
-Berlin’s edema
-Sun eclipse m’pathy

Painless [occasionally,painful red eye if NVG ]
APD –marked
Fundus-“Tomato splash”/ “ thunderstorm”
-Veins- marked tortouosity & engorgement
-Extensive dot- blot & flame-shaped h’ages –
Periphery post- pole
-CW spots =-numerous
-macular edema & h’age
-Optic disc edema-sev
-Disc-hyperaemia
* FA-Retinal h’ages→ hypofluorescence
-Extensive capillary non-perfusion

COMPLICATIONS-
2 most dreaded –
1] MACULAR EDEMA
2]CRVO → 100 day glaucoma→ NEOVASCULAR GLAUCOMA
Non-ischaemic CRVO- vision loss d/t macular edema
Ischaemic CRVO-vision loss is d/t
1.macular edema
2.ischaemic maculopathy
3.NVG [d/t anterior segment NV]
4VH [traction from the vitreous on the NV]

FOLLOW-UP- monthly for 6 mo to detect ant. Segment NV

Angle NV is the best clinical indicator of the eventual risk of NV glaucoma b’cos it may occur in the absence of NV at the pupillary margin
Therefore, routine gonioscopy of eyes at risk shud be performed,mere SLE of iris is inadequate

TREATMENT-Indication for PRP-Iris NV-
1 . PRP- All 4 quad
-medium white burns
-spot-400-500µm’,0.1-0.2sec,
-Total-1000-2000 burns,1 burn width apart
* Prompt PRP shud be done if iris NV dev.
*PRP shud not be done until most of intraretinal bld is absorbed, which occurs 1-2mo after occlusion
2. Reduce IOP
3. For CME- Grid photo + Anti VEGF
4.For NVG- Trab + MMC
↓
Drainage valve ( Ahmed) to maintain patency which may get occluded by NV tiss
If bad visual prognosis-
Pain reducing Rx- Retrobulbar alcohol
-Enucleation

NON-ISCHAEMIC ISCHAEMIC

1.Vision loss - mod-sev - profound
2.APD - absenr/mild -marked
3.Cw spots - few -numerous
4.disc edema –mild-mod -sev
5.Iris NV& NVG- absent -present
6.Cap.non-perfusn – min/- -extensive

SIGNS OF ISCHAEMIA-
-Fall in central V/A
-Multiple CWs
-Central scotoma
-FA- Increased FAZ & capillary non-perfusion

RECENT MGT-
RETINAL ENDOVASCULAR SURGERY[REVS]
Thrombolytic agents [urokinase,tpa ] are injected directly by cannulating branch retinal vein after a v’tomy

2.SUPERSELECTIVE OPHTHALMIC ARTERY FIBRINOLYTIC THERAPY [SOAFT]
Urokinase is infused into the ostium of oph A with a microcatheter via the femoral A

3.RADIAL OPTIC NEUROTOMY-
A radial cut is made in the optic N from the vitreous side upto the lamina cribrosa & cutting the circle of zinn haller.

4.IV TRIAMCINOLONE-
4mg/0.1ml CMO in CRVO

5.RETINOCHOROIDAL ANASTOMOSIS

CRVO STUDY-
This study has recommended PRP for eyes with atleast 10 disc areas of capillary non-perfusion & iris NV & Grid photo for macular edema

D/Ds-
1.DR
DIFF bet
CRVO DR
1. UL 1.BL
2.Sudden DOV 2.Gradual
3. Tortuousity is more 3. venous changes
4. OD swelling 4.Absent
5. HE –absent 5.present
6.H’age-flame shaped 6. Dot-blot

Papilloedema-
-Transient LOV [CRVO-acute]
-BL disc swelling
-Flame-shaped h’ages around disc [CRVO-beyond peripapillary area]

Ocular ischaemic syn-
-Veins are dilated but not tortuous
-NVD +
-Transient LOV
-Orbital pain
-Ophthalmodynamometry—ophthalmic A pressure is low in carotid dis but not in CRVO

4.Radiation RP

BRANCH RETINAL VEIN OCCLUSION -case [d-05]

DEF-obstrn of a branch ret V

EPIDEMIOLOGY-
thrice MC than CRVO
M=F
Age-60-70 yrs
Usually U/L, only 9%- B/L

PATHOGENESIS-
Arteriolar dis is the underlying cause
Almost always occurs at the A: V crossing,where the A & V share a common adventitial sheath
The A is nearly always anterior to the vein
Rigid arteriosclerotic A compresses the V→ Turbulent bld flow & endothelial damage→ Thrombosis of vein→ venous obstrn→Elevation of venous & capillary pressure & stagnation of bld flow→ hypoxia of retina drained by the obsrtd vein→ damage to capillary endothelial cells→ extravasation bld constituents→ rise in tissue pressure→ further stagnation
Most BRVO’s occur superotemporally b/o the highest concn of A:v crossings lying here.Visual loss is marked if the suptemp br is inv.
Secondary BRVO-toxoplasmosis [BETS]
-eale’s dis
- Behcet’s
-sarcoidosis
*Associatn-macroaneurysm
-coat’s dis
-retinal capillary haemangioma
-optic disc drusen

RISK FACTORS
1]advancing age
2]Systemic-HT
-DM
-hyperlipidemia
-smoking
-obesity [increase in BMI]
3] Rise in IOP- POAG
-Ocular HT
4]Inflam-Sarcoidosis
-Behcet’s
-Syphyllis
-SLE
5] Hyperviscosity-Polycythemia [nml platelet-1.5-3.5lac]
-myeloma
-Waldenstrom’s macroglobulinemia
-Leukemia
-SC anaemia
-lymphoma
-Cryoglobulinemia
6] Acquired thrombophilic dis-
-Hyperhomocystenemia
-Antiphospholipid antibody syn
7] Inherited thrombophilic dis
-Increase in factor VII &XI
-Decrease in anticoagulants-antithrombin III,protein C & S

CLASSIFICATION-
MAJOR BRVO-
-Occlusion of a 1st order temporal br at the Optic disc.
-Occlusion of a 1st order temporal br AWAY from the optic disc, but inv br to the macula
2.MINOR MACULAR BR OCCLUSION-inv only a macular br
3.PERIPHERAL BR OCCL-not inv macular cir.

BRVO-
Ischaemic BRVO-> 5disc areas of retinal capillary non-perfusion.
Non-ischaemic BRVO- < 5 disc areas of ret capill non- perfusion

CLINICAL FEATURES-
sudden onset of blurring of vision
visual field defect
metamorphopsia
Fundus-venous dilatation & tortuousity peripheral to the site of occl.
-flame-shaped h’ages
-Dot-blot h’ages
-retinal edema
-CW spots
All these affect sector of retina drained by the obstructed vein.
As a result of distribution,the h’ages assume a triangular appear,with the apex at the site of blockage

MILD OBSTRN-small amt of h’age
COMPLETE OBSTRN-extensive intraretinal h’ages,CW spots, & widespread capillary non-perfusion

Shows collaterals

Retinal NV
VH
Ant segment NV-rare
Collateral Vs & microvascular abnormalities.collaterals cross the horizontal raphe
Proximal to the site of blockage,the retinal veins become sclerotic
The retinal A that feeds the affected zone may become narrowed & sheathed
Microaneurysms & lipid exud
Capillary non-perfusion seen after h’ages hav cleared
Late phase of BRVO-chronic CMO→ epiretinal memb &macular RPE changes
RD – rhegmatogenous & tractional
If sev ischaemia-exudative ,localized RD in the distribution of BRVO
Macular edema is exudative or ischaemic.? [ VIVA]

MCC of vision loss in BRVO- [VIVA]
Non-ischaemic BRVO- d/t macular edema
Ischaemic BRVO- d/t-macular edema
-ischaemic maculopathy
-VH
FA-
Arterial filling –nml
Venous filling-in affected v delayed
Hypofluorescence-h’age & capill non-perfusion
Dilated & tortuous capillaries
Collateral Vs may cross horizontal raphe
Retinal vein walls stain at the site of occln
NV fronds leak dye,but collaterals DO NOT leak
Classic petalloid CME

D/D-
HTR-
-narrowed retinal arterioles
-A: V crossing changes
-Haem are not confined to a sector & usually cross the horizontal raphe.
-mostly BL
DR-
-Haem extend across the horizontal raphe
-BL
Ocular ischaemic syn
Juxtafoveal retinal telangiectasia-
-retinal telangiectasia of capillary bed
-hard exud
Combined BRAO + BRVO
Radiation RP-
-focal retinal capillary non-perfusion
-papillopathy
-hard exud

SYSTEMIC ASSTN
HT [MC]
CV dis
Increase in body mass index
Glaucoma
Raised serum α2 globulin

REDUCED RISK-
alcohol
raised HDL cholesterol

COMPLICATIONS-
Macular edema
NV [due to traction from NVE]

MEDICAL EVALUATION-
1. BP
2.Fasting BSL & glycosylated Hb
3.Complete bld count & DLC
4.prothrombin time
5.partial thromboplastin time
6.ESR
7. Lipid profile
8. ANA
9.Homocysteine
10. Cryoglobulins
11.Anti-phospholipid antibodies
12. Ser protein electrophoresis
13. Tests for syphilis,sarcoidosis

TREATMENT-
FOR MACULAR EDEMA & BRVO→
Wait for clearance of retinal h’age for 3-6mo to allow adequate FA
Determine if V/A is caused by – macular edema or macular non-perfusion
If macular edema→no spontaneous improvement for 3mo→Grid photo
IF macular non-perfusion [FA-enlarged & irregular FAZ]→ Laser NOT advised

FOR NV & BRVO→
Good quality FA obtained after h’ages have cleared
If > 5DD of non-perfusion→foll-up at 4mo interval to see for dev of NV
If NV dev→ PRP to inv sector with argon,med white burns,200-500µm,1 burn width apart
Vitrectomy→for-non-clearing VH
-epiretinal memb
-tractional RD with macular edema

NEW T/T→
Sheathotomy
IV. Triamcinolone [ 4mg/ 0.1ml ] & anti-VEGF
vitrectomy
`
EALE’S DISEASE-case

DEF-Idiopathic obliterative vasculopathy

EPIDEMIOLOGY-
Henry eales
Healthy young adult men

AETIOLOGY-
1.allergy to tuberculoprotein
2.focal sepsis
3.thromboangittis obliterans
4.inf- brucellosis
-infectious mononucleosis
-leprosy
-syphyllis
5.Immune mediated-
* sarcoidosis
*Behcet’s
* SLE
* Weg granul
6.Toxocariasis
OCULAR-
Pars planitis
Viral retinitis
Birdshot retinochoroidopathy
Coat’s

PATHOLOGY-
Chronic & incomplete vascular obstrn→ Tiss. Hypoxia which causes →capillary microaneurysm
→NV
Perivascular / intramural infiltration of lymphocytes/granulation tiss without giant cells.
Lymphocytes are T-cell types i.e cell mediated immune reaction
Vasculitis starts in the retinal periphery→ extends posteriorly
Retinal phlebitis leads to CRVO or BRVO

STAGES-
stg of inflammation
stg of ischaemia
stg of NV

SYMPTOMS
-VH → black spots
Floaters
Cobwebs
-Blurring of vision
Pt complains of blurred vision in only one eye, but always examine the other eye.

