CASE PRESENTATIONCASE PRESENTATION

Dr Kanav GuptaDr Kanav Gupta

29/07/09 29/07/09

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Mrs Sakunbai Meshram, 45 Year old Female Mrs Sakunbai Meshram, 45 Year old Female with H/O…with H/O…

GPDOV – LE>RE since 1 monthGPDOV – LE>RE since 1 month

H/O RE Cataract surgery + PCIOL 4 yrs back at HingnaH/O RE Cataract surgery + PCIOL 4 yrs back at Hingna

H/O Redness and eyeacheH/O Redness and eyeache

K/C/O HTN since 15 years under irregular treatmentK/C/O HTN since 15 years under irregular treatment

No H/O ocular trauma / dischargeNo H/O ocular trauma / discharge

No H/O spectaclesNo H/O spectacles

No H/O any systemic illnessNo H/O any systemic illness

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Ophthalmic examinationOphthalmic examination

Visual Acuity – RE – 6/60p with pinhole NIVisual Acuity – RE – 6/60p with pinhole NI LE – PL+ PR AccurateLE – PL+ PR Accurate SLESLE RERE LELELids WNL MeibomiantisLids WNL MeibomiantisConjunctiva WNL Mild congestion, CCCConjunctiva WNL Mild congestion, CCCCornea Clear ClearCornea Clear ClearAC ND Slight shallowAC ND Slight shallowIris CPN Atrophic patch at 7-9o`clockIris CPN Atrophic patch at 7-9o`clockPupil NSRTL SD Fixed, posterior synechiaePupil NSRTL SD Fixed, posterior synechiaeLens PCIOL ISC Lens PCIOL ISC

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Contd….Contd….FundusFundus: RE – Media clear LE – No View : RE – Media clear LE – No View O.D : normal margins,circular,slight pale O.D : normal margins,circular,slight pale C:D : 0.3 C:D : 0.3 B.V : mild venous tortuosuty,A.V. changes B.V : mild venous tortuosuty,A.V. changes present present with A.V. ratio of 1:4 with A.V. ratio of 1:4 Macula : dull with exudates Macula : dull with exudates FR : Not seen FR : Not seen Hemorrhages from 6-9.30 o` clock involving macula Hemorrhages from 6-9.30 o` clock involving macula TonometryTonometry: RE – 14.6 mm Hg LE – 46.9mm Hg with 10 gms: RE – 14.6 mm Hg LE – 46.9mm Hg with 10 gms

Sac SyringingSac Syringing : RE – Patent LE - Patent : RE – Patent LE - Patent4

SYSTEMIC EXAMINATIONSYSTEMIC EXAMINATION Temperature – Afebrile Temperature – Afebrile

BP – 130/80mmHgBP – 130/80mmHg

Pulse – 80/minPulse – 80/min

RR – 18/minRR – 18/min

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Lab InvestigationsLab Investigations CBC – WNL CBC – WNL

Urine R & M – WNLUrine R & M – WNL

ECG – T inversion V1-V3ECG – T inversion V1-V3

2D ECHO – IHD, Septal Wall hypokinesia, EF-45 – 55%2D ECHO – IHD, Septal Wall hypokinesia, EF-45 – 55%

RBS – 90mg/dlRBS – 90mg/dl

Conjunctival smear LE – negativeConjunctival smear LE – negative

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TREATMENTTREATMENT

Initially started with - I.V. Mannitol 100cc statInitially started with - I.V. Mannitol 100cc stat

T.Diamox 250 mg tdsT.Diamox 250 mg tds

Iotim 0.5% bd in LEIotim 0.5% bd in LE

Pressure controlled : added :LE – Predfax E/D Qid Pressure controlled : added :LE – Predfax E/D Qid

Homide E/D bdHomide E/D bd

LE cataract surgeryLE cataract surgery

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Retinal Vein OcclusionsRetinal Vein Occlusions

MorphologyMorphology

CRVOCRVO

BRVOBRVO

Hemispheric VOHemispheric VO

Hemicentral VOHemicentral VO

PapillophlebitisPapillophlebitis

Macular BRVOMacular BRVO

CENTRAL RETINAL VEIN CENTRAL RETINAL VEIN OCCLUSIONOCCLUSION

Mechanism :Mechanism :

1.1. Conditions producing Conditions producing a physical blockage a physical blockage at the level of the at the level of the lamina cribrosa. lamina cribrosa.