SIGNS-

A. Stg of inflam- * venous dilatation & tortuousity
perivascular exud
sheathing
superficial h’ages
aq. Flare & cells
KPs

B. Stg of ischaemia-
* intraretinal h’ages
* vascular tortuousity & collaterals around the occluded Vs
* solid white lines-remains of obliterated Vs
*junctn betn perfused & non-perfused retina is well- demarcated with-MA
-AV shunts
-venous beading
-hard exud
-CW spots

C. Stg of NV→ NVE
→NVD
→rubeosis iridis→ NVG
Other changes-
* Healed chorioretinitis
* BRVO
* vitreous condensation→ PVD
* macular changes→ mac. Edema
Ischaemic maculopathy
Macular hole
INV-
X ray chest
Montoux test ( erythema -20×20mm is positive)
Sputum exam
FFA-staining of v wall
-Haem-hypoflu
-Delayed filling
-Capillary non-perfusion
-microaneurysms
-NV

TREATMENT-
1. Medical Rx-
oral prednisone
Anti-TB drugs-HRSEZ
HRZE – 2MO
HR-4MO

2.ANCHORING PHOTOCOAGULATION
In the presence of significant phlebitis with PVR, inflamn is brought under control with oral steroids b4 commencing retinal ablation.
Anchor photo is done to prevent complication resulting from Gliosis i.e –mac det/ distortion
-retinal breaks near the feet of NV mass→ rheg RD
-retinal folds /stress lines across the macula→ cystoid mac degeration

200-300µ spots placed around NV tiss facing the macula → after 3 wks→ photo scars are well formed [thereby anchoring the retina to the underlying choroid→peripheral retinal ablation is done by PRP
-
3.RETINAL CRYOPEXY-for hazy media d/t florid new Vs / VH
4.VITRECTOMY- for longstanding ,non-resolving VH
-Wait for 4-6 mo for VH to absorb on its own.
-During the waiting period do B-scan to r/o RD & PVD which makes Sx easy.
Ind for vitrectomy-
TRD threatening macula
RRD
Rubeosis iridis
BL VH
No sign of clearance of VH in one eyed
Recurrance of VH before full clearance

D/Ds OF VASCULITIS-
PERIPHLEBITIS-
Sarcoidosis-‘ candle wax ‘ exud around veins
Syphillis
pars planitis-most prominent in inferior periphery
Eale’s dis-peripheral NV + avascular retina
Behcet”s dis
Crohn”s dis

ARTERITIS-
1.GCA
2. PAN
3.ARN
4. Behcet’s dis
5. SLE
6. IRVAN (idiopathic retinal vasculitis,aneurysms & neuroretinitis)
7 Crohn ‘s dis
Fresh Vasculitis-
Cuffing
Surrounding retinal edema
Superficial h’ages
Old Vasculitis-
sheathing
Surrounding ret is nml
Sclerotic V

CYSTOID MACULAR OEDEMA-case
[j-o5]
DEF-Fld accumulation in the outer plexiform layer of the macula [henle’s layer] that results in the formtn of visible cystic spaces.

CAUSES-
Postoperative-cataract surg [Irvine Gass syn]
-penetrating KP
-astigmatic cor incision
-scleral buckling
-YAG capsulotomy
-Laser iridotomy
-PRP
-cryotherapy
2.Inherited/dystrophies- RP
-Gyrate atrophy
3.Drugs-topical epinephrine
-nicotinic acid
-OCP
-hydrochlorothiazide
-latanoprost
4.Tumours-malignant melanoma
-choroidal haemangioma
5.Tractional-epiretinal memb
-vitreomacular traction
6.Vascular- retinal vein occlsn
-DR
-HTR
-coat’s dis
-radiation RP
7.ARMD
8.Trauma-cellophane RP
-blunt trauma
-electric inj
-solar RP
-ocular hypotony
9.vitreous pathology-VL
-vitreous adhesion to wound
10.uveitis-ant-non-granulomatous iridocyclitis
-intermed-pars planitis
-post-Behcet
11.Vasculitis- Eale’s dis
-behcet’s
-Sarcoidosis
-CMV retinitis
-Necrotizing angiitis
-MS


CLINICAL FEATURES-
decreased central V/A
metamorphopsia
micropsia
central scotoma
photophobia
conj.injn

DIAGNOSES-
Fundus-altered foveal reflex
Slit lamp biomicroscopy-change in volm
-thickness
-cystoid spaces

FFA- flower petal

*Vitreous fluorophotometry-leakage at BRB can be measured
*Recent-confocal SLO
-OCT

-Retinal thickness analyzers

PATHOLOGY-[d-04]
Large cystic spaces in the –OPL
-INL
-NFL
RPE changes-vacuolization
-depigmentation
-disruption
-atrophy
MGT-[j-05]
1] Topical Indomethacin 1% or Ketorolac 0.5% e/d TDS for 2-6 wks
2]Steroids-
* Topical Prednisolone acetate 1%
*Post subtenon’s methylprednisone or triamcinolone 40mg per 1ml.Total 3 inj at 1mo interval
*Systemic prednisone 1mg/kg
*Intravitreal triamcinolone 4mg/0.1ml
3] T/T according to cause-
* Retinal vascular dis- laser photo
*Inflam dis- steroids/immunosuppressives
*intermed uveitis-sys CAI.steroids,cryotherapy,immunosuppressants,PPV
*Post-cataract surgery-vitreous incarceration
-ant.v’tomy orYAG laser disruption of vit adhesion
-AC IOL removal
-PPV
YAG capsulotomy shud be delayed for 6mo after cat surg
*Drug induced- stop drug
* RP- sys CA inhibitor
* vitreomacular traction- v’tomy
* Epiretinal memb-excision of memb
*ARMD- Intravit steroid
-PDT
-TTT
4 Anti-VEGF
MYOPIC FUNDUS –FFA

MACULAR HOLE-case[j-07]

DEF- Full thickness depletion of retinal neural tiss in the centre of macula

Elderly ( 6th-8th decade) females
bilateral

AETIOLOGY-
Vascular-HTR
-DR
2.Trauma- Blunt trauma
-lightening strike inj
3.CME
4.Epiretinal memb
5.Vitreomacular traction
6.Rheg RD
7.Best’s dis
8.High myopia
9.Inadvertant exposure to laser
10.Idiopathic

PATHOLOGY-
Shrinkage of adherent vit cortex→ Tangential vit traction→circumscribed foveolar detachment→enlargement of macular hole with vitreofoveal separation→ complete PVD

CLINICAL FEATURES-
Hallmark-painless central visual distortion

DIAGNOSES-
1.Slit lamp biomicroscopy
2.WATZKE ALLEN TEST-.
A narrow slit beam is projected over the centre of the hole both vertically & horizontally with a 90D / 78D lens .A pt with a macular hole will report that the beam is broken or thinned.
-Positive in stg III MH

3.LASER AIMING BEAM TEST-
50µm He-Ne beam is projected at the hole. In mac hole the spot disappears. ( which laser used?)

4.FA-corresponding area of hyperfluorescence
Centrifugal displacement of xanthophylls→window defect→ unmasking of choroidal fluor→ thus hyperfluor

5. B-SCAN –for staging of the dis

6 OCT-For diagnoses &stging. Gold std
For volume of full-thickness hole

7. SCANNING LASER O’SCOPY
8 .CONFOCAL TOMOGRAPHY
GASS STAGING-
0 → PRE-MACULAR HOLE
* D/t perifoveal vitreous detachment
* Loss of foveal depression
* Nml V/A
IA→IMPENDING HOLE
*Yellow spot at foveola
Intrafoveal pseudocyst

IB→OCCULT MACULAR HOLE
Centrifugal displacement of foveal retina &xanthophylls
Yellow ring with a bridging interface of vit cortex

II→EARLY FULL THICKNESS MACULAR HOLE
100-200µm
+/- pseudoperculum ( condensed vitreous)
Posterior hyaloid attached

III→ESTABLISHED FTMH
>400µm ( 350-600µm)
Attached post vit phase

IV→ENLARGED HOLE
Complete PVD
Cuff of SRF


LAMELLAR MH-
-Round, central,inner retinal defect without thickening,cystic change or SRF .
-Vitreofoveolar separation occurs with loss of inner retinal layers,however outer photoreceptor layer is intact.
-V/a is good ( 6/6-6/9)

TREATMENT-[j-07]
Stg I holes undergo spontaneous improvement

SURGERY-INDICATIONS-
FTMH upto Stg III
V/A < 6/18
Duration < 1year

CONVENTIONAL VITRECTOMY-
under LA/GA
3 port CORE vitrectomy
Critical step appears to be removal of perimacular tractionSo posterior hyaloid,ILM & ERM shud be removed.
A] POSTERIOR HYALOID-
is removed by inducing complete PVD by suction with a soft tipped cannula.A fish-strike sign or bending of silicon cannula is a sign that post hyaloid has been engaged.Then it may be pulled carefully & removed with a v’tomy cutter

B] ILM-
is first stained with ICG or trypan blue & then peeled off.Recent innovation is scraping the ILM with Diamond Dusted membrane scraper

C] ERM-
is removed with a microvitreoretinal [MVR] blade or fine membrane pick
Air-fld exchange.[C3F8 preferred over SF6]
Strict face-down pos for 4-6 wks

COMPLICATIONS-
Cataract ( MC, d/t accelerated nuclear sclerosis)
Retinal tear/ RD
Intraoperative light/ mechanical toxicity to macular RPE
Enlargement of macular hole
Reopening of successfully closed holes
Dense temporal field defect

D/Ds-
macular pucker-
-Glistening membrane( cellophane mp) to thick gray white memb.
2. CME-cystoid spaces on SL biomicro
-FA-flower petal
3. Vitreomacular traction
4. CNVM
5.CSR
6. Lamellar MH
7.solar rp
PROGNOSIS-VIVA
Anatomical success is defined as complete disappearance of the cuff of SRF that surrounds the MH.When this occurs,the edges of the MH are opposed firmly to the RPE.

Visual success is defined as improvement in postoper V/A of atleast 2 / more Snellen lines over pre-oper acuity

CHEMICAL VITRECTOMY-
For stg III hole
Plasmin is injected into the vit which detaches the vit from the retina without manipulation of the post hyaloid

- MACULAR PSEUDOHOLE-
Within premacular fibrosis
2.Lamellar hole resulting from longstanding CME
3.White dot fovea-white dots arranged in a ring around foveolar margin
EPIRETINAL MEMBRANE-case

DEF-Consists of proliferation of retinal glial cells which hav gained access to the retinal surf thru breaks in ILM

Healthy elderly
Bilat – 10%

CLASSIFICATION-
Grade a-CELLOPHANE MACULOPATHY-
Translucent memb
No tortuousity / obscuration of underlying Vs

Grade b-SURFACE WRINKLING RP
*Memb causes irreg wrinkling of inner retina but details of BVs is visible

Grade c-MACULAR PUCKER
Distortion of full thickness of retina & obscuration of underlying BVs

AETIO-
Surgery-cataract,RD
Ocular dis-retinal vas occlus
-DR
-ocular inflam
-VH
3.Trauma- blunt
-penetrating
4.Foll laser / cryo for ret breaks

CLINICAL FEATURES-
Asymptomatic
Metamorphopsia
Waxing & waning of vision
Fundus- irreg light reflex / sheen at macula
-memb contractn→nerve fib layer distortion→blockage of axoplasmic flow→CW spots
-Pseudoholes
-Ectopia of fovea
-Traction of BVs→ vas. Leakage→ CME
-A pseudohole may dev
Distortion of macular BVs-AV phase
INV-
1.FA-Retinal vas. Tortuousity
-vas leakage
-Diff bet pseudohole & true hole

2.OCT-Thickness of ERM
-Attachment to retina-focal / global
-macular status

ERM
3.VEP-Pattern reversal- prolonged latency & reduced amplitude

4.Pulfrich’s psychophysical stereoillusion +

T/T-If asymptomatic→ no t/t
If vision reduced/ metamorphopsia→ PPV
PPV→ if aphakia/ pseudophakia→complete V’tomy
→if phakic→ant vit behind the lens is left undisturbed to avoid cataract

Edge of ERM is picked up with end opening forceps.

If firmly attached→DELAMINATION→ vitreoret. Scissor[best]
→ viscoelastic delam
OR →ERBIUM YAG LASER→ incision/ ablation

ERM shud be removed after maturation [6-8wks after symptoms]
-Delamination-Horizontal cutting of vascular pegs connecting the memb to the retinal surf
-Segmentation- Vertical cutting of ERM into smaller seg

COMPLICATIONS-
retinal tear
RD
Nuclear sclerosis-to prevent this, cold infusion fld [-4deg c] with high glucose is recommended
DDs-
DR
CME

CENTRAL SEROUS RETINOPATHY-case

DEF- Localized detachment of the sensory ret at the macula +/- PED

EPID-
young / middle aged healthy adult males (25-55yrs)
type A personality
unilateral
self limited

AETIO-
Emotional stress
HT
SLE
Sys steroids
Smoking
Alcohol
Vasoconstrictors
Antibiotics
Antihistaminics

PATHOGENESIS-
Abnormal choroidal cir→ischaemia→choroidal exud→focally hyperpermeable choroid→excess choroidal fld accumulates→RPE detaches→target junc bet RPE cells are broken→bld barrier defect→choroidal fld passes thru this defect→sensory RD

CLINICAL FEATURES-
unilat blurred vision
positive relative scotoma
micropsia/ metamorphopsia
Defective colour vision
V/A-6/9-6/12, correctable to 6/6 with weak plus lens.Elevation of sensory ret →acq hypermetropia→disparity bet sub & objective refraction
FUNDUS-Round/oval detachment at post pole
-SRF – clear/turbid,small ppts on surf of det
INV-
1] Amsler grid
2] Slit lamp biomicroscopy-to rule out CNV
3] FFA-1. SMOKE STACK →
Small hyperfluor spot d/t leakage thru RPE→ flu passes into subret space & ascends vertically from the pt of leakage upto the border of det→ spreads laterally like a mushroom / umbrella until the entire area of det is filled
This unique pattern is d/t convection currents & a pressure gradient bet the protein conc of the SRF & the fluorescein dye.

INK-BLOT→
Small hyperflu. Spot→ enlarges centrifugally
4]OCT-hyporeflective optically clear space s/o serous RD
-PED

5] ICG –to distinguish atypical CSR in older pts from occult CNV in exud AMD & idiopathic polypoidal choroidal v’pathy

D/D-
1] ARMD-> 50 yrs
-drusen
-pigment epith adnmlity
-CNV
2]optic pit-small defect in ON tiss
-serous RD contiguous with OD
-no pin-point leakage ( CSR-pin-pt leakage)
3] Macular detachment foll RRD or macular hole
4]PED
5] Idiopathic polypoidal choroidal v’pathy

T/T-
Wait for 4mo before considering t/t for 1st attack & 1mo for recurrence.
Prognosis for spontaneous recovery is excellent.
Worse prog-Recurrent dis
-multiple detachment
-prolonged course
Ind of laser-
Persistence of serous detachment FOR SEV MO
Recurence in an eye with permanent visual deficit from a previous episode
occurrence in the C/L eye after a permanent visual def from a prev episode
for prompt recovery of vision (occupational need)
C/I-leak in / within FAZ
Argon laser
2-3 low-mod intensity burns are applied to leakage site
200µm,0.2sec

RETINOBLASTOMA-PATHO

DEF-RB is a proliferation of neural cells which hav failed to evolve normally

EPIDEMIOLOGY-
incidence-1 in 34000 to 1 in 14000
avg age of diag- 18mo
u/l or b/l
M= F
Mutation of q14 band of chromosome 13 which is responsible for controlling cell div
Consanguineous marriages

CLINICAL FEATURES-
Amaurotic cat’s eye/ leucocoria –MC,ie yellow reflex from the pupil
Strabismus 2nd MC
cataract
buphthalmos
hypopyon
proptosis

STAGES
Quiescent stg
Tumor is intraretinal without any choroidal invasion
Cat’s eye reflex
Squint

2.Glaucomatous stg-Due to
* NV of iris & TM
*Toxic endophthalmitis from necrotic end products of tum
*Vol of tum may push the iris-lens diaphragm forward & block the angle
*Tum cells may block the TM pores.

3.Stg of extraocular extension-
Tum extends thru the natural opening in * *sclera→orbit→proptosis
*optic N→ cranial cavity

4.Stg of metastasis-
* choroidal Vs
*long bones of limbs,ribs,sternum,cranium
* preauricular glds→ Cx, mediastinal,axillary & inguinal

RB → Exophytic- grows towards the subretinal space
→Endophytic- towards the vit cavity

REESE ELSEWORTH CLASSN-
VERY FAVOURABLE
solitary tum < 4DD at/ behind the equator
multiple tum ,none >4DD & all behind the equator

II.FAVOURABLE-
A.solitary tum 4-10DD at / behind the equator
B.multiple tum 4-10DD behind the equator

III.DOUBTFUL-
A.any tum ant to the eq
B.solitary tum > 10 DD behind the eq

IV.UNFAVOURABLE-
A.multiple tum >10DD
B.any lesion ant to ora serrata

V.VERY UNFAVOURABLE-
A.massive tum inv more than half retina
B. vit seed

INVESTIGATIONS-
ORBITAL X-RAY- Calcification
CT SCAN-HRCT- detects very small calcification, optic N extension & pinealoblastoma
FFA-vascular pattern & degree of vascularization
BIOCHEM TEST-raised aqueous /plasma LDH,phosphoglucoisomerase
FNAB CYTOLOGY-small , round , highly, basophilic cells in clumps/ rosettes

PATHOLOGY-
Poorly differentiated-small to med sized cells
-intensely hyperchromatic nuc [basophilic]
-scanty cyto
-high mitotic figures

B.Well-differentiated-
ROSETTES-better prognosis
FLEXNER WINTERSTEINER RO-columnar cells arranged around a central clear lumen[corresponding to subretinal space]
HOMER WRIGHT RO-tum cells arranged around central
neural fibres.no lumen
[pseudorosettes- tum cells around BVs]
FLEURETTES-flower bouquet type of aggregate of cellular processes that correspond to photoreceptor inner segment that project thru a fenestrated memb

Rb cells tend to outgrow their bld supply & undergo spontaneous necrosis.Necrotic part is eosinophilic [pink] because the dead cells lose their basophilic nuclear DNA

T/T-
Enucleation
Cryotherapy
photo
Radiotherapy
Chemotherapy

ENUCLEATION-
IND-
UL RB provided there is no optic N / choroidal inv & extraocular extension
more affected eye in b/l RB

VIVA- How much length of optic N shud be excised during enuc? & why?
10-12mm [or as much as possible]
-To rule out meningeal inv & vascular inv as CRA supplies the optic N 10 -12mm from behind the lam crib
Enucleation specimen with foll features show poor prog-
ON inv
choroidal inv
scleral inv

CRYOTHERAPY-
IND-
3.5mm dia
3mm thickness
Ant part of sensory ret
No choroidal inv
No vit seeds
TECH-Triple freeze thaw
COMPLICATIONS-
VH
Ret.edema
Ret hole
PVR
TRD

PHOTOCOAGN
IND-
3mm / < dia
2mm thickness
Post sensory ret
No choroidal inv
No vit seeds
C/I-
Within 3mm of foveola
Over papillomacular bundle
TECH-
One/ two rows of confluent burns→obliterate feeding & draining Vs
Repeat after 3-4wks if viable tum left
SUCCESSFUL T/T-
Flat / depressed chorioret scar
No viable tum
No tum vascularity

COMPLICATION-
VH
TRD

RADIOTHERAPY-
IND-
u/l large & multifocal tum
vit seeds
choroidal inv
u/l RB with lesions within 3mm of foveola & over PM bundle or optic disc
residual tum in the distal part of ON
recurrence after enucleation
2 forms-
1. External beam RT
2.Plaque RT

Radioactive isotopes used- I 125,Co-60,ruthenium 106,iridium 192
Avg dose- 4000 rads [40 Gy]

CHEMOTHERAPY-
IND-
orbital ext
choroidal/ ON ext
tum cells on cut end of ON after enuc
trilateral RB
2nd non-ocular malignancy
DRUGS-
vincristine
etoposide
carboplatin

HEREDITY- [j-05]
AD with incomplete penetrance.Therefore does not dev in every person with mutant genes
SPORADIC [60%]- U/L & unifocal

HEREDITARY [40%] → bil. 68%
→ Unil32%
Hereditary RB – younger age
-more Bil
-multicentric
-2nd non-ocular malignancy [osteosarcoma,cutaneous melanoma]-VIVA

* Knudson’s 2 hit hypothesis-
Hereditary-
1st hit occurs in pre-zygotic state→Therefore mutation occurs in all somatic cells
2 nd hit occurs in post-zygotic state→As 1st hit has occurred in all the cells of the body,therefore pts are predisposed to not only RB but also other non-ocular malignancy

Non-hereditary-
Both hits occur after fertilization [post-zygotic state] & in the same retinal cells→ Therefore no risk of 2nd non-ocular malign

GENETIC COUNCELLING

Increase parental age-risk factor
Defective gene-q14 band on long arm of chromosome 13 [13q14]

Parents need clarification on –
1.Possibility of RB if they hav a 2nd issue
2.Possibility of RB in childn of RB survivors

A] HEREDITARY-
*Hereditary & Bil [affected parent & child-Bil.RB]→50% risk in next preg
* Unaffected sibling→ negligible risk for affected child

B] SPORADIC-
No family history + unilat RB in child→ 1% risk in next child
NO family history + BIL RB in child→6% risk in next child

PSEUDOGLIOMAS-
Spectrum of dis that affect lens, vit, retina & choroid.
cong cataract
PHPV
ROP
Toxocara endophthalmitis
Coat’s dis
Retinal dysplasia
Choroidal coloboma

LEUKOCORIA-
same as above

PHPV RB
1. unilat-90% 1.unilat-20-40%
2 .not hereditary 2.AD
3 .microphthalmia 3.nml size eye
4.elongated ciliary processes 4.CP not elongated
5.Retrolental mass early 5.Retrolental mass late
Wen entire globe is
Filled with tum
6.Early cataract 6.Cataract- rare & late
7.Microphakia 7.Nml lens size
8.Hyaloid remnant + 8.Hyaloid remnant –nt
9.No calcification 9.Calcification +
10.Nml aq/ser LDH 10.Abml aq/ser LDH

ENUCLEATION-instrum
DEF-Globe & attached portion of ON are excised from the orbit

IND-ABSOLUTE-
RB.
Malignant melanoma
Sev traumatized eye with ‘no PL’ to prevent sympathetic oph

RELATIVE-1. Painful blind eye-Abs glauc
-chr. Iridocyclitis
-IO h’age
2.Blind & disfigured eye-ant & ciliary
Staphyloma
3.phthisis bulbi
4.endophthalmitis
5.symp oph

C/I-Panophthalmitis [bcos inf can spread via the cut end of ON sheath causing meningitis ]

STEPs-360 deg peritomy→all recti incised except LR 4-5mm stump which is grasped with a clamp for globe removal--. Oblique ms are cut & allowed to retract→ eye is rotated laterally & enuc scissor passed with closed tip from the medial side & abt 10mm of ON cut→ press applied→ tenon’s cap & conj sutured→P & B
Prosthesis may be fitted after 3-4 wks

COMPLICATIONS-
h’age
globe perforation
periorbital swelling & chemosis
inf
discharge from socket
extrusion &migration of implant
ptosis –d/t levator disinsertion
contracted socket-d/t abolition of conj fornix-prosthesis cannot be retained
Post enucleation syn-Deep superior sulcus & inferior displacement of prosthesis d/t vol loss & fat atrophy

EVISCERATION-
DEF-Io contents are removed along with inner 2 coats retaining the sclera & ON
IND-
panophthalmitis
expulsive h’age

STEPS- 360 deg peritomy → whole cor removed→ evis scoop introd bet sclera & uvea & swept 360 deg to separate uvea from the sclera & ON→ IO contents are scooped out specially around the ON & vortex veins→. Press→conj sutured

FRILL EXCISION-A frill / collar of sclera is left around the ON to prevent spread along the ON sheath causing meningitis

COMPLICATION-
globe perforation
excessive blding
cor erosion
sym oph

RETINAL NEOVASCULARIZATION
Sickle cell RP
ROP
DR
CRVO
BRVO
Eale’s dis
Sarcoidosis
Leukemia
VITREOUS HAEMORRHAGE [d-02]-case
TYPES-
1.Intravitreal h’age /Intragel h’age-
Bld within the vit body d/t growth of NVs into the vit
2.Subvitreal / subhyaloid / pre-retinal h’age-
Bld bet the post hyaloid face & ILM-----boat shaped
3. Diffuse h’age-
MC type
4. Retrogel-
When post vit phase has detached

SYMPTOMS-
-Sudden painless DOV
-Floaters [shadows & cobwebs]
-Photopsia

SIGNS-
Best corrected V/A
Ant seg- iris & angle NV
-KPs
-cells in AC
-RAPD
3.IOP-Low- RD, wound leak, open globe inj
-High- NVG, Hemolytic glaucoma,steroid,tum invasion
4. Fundus-
DO- Dark shadow against the glow or no glow
IO- Bld in vit,PVD
CAUSES-ADULTS-
DR
CRVO ,BRVO
Sickle cell RP
Eale’s dis
HTR
Coat’s dis
Radiation RP
Retinal angioma
Uveitis
10.Metastatic IO tum
11.Choroidal mal melanoma
12.Trauma
13. Retinal tear
14. SRNVM
15.Macroaneurysm
16.RD
17.PVD
18. ARMD + CNV
19. Retinal cavernous haemangioma

CHILDREN-
Birth trauma [Terson’s syn]
Shaken baby syn
ROP
Retinal break
RD
RB
Congenital retinoschisis

FATE-
spontaneous absorption-slow & constant process
-seen in dis without tendency of recurrent blding
-syneresis
-aphakia
2.Persist for a long time eg DR
Ochre membrane-VH + RBC +RBC debris+vitreous collagen

INVESTIGATIONS-
Diagnostic USG-
A-scan- chain of low amplitude spikes
B-scan-Dots & short lines
Also reveals- obscured PVD
-RD
-fibrovas proliferation
-tumour
-Retinal tears
2.MRI-To diff subacute VH with RH from uveal melanoma in adults & RB in childn
T/T-
Bed rest & Bil patch with the head end elevated.this reducees the chance of rec blding allows the bld to settle inferiorly→ within 10 days spontaneous absorption is expected→if not, then
Vitrectomy & t/t of underlying cause

Early v,tomy-
Bil VH → blindness
Pre-retinal macular h,age
Acute VH & RD
Type I DM
VH with RD with open globe inj
Advanced PVR where VH does not clear in 6-8 wks

Trauma- time of v,tomy- During prim repair or at an interval, but never beyond 14 days after injury.After 14 days the scleral wound heals & post vit also detaches

Enzymatic v’tomy→ Tissue plasminogen activator→ lysis of clot

Photocoagulation-prophylaxis in-
DR
Eale’s
BRVO

Posterior hyaloidotomy-for h’age bet ILM & ret
Retinal breaks sealed with cryo or laser
RD-scleral buckling+ Drainage + silicone oil

COMPLICATIONS OF VH-
Haemosiderogenic vit syneresis→Hb is broken down→iron toxicity (i.e iron binds with proteins)
Cellophane RP / fixed retinal folds
Siderotic glaucoma
erythroblastic glaucoma-
Ghost cells obstruct the TM
Asstd with broken ant hyaloid phase
5.Erythroclastic glaucoma-
* RBC debris,hb aggregate,& macrophages obstruct Tm
* haemosiderin released from RBCs sticks to the collagen framework of TM→ inflamn of TM→siderotic glauc
6.Necrosis of ganglion cell layer & ON
7.cataract
8.siderosis- cor & retina
9. PVR-MACROPHAGES & CHEMOTActic factors induce fv proliferation→scarring→ RD

D/Ds-
Vitritis-WBCs in vit
-not sudden in onset
-an /post uveitis
-No RBCs in vit
2. RD

RETINAL DETACHMENT -case

DEF-RD is the separation of the neurosensory ret from the RPE with the accumulation of SRF in the potential space bet them

RETINAL BREAK-
A full-thickness break / discontinuity in the neurosensory ret.
a. TEAR-caused by dynamic/static VR traction
b.HOLE-ischaemia→ atrophy→ hole
c. GIANT TEAR-limbus parallel tear greater than 90deg /3 clock hrs
d.DIALYSIS-seperation of the sensory ret from the non-pigmented epith of the pars plana at the ora serrata

VITREORETINAL TRACTION-
A] DYNAMIC-caused by rapid eye movts
-centripetal force exerted

B] STATIC TRACTION-unrelated to ocular movts
1.TANGENTIAL-parallel to the surf of ret with contraction of epiret / subret memb
2.ANTEROPOST-pull from the ret posteriorly to the vit base
3.BRIDGING-[ Trampoline] pull from one part of ret to other along the detached post hyaloid face.

TYPES OF RD-
A] Rhegmatogenous-asstd with breaks
B] Tractional-asstd with traction,but without break
C] Exudative-d/t fluid exudn

DDs-
retinocele
retinal cyst
retinoschisis

SURGICAL ANATOMY-
VITREOUS ADHESIONS
vit base
optic disc
macula
BVs
Chorioret scarring
ORA SERRATA-
Junction bet the ret & the non-pigmented epith of pars plana
Nasal ret has tooth like extensions of the ret onto the parsplana k/as dentate processes separated by oral bays.
The non-pigmented epith of the parsplana adheres to the pigmented epith more densely than the sensory ret to the RPE,thus rheg RD seldom extends beyond the ora

VITREOUS BASE-
4mm wide zone straddling the ora serrata

Sclera is thinnest at the recti insertion

Macula is 1mm above & post to the post end of the inferior oblique ms insertion

APPLIED PHYSIOLOGY-
Ret stays attached bcos-
Acid mucopolysachharide bet the RPE & sensory ret acts as a biological glue
RPE cell sheaths mechanically hold the sensory ret
RPE pump & hydrostatic press-RPE ATP-ase dependant pump→pumps out the SRF→lowers the hyd press & vit press→ flattens the ret.
Vit tamponade-cortical vit impedes movt of liqd vit thru breaks

MECHANICS OF RD FORMN-
vit liquefaction
PVD
ret tears at sites of VR adhesions.
PREDISPOSING FACTORS-
myopia
aphakia
trauma
lattice deg
snailtrack deg
deg retinoschisis
glaucoma
proliferative RPs-DR,BRVO,sickle cell,ROP
infect

MYOPIA & RD-
Myopia-10% popln
40% RD occurs in myopic eyes
In myopia-
Lattice deg is common
Snailtrack deg is common
Diffuse chorioretinal atrophy may cause holes
Macular hole predisposition
High risk of PVD & vit deg
High risk of VL during surg
Post capsulotomy has a high risk of RD
SURGERIES CAUSING RD-
cat
Penetrating KP
PPV
Scleral perforation
Cryotherapy
Photocoagn

RHEGMATOGENOUS RD
-1 in 10,000-incidence
-AETIO-
1. Trauma
2. myopia -↑ -lattice deg
-vit liquefaction
-PVD
3. Peripheral retinal deg-
-lattice deg
-snailtrack deg
-white-with-pressure
-white-without pressure
4. Cataract Sx-common after PCR,needling,yag c’tomy

PATHOGENESIS-
Retinal breaks are caused by an interplay between dynamic Vitreoretinal traction & predisposing peripheral ret deg.
Synchisis ( vit liquefaction)
↓
Hole dev in the thinned post vit cortex which overlies the fovea
↓
Synchitic fld from the vit cavity passes thru this defect into the retrohyaloid space.
↓
This process hydrodissects the post vit surface from the ILM as far as the vit base.
↓
The remaining solid vit gel collapses inferiorly & the retrohyaloid space is occupied by synchitic fld.
↓
K/as acute rhegmetogenous PVD

CLINICAL FEATURES-
RHEGMATOGENOUS RD-
Photopsia-d/t traction on the ret at sites of VR adhesions
-no lateralizing value
* floaters-moving vit opacities wen they cast a shadow upon the ret
3 types-
1. Weiss ring-solitary ring shaped opacity representing the detached annular attachment to the margin of optic disc
2.Cobwebs-d/t condensation of collagen fib within the collapsed vit cortex
3. Sudden shower of red coloured spots-VH d/t tearing of a peripheral BV

Field defect-percieved as a curtain
-The quad of the field in which the defect first appears is useful in predicting the location of prim ret break [which will be in the opposite quad]

SIGNS-
Marcus Gunn pupil[RAPD]
Low IOP < 5mmHg in fellow eye
Mild ant uveitis
Tobacco dust in ant vit-Schaffer’s sign
Ret breaks appear as red discontinuities in the ret surf

FRESH RD-VIVA
convex, opaque & corrugated
Undulates freely with eye movts
Loss of underlying choroidal pattern
Dark appear of ret BVs with lesser contrast bet arterioles & venules
SRF may extend till the ora serrata

OLD RD-
Ret thinning d/t atrophy
Intraretinal cysts [12mo ]
Subretinal demarcation lines [high water marks ] d/t proliferated RPE cells at the junctn of attached & detached ret[ 3mo ]

PROLIFERATIVE VITREORETINOPATHY-
GRADES
Diffuse vit haze
Tobacco dust

Wrinkling of inner ret surf
-Rolled edge of ret hole
-V tortuousity

C.Full thickness fixed ret folds
C 1-one quad
C 2-two -“-
C 3.-three “

D.Fixed ret folds in 4 quad
1. Wide funnel shaped RD
2. Narrow funnel shaped RD
3.Closed funnel shaped RD

T/T of PVR-
NO PVR- scleral buckling
PVR< C2-Scleral buckle
-Drain SRF
-Intravitreal gas
PVR> C2- Vitrectomy
Consider- Sc buckle
-Drain SRF
-Gas inj

C /F
RHEG
TRACTIONAL
EXUDATIVE
Photopsia&floaters
+
-
Phot –nt[no VR tractn] &floaters + [vitritis]
Field defect
Dark curtain
Slow & stationary
Sudden & rapid
Detached retina
Convex
Opaque
Corrugated
Undulates freely,high water marks +,SRF extends upto ora
Concave
Breaks-nt,
SRf shallow
Seldom extends upto ora,
Ret mobility reduced
Shifting fld -nt

Convex
Smooth,
Breaks –nt
Detached ret mobile,
Shifting fld +

RETINAL DIALYSIS-
Seperation of the sensory ret from the non-pigmented epith of pars plana at the ora
MC –inferotemporal quad
Blunt trauma-superotemp
Vit base avulsion with dialysis-pathognomic of traumatic dialysis

SERIOUSNESS OF BREAKS-
tears more dangerous than breaks d/t traction
larger breaks more dangerous than smaller ones d/t increased access to Sr space
symptomatic breaks more dangerous d/t traction
Superior breaks more dangerous bcos SRF spreads more quickly d/t gravity
Equatorial breaks progress more than oral breaks
Sub-clinical break –small break limited by a small amount of SRF
Pigmentation-suggests longstanding break & carries less risk
COLOUR CODE
Attached retina-red
Detached retina-blue
Break-red outlined in blue
Thinning-red cross hatching outlined in blue
Lattice-blue cross hatching outlined in blue
Pigment- black
Exud-yellow
Vit opacity-green

FINDING THE PRIMARY BREAK-
Quadrantic distribution-
60% -UT
15%-UN
15%LT
10%-LN
LINCOFF’S RULE
A shallow inferior RD in which the SRF is higher on the temporal side points toa prim break on that side
A prim break at 6 o’ clock will cause an inferior RD with equal fld levels
In a bullous inferior RD,the prim break usually lies above the horizontal meridian
If the prim break is located in the upper nasal quad the SRF will revolve around the disc & then rise on the temporal side until level with the prim break
A subtotal RD with a superior wedge of attached ret points to a prim break located in the periphery nearest its highest border
When the SRF crosses the vertical midline above,the prim break is near 12 o’ clock,the lower edge of RD corresponds to the side of the break.

LATTICE DEGENERATION-Discontinuity of ILM with atrophy of underlying sensory ret
8% of gen pop & 40% of RD pts
Imp cause of RD in myopes
Seen in –Marfan,s, Stickler,& ehler Danlos
Typical-sharply demarcated
-circumferentially oriented
-spindle shaped area of ret thinning
-bet equator & post vit base
-Bilateral
-Temporal
-Superior
-Arborizing network of tiny white lines
-snowflakes [remnants of deg muller’s cells]
-overlying vit is synchitic, but vit attachments around
the margin of lesion is exaggerated
Atypical-Radially oriented
-continuous with peripheral BV
-may extend post to equator
-stickler syn
Complication- RD d/t tractional tear

SNAILTRACK DEG-
sharply demarcated
circumferentially oriented bands of tightly packed snowflakes
white frost-like
longer than lattice
tractional u-tears rare
complication→hole → RD

RETINOSCHISIS

Splitting of sensory ret into 2 layers-outer-choroidal
-inner-vitreal
2 types-a] Degenerative
b]Congenital

DEGENERATIVE RETINOSCHISIS-
Hypermetropes
Asymptomatic
Often bilateral
Classn-A] Typical-split at the OPL
-anterior to equator
B] -Reticular-split at the NFL
-beyond the equator
Inferotemporal periphery of both fundi
Inner layer-snowflakes, sheathing or silver-wiring of BVs
Outer layer-Beaten metal appear & white with press
Unlike RD ,retinoschisis is immobile
Complications-
1 ] Breaks in reticular type
2] RD in eyes with break in both layers
T/T-
IND-
Schisis threatening the macula
Outer/inner ret break or both
RD with SRF beyond the margins of schisis
Prev H/O RD

1] Cryopexy / Photo scattered thru out the edge of schisis or around the break→breakdown of RPE barrier→ schisis fld gets absorbed by choroidal cir.

2] Conventional Buckling-
-For outer layer holes ant to equator asstd with RD
-Excessive cryo shud not be done to avoid dissolution of outer layer holes
-Only the area surrounding the outer layer holes shud be treated & area beneath the schisis cavity avoided
-If outer layer holes are +nt post to equator → External drainage + cryo

CONGENITAL RETINOSCHISIS-
Bil maculopathy + retinoschisis
Defect is in muller’s cells→splitting of NFL from sensory ret
XL
Age-5-10yrs

SYMPTOMS-
Reading diff
Squint/nystagmus

SIGNS-
A. Foveal s-Tiny cystoid spaces –‘bicycle-wheel ‘pattern & blunt FR
B.Peripheral schisis-inferotemp quad
-inner leaf-oval defects
-sev cases-defect coalesce,leaving ret
BVs floating in the vitreous [vit veils]

COMPLICATIONS-
-VH
-intra-schisis h’age
-RD
INV-
ERG- decrease in b-wave amplitude
EOG-subnormal
CV-tritan defect
FA-window defect
Fields-Absolute defect [RD-relative defect]

TREATMENT OF RD→
PRINCIPLES OF RD Sx- VIVA
1.Find the break & seal it
2.Relieve Vitreoretinal traction
3.Drain the SRF

PROPHYLACTIC T/T-
-Cryotherapy
-Photocoagulation

CRYOTHERAPY-
Lesion surrounded by a single row of cryo applications
Based on Joule Thompson’s principle
Gas used-CO2,NO2
Mech-Compressed gas is passed thru a small delivery tube into a large exhaust chamber→sudden drop in press→rapid expansion of the gas→sudden drop in temp→freezing→intracellular ice crystals→ mech cell damage→ further increase in size on thawing→seperation of water & electrolytes & change in pH→destruction of choriocapillaries,RPE & outer ret layers→firm chorioret scar
Cryoprobe shud not be removed unless it has defrosted completely as premature removal may crack the choroids→choroidal h’age
Pigmentation occurs after 5days
Problems-chemosis & lid edema
-transient diplopia
-vitritis
-maculopathy
* ADVANTAGES-
-Full thickness buckle can be applied to full thickness sclera
-No thermal damage to vit or sclera
-Less risk of ant seg ischaemia
-Can be applied over staphyloma
-Applicable to wet sclera
-Lower incidence of macular pucker

*DISADVANTAGE-
-Diff to see reac in deep SRF
-Excessive cryo→release of RPE cells into vit→PVR

PHOTOCOAGULATION-
200µm, 0.1-0.2sec
Panfundoscopic lens used
2 rows of confluent burns
Thermal effect confined to retina & RPE,sparing the choroid & sclera
Problems-
CMO/macular pucker
choroidal detachment→forward rotation of CB→sec angle closure glauc
exud RD
Rheg RD
Retinal h’age

SURGERY-[ D-02]
SCLERAL BUCKLE
DEF- Creation of inward indentation of sclera [‘buckle’]

2 main purpose-
1.To close ret break by opposing RPE to sensory ret
2.to reduce dynamic VR traction

EXPLANTS-
Material sutured directly onto the sclera to create buckle
1,Local explant
2.encircling explant
LOCAL a) Radial explant-placed at right angle to limbus
b)Circumferential ex-parallel to limbus

INDICATIONS
RADIAL BUCKLE-
Large U-tears[less tendency to fishmouth]
Posterior breaks

CIRCUMFERENTIAL BUCKLE-
Multiple breaks in 2/more quad
Ant breaks
Wide breaks such as dialysis

ENCIRCLING EXPLANT-
Placed around entire circumference of globe to create a 360 deg buckle.
2mm strap used
Supplemented with radial sponge/circumferential silicone tyres
2mm high buckle may be produced by tightening the strap by 12mm
Indications-
Breaks in 3 / 4 quad
lattice / snailtrack deg in 3/ more quad
extensive RD without detectable break in hazy media
failed local procedure

DRAIN-AIR-CRYO-EXPLANT [D-A-C-E]
Useful in bullous RDs,esp if breaks are postequatorial
SRF is drained to bring ret closer to RPE
Air is injected to counteract the hypotony induced by drainage
Breaks accurately localized & treated with cryo
Explant inserted.

DRAINAGE OF SRF * * *
IND-[ viva]
Diff in localization of breaks in bullous RDs with postequatorial breaks
Immobile retina
Longstanding RD,as SRF is viscid & takes a long time to absorb
Inferior RD with equatorial tear,bcos wen the pt assumes an upright posn postoperatively,residual SRF gravitates inferiorly &reopens the break.

TECH-2 methods-
Radial 4mm sclerotomy over the area of deepest SRF→knuckle of choroid prolapsed→knuckle is perforated tangentially with a 25G needle
Direct perforation made thru sclera,choroid& RPE with a 27 G needle bent 2mm at its tip.

COMPLICATIONS-
H’age d/t perforation of a large choroidal V
Dry tap d/t incarceration of IO struc in the ostium
Iatrogenic break
Ret incarceration
Fishmouthing

PNEUMORETINOPEXY [J-03,05]

DEF-Intravitreal gas bubble is used to seal a ret break & reattach the ret without scleral buckling

HOW IT WORKS?
As the IO gas is lighter it floats up & produces a buoyant force ,thereby forcing the detached ret against the ret-choroid complex
Surface tension of the air bubble closes the break→RPE pumps & removes the SRF

IV GAS
AVG DURATION
LARGEST SIZE
AVG EXPANSION
AIR
3 days
immediate
No exp
SF6[sulphur hexafluoride]
10 days
36 hrs
Doubles
C3F8[perfluoropropane]
28 days
3 days
Quadruples

IND-
macular hole
posteriorly located hole
superior hole < 1 clock hour
Redetachment after scleral buckling
Giant tear
Large tear with fishmouth

C/I-
Multiple holes
> 1 clock hour
Breaks in inf quad
Physical disability/MR
Cloudy media
PVR-Gr C or D
Iris clip IOLs

TECH-
Ret breaks t/ted with Cryo
IV inj of 0.5ml 100% SF6 or 0.3ml 100% C3F8
Po, pt is so positioned that break is uppermost & rising bubble remains in contact with the tear

COMPLICATIONS-Intraoper-
Rise in IOP
VH
Vit incarceration
Subconj gas
Subret gas
Multiple gas bubbles [Fish eggs ]
Extension of detachment
Enlargement of tears

Postoper-
1.New/missed breaks
2.Redetachment
3.PVR
4.Macular pucker
5.Persistence of SRF
6.Endophthalmitis
7.Cataract

Q- What precautions ?
1. Avoid air travel
2.Dont use expansile air ( conc >13- 15%)→ CRAO


PERFLUOROCARBONS

Tamponading agents
High specific gravity→Flatten the ret
Low viscosity→Facilitates easy introd & aspiration from the eye
Commonly used PFCL-
Perfluorotributylamine
Perfluorodecalin
Perfluorooctane
Perfluorophenanthrene

IND-
RD + PVR
RD+ ret break
Traumatic Rd
DR & other PRP
Lens/IOL dislocation into vit
Suprachoroidal h’age
GRT-to unfold the rolled edges

C/I-
Post ret break
Passage of liqd under the ret shud be avoided

TECH-
Inj with a 23- 25 G needle
Inj shud start a mm over the disc & during progressive inj edge of the needle is maintained inside the bubble of liqd to avoid fragmentation of the agent
Inj is stopped wen the post end of the tear is reached to avoid any passage under the ret
After retinopexy,the PFCL is removed by fluorocarbon / gas exchange or fluorocarbon/silicone oil exchange or by aspiration with a Charle’s flute needle

PRECAUTIONS-
1.Meant for IO use only.Therefore shud not be left in the eye at the end of the surg
2.Shud not be resterilized
3.Glass syringe shud not be used

COMPLICATIONS-
New ret breaks
CRAO
Subret migration
Dispersion into multiple gas bubbles
Residual droplet
Retinotoxic if left for > 1 wk

SILICONE OIL

PDMS-Polydimethyl siloxane polymer
Transparent
RI -1.4 [higher than vit]→ optics of silicone oil filled eye gets changed.
Phakic eye-Increase hyperopia[+5D]
Aphakic eye-Decrease hyperopia
Viscosity 1000-5000 centistokes
Low specific gravity
Silicone oil→Internal tamponade to ret breaks→counteracts the tractional forces→prevents rec RD

TECH-
Inj manually/ with viscoelastic inj
Prior to inj ,a large inf iridectomy is done to prevent pupillary block glauc
Removed wen ret & dis process are stabilized & further int tamponade is not reqd
After 4-6mo chances of reproliferation &redetachment are min

IND-
PVR
PDR
To unfold post edge of a giant ret tear
Trauma
CMV related RD in AIDS

SILICONE OIL
IO GAS
Immed ability to see object
Inability to see thru the bubble for 4-6 wks
Avoid prob of positioning
Necessity of positioning
Air travel allowed
Avoid air travel
Hypotony-less
Hypotony-common

Recurrent perisilicone proliferation

Drying effect on ret & conc of mitogens encourage rec proliferation
Alteration in ref power
No alteration

COMPLICATIONS-[J-07-comp & mgt]
Emulsification
Finely emulsified bubbles collect in AC-‘Inverse hypopyon’
They can also collect in the retro-oil space in front of the ret
Oil bubbles can get embedded in vit memb,ciliary processes,iris & angle of AC
Causes persistent sec glauc
Removal of oil may not reverse glauc.
Med & surg Rx of persistent glauc is reqd

Band KP/stromal opacification
Intermittent contact of the oil with cor → progressive decompensation & BK
Rx-EDTA [Ethylenediaminetetraacetic acid]
Keratoplasty
Silicone oil removal

Glauc
-Due to- occlusion of 6 o’clock iridectomy.Rx- Reopen the iridectomy with YAG laser
-Inflamn- Rx- steroids
-Emulsified oil→chr inflamn {Rx above]

Cataract
-Phakic eyes with oil for a long time dev cat
-Rx- Remove cat + sil oil
-If oil needs to be retained,a 6 o’clock I’dectomy & topping of the oil done along with cat extraction

Hypotony
Perisilicone proliferative macular pucker
Recurrent RD
Silicone oil migration under the retina-
-Failure to relieve all traction on the ret→ entry of oil into the subret space
-If oil enters subret space
↓
stop oil injection
↓
-Residual traction is relieved by membrane surg
-If ret remains stiff despite of removal of memb
↓
relaxing retinotomies may be needed
-Subret oil can be removed by injecting RL in front of the disc & gently kneading the oil out thru the ret break or slow suction of oil directly with a cannula
-Fluid –air exchange will push the trapped oil down & out thru the posterior ret break.

9. Visualisation problem-
- Oil in the pupillary space may have a convex surf causing optical distortion of fundus image
-Rx-Evacuate the AC of all the fluid & allow the oil to fill the AC.At the end of the surg,AC can be reformed with RL

10 Vitreous floaters
-Due to rubbing action of the oil, impurities in the silicone tubing,syringes & needles will be washed into vitreous cavity as white floaters. These disappear on the 1st PO day.

Silicone oil Removal-
-Fluid is introduced thru one sclerotomy,oil is allowed to float up & come out of another.
-May be removed by suctioning with a wide bore cannula

COMPLICATIONS OF RD SURGERY-
INTRAOPER-
Anaesthesia-scleral perforation &RBH
Exposure-Scleral rupture/perforation - -Rectus ms rupture ------- -Vortex vein damage
Decrease visualization-cor opacity -
-miosis
-hyphaema
-VH
- Multiple gas bubbles
4.Drainage-VH
-Ret/vit incarceration
-Hypotony
-Iatrogenic breaks
-Fishmouthing
-Dry tap
5.Buckling-VIVA
-Corneal exposure
-Radial ret folds
-Fishmouthing
-Rise in IOP
-CRAO
EARLY-
Angle closure glaucoma dt compression of veins draining the CB & forward displacement of CB
IO gas- glauc
-new breaks
-extension of detachment
3.Symblepharon
4.Ant seg ischaemia
D/t- diathermy occluding long ciliary As
- Tenotomy
- Tight encircling band
C/F-SK
-chemosis
-white flakes floating in AC/deposited on lens
-fall in IOP
-irreg dilated pupil
-sector iris atrophy
-uveitis
-cataract
5.local inf
6.choroidal det
7.pigment fallout foll cryo

LATE-
Myopia induced by encircling band
Strabismus & diplopia
Extrusion of implant
mac pucker
CME
PO exud RD

DIFF BET RD & RETINOSCHISIS-
RD- Tobacco dust
-VH
-Corrugated & irreg surf
-RPE atrophy
-Relative scotoma [Retinoschisis- Absolute scot]
- Demarcation line
-No photo burns in RD d/t SRF

EXUDATIVE RD
CAUSES-
neoplastic- choroidal MM
-choroidal haemangioma
2. inflame- VKH sy
-symp oph
-posterior scleritis
3.Congenital- optic pit
-morn glory syn
-choroidal coloboma
4. Vascular- Coat’s dis
-malignant HT
5Nanophthalmos
6.CSR
7. Uveal effusion syn-BL detachment of ret,CB & choroid, leopoard spot RPE change, cells in vit,dilated episcleral Vs
C/F see table

TRACTIONAL RD

CAUSES-
PDR
Sickle cell RP
ROP
Familial exudative vitreoretinopathy
Toxocariasis
Trauma

C/F- see table
DDs-
1.Retinoschisis.
C/F
RD
RETINOSCHISIS
Surface
Corrugated
Smooth-domed
H’age or pigment
present
Absent
Scotoma
relative
absolute
Reaction to photocoag
absent
present
Shifting fld
variable
Absent

POSTERIOR VITREOUS DETACHMENT
-Senile form
-common in diabetics
-May be asstd with retinoschisis,retinal break orDR
SYMPTOMS-
-Floaters
-blurring of vision
-Photopsia- common in dim light & temporally located

SIGNS-
-Vitreous opacities-Weiss ring
- Retinal break,
- RD
-peripheral retinal & disc h’ages
-pigmented cells (released RPE cells) in ant vit or VH with acute PVD indicates a high probability of a coexisting ret break

T/T- no T/T
-For acute break→photo or cryo
-for break s/b pigment → no t/t
VH with PVD

VIVA-
BONE SPICULES-
RP
Chorioretinitis
Cystinosis
Vascular occlusions
CHOROIDAL FOLDS-
Pseudotum
Post scleritis
Hypotony
RD
Scleral laceration

COTTON WOOL SPOTS
AIDS
HTR
DR
SLE
CRVO
BRVO
Carotid A occlusion
Purtscher RP
Anemia
10.Leukemia

MACULAR EXUDATES-
HTR
DR
SRNVM
Macroaneurysm
Coat’s dis
Papilledema
CRVO
radiation
9.neuroretinitis

NORMAL FUNDUS WITH DECREASED VISION-
Retrobulbar neuritis.
Cone degeneration
Stargardt’s dis
Fundus Flavimaculatus
Optic neuropathy ( alcohol / tobacco)
Rod monochromatism
Amblyopia
Non-physiologic visual loss

ROTH SPOTS-
1 .Leukemia
2. SABE
3. Pernicious anemia
4. Sickle cell RP
5.SLE

SHEATHING / PERIPHLEBITIS-
Sickle cell dis
Sarcoidosis
Pars planitis
Eale’s dis
Viral retinitis ( AIDS, Herpes)
Fungal retinitis
Tb
MS
Behcet’s dis
10.Syphillis

DIFF BET OPTOCILIARY SHUNT & NV-
NV- Thin & wispy
nV show leakage whereas shunt Vs do not leak.

OPTIC DISC COLOBOMA-
Due to failure of closure of fetal fissure.

CHARGE SYN-
C-coloboma
H- Heart dis
A- Choanal Atresia
R- Mental retardation
G- Genitourinary anomalies
E- Ear deformity

Field defect-
-Enlarged blind spot
-Arcuate scotoma
-Altitudinal defect

ASTEROID HYALOSIS
SYNCHISIS SCINTILLANS
White
Golden
Calcium soap [stearate & palmitate]
Cholesterol crystal
Less refractile
More refractile
Not mobile as they are attached to the vit
Mobile

Suspended in the vit
Settle at rest

RETINITIS PIGMENTOSA-[VIVA Q]
Q. Types of maculopathy in RP?
A. 1. Cellophane MP
2.Atrophic mp
3. Cystoid MP

Q. OCULAR ASSTN-
A. * Optic disc drusen
* PSC
* Glaucoma
* Keratoconus
* Vitreous cells

Q. ERG findings ?
A- Early stg- Reduced amplitude
Later- Extinguished

MACULAR FUNCTION TESTS
1.TWO LIGHT DISCRIMINATION TEST-
* Dark room
*Pt is asked to look thru an opaque disc perforated with 2 pinholes close together behind which light is held.If he can appreciate, MFT is good

2. PINHOLE TEST-
* Pinhole [1mm] →increases the depth of focus→Limits scattering effect of cor scars & lenticular opacities
* Smaller the aperture→ Greater the depth of focus
* Useful in –small cor opacities
-Small lenticular opacities

3. MADDOX ROD TEST-
Ask the pt to look thru the Maddox rod→ if the red line is continuous & unbroken→ good MF

4.RELATIVE LUMINANCE-
* Two identical pentorches are brought close towards each eye till the pt judges the illumination of each to be equal
* If ret functn is equal→ the distance where this happens will be equal.
* Useful in UL cataract with other eye nml

5. AMSLER GRID-
* Evaluates the 10 deg of visual field surrounding the fixation
* Useful for monitoring macular dis
* 7 charts.
* Each chart- 10 cm square
* CHART 1- 400 smaller 5mm squares
-Each sq subtends an angle of 1 deg
* CHART 2- Similar to chart 1, but has diagonal lines that aid fixation in pts unable to see the cental spot
* CHART 3-Identical to chart 1 , but has red sq which help in detecting color desaturation in optic n lesions
* CHART 4- Consists of random dots
-Seldom used
* CHART 5- Consists of horizontal lines
-To detect metamorphopsia along specific meridian
Esp horizontally to investigate diff reading
* CHART 6-Similar to chart 5, but has white background &
Central lines are closer together
* CHART 7-Exhibits a central fine grid, each sq subtending an
Angle of ½ deg & is more sensitive
Method- Pt wears reading specs & covers one eye
-Asked to look at the central dot with uncovered eye
& report –
-Maculopathy→ Lines appear wavy
-Optic neuropathy→Some lines will be missing or
Faint but not distorted

6. PHOTOSTRESS TEST-
* Best corrected V/A
* Pt fixates pentorch / o’scope light at 3cm for 10 sec
* Photostress recovery time-Time taken to read any 3 letters of the pre-acuity line- N-15-30sec
*Performed on the other eye & results compared.
* PSRT –prolonged in macular dis & not in ON

7.PUPILLARY REACTION
* Macular dis- N
* ON- RAPD

8. COLOUR VISION TEST-
* If the pt can identify red, green or blue in the presence of an opaque medium –his MFT is nml

9. PURKINJE VESSEL SHADOW/ PURKINJE’S ENTOPTIC VIEW OF RETINA-
* Pt can see his whole ret BV after pressing the LL against the sclera with an illuminated bulb.
* An intelligent pt may be able to detect a patch of choroiditis / macular degeneration

10.BLUE FIELD ENTOPTOSCOPE-
PRINCIPLE- Hb in RBCs absorbs blue light & so no stim of ret receptors occurs
-Leucocytes contain no Hb.So visual sensation is perceived as flying corpuscle effect
* Pt with dilated pupils is seated in adark room & observes a 20deg uniform blue field split into 4 quad by a black graticule
* Pt is asked to state-
-If flying corpuscles are visible
-No seen in each quad
-Sinuous movts
-Relative speed of movt in two eyes

11.INTEROFEROMETER-
* When 2 / more light waves fall on the same point→ amplitudes of respective electrical & magnetic fields add→third wave [ summation of respective pts]
* If the waves are in phase with each other→Maxima adds upto maxima &minima to minima→Third wave which is 4 times the intensity of the initial wave.
* If the waves are 180 deg out of phase→ maxima adds to minima→ Destructive interference occurs→ Pattern of alternate light & dark fringes→ k/as Interference pattern
* Coherant laser light can pass thru openings in lens opacities & transmit patterns of diff sizes to the macula for recogonition.
* There is a good correlation bet the size of the pattern recogonized & PO V/A.

12. POTENTIAL ACUITY METER-
* Snellen’s image is projected by a narrow beam [0.1mm] thru a special attachment in the slit lamp on the central retina in an opaque media
* Ability to read projected letters correctly ensures good macular function

13. ELECTROPHYSIOLOGICAL TESTS-
A) ERG-
B) VEP-
1.Pattern appearance
2. Pattern Reversal
Reduced amplitude of 2nd peak→ noted in pts with reduced V/A

14. USG-
* TO assess anatomic integrity
* Does not indicate abt functional status of macula

HAIDINGER’S BRUSHES

SRNVM- CAUSES
High myopia
Angioid streak
Presumed ocular histoplasmosis syn
photocoagulation
Choroidal naevus / melanoma
choroidal rupture
RP.
ARMD

AGE RELATED MACULAR DEGENERATION[[j-07] -case
ARMD-Early
-Late
EARLY-
Discrete yellow spots at the macula
Hyperpigmentation of RPE
Sharply demarcated areas of RPE depigmentation
LATE-
Geographic atrophy of RPE with visible underlying choroidal Vs
PED with / without neurosensory detachment
Sub-retinal /sub-RPE NV
Fibroglial scar tiss,h’age & exudates
2types-Atrophic
-Exudative

ATROPHIC-
Dry / Non-exudative
MC
Slowly progressive
Drusen & Geographic atrophy of RPE

EXUDATIVE-
Wet / Neovascular
Less common
Devastating
CNV & subretinal scarring
DRUSEN- H/P
Discrete deposits of abnml material located bet the BM of RPE & inner collagenous layer of Bruch’s memb
This material is derived from the RPE & accumulates d/t failure to clear the debris
SIGNS-
HARD DRUSENS-
Small, round, discrete,yellow –white spots
Focal dysfunction of RPE

SOFT DRUSENS-
Larger
Indistinct margins
Slowly enlarge & coalesce to form drusenoid detachment of RPE.

SMALL DRUSENS-< 64µm dia
INTERMEDIATE DRUSENS- 64-124 µm
LARGE DRUSENS - > 125 µm

FFA-

HYPERFLUORESENCE-
D/t –Atrophy of overlying RPE→window defect
-Late staining
* Hydrophilic [low lipid content]
* Predispose to CNV

HYPOFLUORESENCE-
Hydrophobic [high lipid content]
Predispose to RPE detachment

T/T- Prophylactic-
Low-energy Argon laser photo-
Reduces the no & extent of drusen
May predispose to CNV → so not recommended
Antioxidants- Vit A, C, E & Beta- carotenes

ATROPHIC ARMD-
Slowly progressive atrophy of photoreceptors, RPE & choriocapillaries
C/F- Gradual impairment of vision
-BE & asymmetric
SIGNS-
Focal hyperpigmentation or atrophy of RPE + drusen
Sharply circumscribed,circular areas of RPE atrophy with variable loss of choriocapillaries
Enlargement of atrophic areas within which larger choroidal Vs become visible & pre-existing drusens disappear-Geographic atrophyGeographic Atrophy
FA-Hyperfluoresence d/t unmasking of background choroidal fluor
T/T- LVA

RETINAL PIGMENT EPITHELIAL DETACHMENT-
Thickened Bruch’s memb→ reduced hydraulic conductivity→impedes movt of fld from RPE towards choroid
C/F- UL metamorphopsia
-Impaired central vision
-Sharply circumscribed , dome shaped elev
-Sub-RPE fld clear / turbid

PED can occur in-
AMD
CSR
Polypoidal choroidal vasculopathy
FA-Well-demarcated area of hyperfl d/t pooling of dye under the detachment- Early phase
- Late phase-Increased hyperfl but no change in size

* ICG- Oval area of hypoflu with a faint ring of surrounding hyperflu.

* Laser photo shud not be performed in PED d/t risk of retinal tear

* Course-
- Spontaneous resolution
-Geographic atrophy
- Detachment of sensory retina- D/t breakdown of outer BRB allowing passage of fld into subretinal space
- Occult CNV
-RPE tear

EXUDATIVE ARMD-
PATHOGENESIS-
Exud ARMD is caused by CNV originating from choriocapillaris which grows thru defect in Bruch’s memb.
Type 1- confined to sub-RPE space
Type2- extends to sub-retinal space
C/F-
Metamorphopsia
Blurred central vision
Sub-RPE CNV- Grey-green or pinkish yellow elevated lesion
Sub-retinal CNV-Subretinal halo / pigmented plaque

FA- CLASSN OF CNV
CLASSIC CNV-
Well-defined membrane which fills with dye in a lacy pattern
A) EXTRAFOVEAL CNV-
CNV is more than 200μm away from the centre of FAZ
B) SUBFOVEAL CNV-
Centre of FAZ is involved either by an extension from an extrafoveal area or by originating directly under the centre of the fovea
JUXTAFOVEAL CNV
CNV is closer than 200μm from the centre of FAZ but does not inv it

CLASSIC CNV-
Predominantly classic CNV- CNV > 50% of lesion
Minimally classic CNV-CNV -1-49% of lesion
Occult with no classic CNV-NO classic CNV ,only occult CNV.
Poorly defined CNV-Ill-defined boundaries of CNV
Well-defined CNV-well-defined boundaries

OCCULT CNV-
Poorly defined membrane

FIBROVASCULAR PED-
CNV + PED
CNV fluoresces more brightly [ hot spot] than the PED-ICG

COURSE OF CNV-
HAEMORRHAGIC PED-
Caused by rupture of BVs within the CNV
Initially bld is confined to sub-RPE space- dark elevated mound
Later the h’age may break into the SR space- more diffuse outline & lighter red colour

2.VH-
Wen sensory h’gic detachment breaks into vitreous cavity

3.SUBRETINAL / DISCIFORM SCARRING-H’age→ gradual organization of bld→ingrowth of new Vs from the choroid→Fibrous disciform scar→ permanent LOV

4.MASSIVE EXUDATION-
Chronic leakage from CNV→ intraretinal &subretinal exudn

D/D-
1.Myopic deg- peripapillary & macular deg changes.No drusens
2.CSR-parafoveal serous retinal elevation
-RPE detach
-Mottled RPE atrophy
-No drusens
-age < 50 yrs
3.Inherited central retinal dystrophies-
-Stargardt’s dis
-pattern dystrophy
-Best dis
4. Toxic RP-chloroquine MP
5. Inflamatory maculopathies-
-Multifocal choroiditis
-rubella
-serpiginous choroidopathy

T/T-
1.ARGON LASER PHOTOCOAGULATION-
IND- Extrafoveal / juxtafoveal CNV with classic membranes
C/I-
poorly defined CNV [as the memb is either occult / obscured by bld/serous RPE detachment.]
Poor V/A- < 6/36
TECH-
FA , not more than 72 hrs old
Perimeter of the lesion is t/ted with overlapping 200μm burns, 0.2-0.5 sec.
T/T must extend beyond the margins of the memb.
FU- after 1-2 wks
Monitoring- Amsler’s grid

2.TRANSPUPILLARY THERMOTHERAPY-
Heat is delivered to the choroid & RPE thru the pupil with diode laser.
Based on the principle of hyperthermia
Differs from photo-Temp rise at RPE is less than 10deg c compared to photo which is 40 deg c
-Intracellular breakdown of organelles rather than coag necrosis
* Spot size- larger [1.2,2,3mm]→Allows the laser to select the most appr one based on size of NV memb
* Longer duration-1min
* Subthreshold-barely discernible burn
* Longer wavelength-810nm
* Power-800mW
* USES-Choroidal melanoma
Capillary & choroidal haemangioma

3. PHOTODYNAMIC THERAPY [PDT]
* A special laser activated dye is used to cause damage selectively to abnml BVs while minimizing damage to the nearby retinal tissue

* IND- ARMD
-malignant melanoma
-RB

* MECH-
-Photosensitizing dye –verteporfin is injected IV
-Dye binds to low-dose lipoprotein in NV & neoplastic tiss[ as these hav high expression of LDL receptors]
-Receptor mediated endocytosis
-LDL bound dye is taken in the cells
- This tiss is now subjected to photothermal elev of temp by laser
-Release of singlet O2
-Vascular endothelial damage + platelet aggregn + V thrombosis [sparing of overlying receptors & adjacent extravas tiss

-Photosensitizer- verteporfin [BPD-MA liposomal benzoporphyrin] & SnET2 [tinethyl etiopurpurin]
TECH-
-Verteporfin 6mg/m2 IV over 10 min
-Allow the dye to accumulate in the NV tiss for 5min
-Diode applied for 83 sec
-wavelength-689nm
-power-600mW/cm2
S/E-
-Avoid direct exposure to light for 5 days→ damage to skin & retina
-Blurring & DOV
-Field defect
-Extravasation & reaction at inj site
-Allergic rec
-Back pain

4. SUBMACULAR SURGERY-
SRNVM REMOVAL is indicated in-
1.ARMD
2.High myopia
3.Angioid streaks
4.POHS
5.Multifocal choroiditis

TECH-
3 port v’tomy
Induction of PVD
Retinotomy [usually temporal location] Made with MVR blade or subretinal pic]
BSS injected subretinally
Subretinal pic is used to lift & pick SRNVM
Once it is loosened, it is grasped with a subretinal forcep & removed.
Just before the membrane is pulled off,the iop is raised to 80 mmHg to prevent subretinal bleed.after 1min the IOP is lowered by reducing the height of the bottle.

MACULAR ROTATION SURGERY-
Diseased submacular RPE is replaced by-Relocation of fovea to an adjacent area of intact RPE & choriocapillaris

RELOCATION OF FOVEA-
TECH- Retina is detached by trans-scleral subretinal inj of fluid
-360 deg peripheral retinotomy
-Retina is rotated for 10-45 deg around the optic disc under silicone oil
-Retinal translocation is supplemented by counter rotation of the whole globe by EO ms surgery
-Strabismus surg consists of partial transposition of all 4 recti ms & folding & retropositioning of oblique ms

COMPLICATIONS-
Cyclotropia & tilted image- regress over 3-6 mo
PVR-causes- Large area of RPE exposure to vitreous cavity
-Intraoperative seeding of RPE cells
-Retinal trauma
3.CNV recurrence
4.Late macular edema
5 ocular hypotony

RPE TRANSPLANTATION-
Aims to replace the sick cells in the macula which have lost their junction & adhesive matrix with the healthy cells
-Transplant from –Iris pigment epith cells or RPE
-Cells are harvested from nasal retina as RPE cells are denser here & r’tomy is less likely to cause RD

PNEUMATIC DISPLACEMENT OF SUBMACULAR H’AGE-
-Inj of gas into vitreous cavity→displaces bld from the fovea
-tPA may also be used

Extrafoveal / Juxtafoveal CNV→Photocoagulation
Subfoveal CNV→- PDT
-Intravitreal steroids
-Anti-VEGF
1.Pegaptanib [macugen]-
-anti-VEGF aptamer
-0.3mg intravitreal every 6weeks for 1-2 years
2.Ranibizumab [lucentis]-
-0.5mg/o.o5ml
-anti-VEGF antibody fragment
-highly effective in reducing exud
3. bevacizumab [ Avastin]
-Anti- VEGF antibody
-1.25 mg/0.05ml IV

RETINOPATHY OF PREMATURITY-j-05
Read from notes
DEF-
Proliferative RP
Pre-term infants
Low-birth weight
Exposed to high ambient O2 conc
PATHOGENESIS-
No BVs until the 4th mo in the retina,at which hyaloidal Vs at the OD grow towards the periphery.
These Vs reach the nasal periphery after 8mo of gestation,but do not reach the temporal periphery upto 1mo after delivery
Therefore the incompletely vascularized temporal ret is particularly susceptible to oxygen damage.
Mechanism of injury-
Initial insult→ Hyperoxia /hypoxia/ Hypotension→
Vasoconstriction→ ischaemia→ arrest in vascular dev→ release of angiogenic factor→NV→ extensive fibrovascular proliferation→ RD

ACTIVE ROP
LOCATION-3 ZONES CENTERD AROUND OD
Zone 1-Imaginary circle,the radius of which is twice the distance from the macula to the disc
Zone2-Edge of zone 1 to the nasal ora serrata & to an area near the temporal quad
Zone 3-Residual temporal crescent anterior to zone2

Extent of severity is determined by the no of clock hours

STAGES-
Demarcation line – runs parallel to ora serrata & separates avascular immature peripheral ret from vascularised posterior ret
Ridge- Line dev into an elevated ridge which represents a mesenchymal shunt.Isolated NV tufts seen post to ridge
Ridge with extraretinal fibrovascular proliferation-Ridge becomes pink.Vas tortuousity,RH & VH
Subtotal RD-wen the infant is 10 weeks old
Total RD

PLUS DISEASE-
Failure of pupil to dilate
Iris vascular engorgement
Vitreous haze
Dilated veins & tortous As
Pre-retinal VH

THRESHOLD DISEASE
5 contiguous clock hours or 8 non-contiguous clock hours of extraret NV in zone 1 or 2 asstd with plus dis & is an indication for t/t

SCREENING-
6 & 7 weeks post-natal age or 34 weeks post-conceptual age [whichever is earlier], but not b4 5 weeks post natal age

Pupil in a pre-term shud be dilated with 0.5 % cyclopentolate +/- 2.5 % phenylepherine

T/T
1] CRYOTHERAPY-
IND-Rx shud be witheld till stg 3 ROP& wen confluent fibrovascular proliferation of more than 3-6 clock hours are found

TECH-
Done wen infant is 7-20 wks of age
Under GA
Cryo applied to entire avascular zone ant to the ridge
Temp→-25 to-55 deg c

COMPLICATIONS-
VH /RH→ more chance of PVR
CRAO d/t pess by cryoprobe
Bradycardia d/t oculocardiac reflex
Macular coloboma like lesion
macular pigment abnmlities

2] PHOTO-
* Argon / diode
* Burns are placed one half width apart,from the ora serrata upto,but not including the ridge for 360deg
ADV-
Adv in zone 1 dis where cryo is diff
Scars are less pronounced & discrete
No need of conj incision & intense scleral depression

COMPLICATIONS-
Ant seg ischaemia
cat
Burns of cor, iris or tunica vasculosa lentis

3]SURGERY-
VITRECTOMY SCLERAL BUCKLING
IND-
Extensive BL subtotal /total RD
UL RD with high rsk of RD in other eye

C/I-1. Subretinal memb
2.Exud
3. Blood

ANTI-VEGF
VEGF-
The term Vascular endothelial growth factor refers to a collection of related protein iso-forms derived from the same gene.

-Initiating stimuli for pathological VEGF-
* Hypoxia
* Reduction in choriocapillaris blood flow
* Accumulation of lipid metabolic byproducts
* Oxidative stress
* Alterations in bruch’s memb

-Effects of pathological VEGF-
* Cytokine & protein release
* Monocyte recruitment
* Breakdown of BRB
All theses lead to pathologic NV

CLASSIFICATION-
I] Manufactured / Synthesized /Pharmacological products-
A] Direct VEGF Inhibitors:
Oligonucleotides-
a} Aptamers ( Pegaptanib sodium) MACUGEN-single stranded
S/E-Endophthalmitis
-Traumatic injury to lens
-RD
b} Small interfering RNA ( siRNA)-double stranded

B] Monoclonal antibodies
a}Bevacizumub ( AVASTIN)
b}Ranibizumab – rhuFab ( LUCENTIS )
-Lucentis 0.5mg is recommended for intravitreal inj once a month.if not feasible, t/t can be reduced to one inj every 3 mo after the first 4 inj.
-S/E-Conj H’age
-Eye pain
-vitreous floaters
-Increased IOP
-IO inflamn
-C/I- Hypersensitivity
-ocular/periocular infections

C]VEGF Tyrosine kinase receptors [VEGFR] Inhibitors

D] Intracellular Signalling Blockers
a]Nitric oxide synthetase [NOS] inhibitors
b]TrpRS inhibitors-Inhibit human aminoacyl-t-RNA synthetase
c]PKC inhibitors-[protein Kinase c]

II] Naturally occurring Inhibitory Polypeptides & Inducible Cleavage products-
A] PEDF- Pigment Epithelial derived factor-
Downregulates endothelial cell migration
B] Pathologically expressed circulating Angiostatins & Endostatins

III] Extracellular Matrix Modulators-
A] Integrin Antagonists
B] MMP Inhibitors-TIMP 3 ( Tissue inhibitors of metalloproteinase)

IV] Miscellaneous-
A] Combrestatin A-4
B] Squalamine
C] Verteporfin

CHOROIDAL NEOVASCULARIZATION-CASE

DEF-Inappropriate ingrowth of BVs & accompanying cellular infiltrates originating in the choroids,which extends thru the bruch’s memb to proliferate under the ret,RPE or both.

CAUSES-AJO
Degenerative-
ARMD
myopia
Angioid streaks

Heredodegenerative-
Vitelliform macular dystrophy (Best’s dis)
Fundus flavimaculatus (Stargardt’s dys)
ON head drusen

Inflammatory—
Ocular Histoplasmosis syn
Multifocal choroiditis
serpiginous choroiditis
Toxoplasmosis
Toxocariasis
Rubella
VKH syn
Behcet’s sy
Sympathetic oph

Tumour-
Choroidal naevus
choroidal haemangioma
Metastatic choroidal tum
Hamartoma of RPE

Traumatic-
Choroidal rupture
Intense photocoagn

6) Idiopathic

PATHOGENESIS-
-CNV occurs in response to disturbance of the RPE or bruch’s memb or loci of inflammn adjacent to these struc.
-Traumatic →Rupture of bruch’s mem
-common in young
-Inflamn→directly causes CNV or scarring & disruption of nml ocular architecture→ Vs ingrowth.seen in young-mid age
-Pathological myopia→ fracture in BM (lacquer crack) + atrophy→ CNV .Occurs at any age.
-Idiopathic→< 50 years without any e/o inflamn,myopia,chorioret scar or chorioret deg

Theories to explain CNV-
Release of cytokines ( VEGF)
Rupture of BM
Inflamn
Oxidative stress of RPE
Abnml accumulation of lipid by-prod
Vascular insufficiency

C/F-
SYMPTOMS- Decreased central V/A
metamorphopisia
SIGNS-
Grayish discolouration under the ret
Vs are incompetent with varying degree of leakage
Leakage
↓
Excessive fld accumulates within the tissue or between tiss planes.
↓
Detachment of RPE ,macula & intraretinal edema
-Tensile stress from the contracting fibrovascular memb
+
Excessive hydrostatic pressure
↓
Rips in the RPE
-Chronic leakage→ lipid deposition & degenerative changes within the deatached ret
-NVs have a tendency to bleed→ H’age under the RPE or retina or breakthrough h’age into the vitreous cavity
-Eventually,proliferation of ret glial cells,RPE & fibroblasts→ scar tiss (disciform scar)→ whitish accumulation under the macula

INV-
FFA-
Acute ingrowth of Vs in the inner portion of bruch’s memb or subretinal space→ vascular network→early hyperfluorescence ( foll dye inj) with late leakage-lacy pattern→ classic CNV
Occult CNV-obscuration of fibrovascular ingrowth by intervening tiss.Two types-
Fibrovascular PED-RPE elevation d/t fibrovascular ingrowth.Here hyperfluorescence slowly increases& later retention of dye leads to staining
Late leakage of undetermined source-there is little or no early hyperfluorescence & leakage from poorly defined areas

ICGA- offers additional insight
Classic CNV does not show prominent leakage d/ t higher protein binding
Areas of CNV which appear very poorly defined during FFA can be well-defined during ICG
Occult CNV appears as large plaques
OCT-
Classic CNVM-thickening or disruption of RPE-choriocapillaris complex & thickness or ret & SRF
Occult CNVM – Disruption of RPE –choriocapillaris complex & most of the fv complex lies under RPE

D/Ds-
1.Acute posterior multifocal placoid pigment epitheliopathy
2. serpigeneous choroidopathy
3.CSR
4. CME
5.ERM

SYSTEMIC RISK FACTORS-
-HT
-Hypercholestrolemia
-Smoking
Rx- pg 97Best Vitelliform Macular Dystrophy

BEST VITELLIFORM DYSTROPHY

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Vogt-Koyanagi-Harada syndrome

Vogt-Koyanagi-Harada syndrome

COMMONLY USED DRUGS IN ENDOPHTHALMITIS

White dot syndromes

White dot syndromes

Source: Kanski, Yanoff, Sankara Netralaya atlas of FFA

CENTRAL SEROUS CHORIORETINOPATHY

CENTRAL SEROUS CHORIORETINOPATHY

Definition

RETINA NOTES

R E T I N A

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Ophthalmology Notes

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Vogt-Koyanagi-Harada syndrome

Vogt-Koyanagi-Harada syndrome

COMMONLY USED DRUGS IN ENDOPHTHALMITIS

White dot syndromes

White dot syndromes Source: Kanski, Yanoff, Sankara Netralaya atlas of FFA

CENTRAL SEROUS CHORIORETINOPATHY

CENTRAL SEROUS CHORIORETINOPATHY

Definition

RETINA NOTES

R E T I N A

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White dot syndromes

Source: Kanski, Yanoff, Sankara Netralaya atlas of FFA