2. Hemodynamic factors 2. Hemodynamic factors resulting in an resulting in an obstruction to the obstruction to the flow of blood. flow of blood.

"Blood and thunder" appearance of a central retinal vein occlusion.

CRVOCRVO

PATHOLOGY PATHOLOGY

Histopathologic evaluation of eyes removed Histopathologic evaluation of eyes removed because of a central retinal vein occlusion because of a central retinal vein occlusion demonstrates an occlusion at or just behind the demonstrates an occlusion at or just behind the level of the lamina cribrosa.level of the lamina cribrosa.

At this location, the lumina of the central retinal At this location, the lumina of the central retinal artery and central retinal vein are narrower than artery and central retinal vein are narrower than they are in the orbital optic nerve, and the they are in the orbital optic nerve, and the vessels are bound by a common adventitial vessels are bound by a common adventitial sheath.sheath.

CRVO ANATOMYCRVO ANATOMY

Anatomical StudiesAnatomical Studies

In a study of 29 eyes that were enucleated 6 In a study of 29 eyes that were enucleated 6 hours to 10 years after occlusion. It was hours to 10 years after occlusion. It was hypothesized that the flow of blood through the hypothesized that the flow of blood through the central retinal vein becomes increasingly central retinal vein becomes increasingly turbulent as the vein progressively narrows at turbulent as the vein progressively narrows at the lamina cribrosa, where it also may be further the lamina cribrosa, where it also may be further impinged upon by arteriosclerosis of the impinged upon by arteriosclerosis of the adjacent central retinal artery. This turbulence adjacent central retinal artery. This turbulence damages the endothelium in the retrolaminar damages the endothelium in the retrolaminar vein, which exposes collagen and initiates vein, which exposes collagen and initiates platelet aggregation and thrombosis.platelet aggregation and thrombosis.

In another study of enucleated eyes with In another study of enucleated eyes with CVO and NVG, intraretinal VEGF CVO and NVG, intraretinal VEGF production from areas of ischemic retina production from areas of ischemic retina was demonstrated.was demonstrated.

Aqueous VEGF levels increase prior to the Aqueous VEGF levels increase prior to the development of NVI and decrease with development of NVI and decrease with regression of NVI after panretinal photo regression of NVI after panretinal photo coagulationcoagulation

Risk FactorsRisk Factors

Increasing Risk : Hypertension (BRVO)Increasing Risk : Hypertension (BRVO) Diabetes MellitusDiabetes Mellitus Advancing AgeAdvancing Age HyperlipidemiaHyperlipidemia Raised IOP (increases risk of CRVO)Raised IOP (increases risk of CRVO) Increased ESR(females)Increased ESR(females)

Decreasing Risk : Physical ActivityDecreasing Risk : Physical Activity Increased Alcohol ConsumptionIncreased Alcohol Consumption Exogenous Oestrogens(females)Exogenous Oestrogens(females)

The Eye Disease Case-Control Study Group: Risk factors for central retinal vein occlusion.

Arch Ophthalmol 114:545, 1996

UNCOMMON FACTORSUNCOMMON FACTORS

Myeloproliferative disordersMyeloproliferative disorders: Polycythemia, Abnormal : Polycythemia, Abnormal plasma proteins(myeloma).plasma proteins(myeloma).

Acquired hypercoagulable statesAcquired hypercoagulable states: : Hyperhomocysteinemia, Lupus anticoagulant, Hyperhomocysteinemia, Lupus anticoagulant, Antiphospholipid antibodies.Antiphospholipid antibodies.

Inherited hypercoagulable statesInherited hypercoagulable states: Activated protein C : Activated protein C resistance, Protein C,S deficiency, Antithrombin resistance, Protein C,S deficiency, Antithrombin deficiency,Factor XII deficiency.deficiency,Factor XII deficiency.

Inflammatory diseaseInflammatory disease: Bechet syndrome, Sarcoidosis, : Bechet syndrome, Sarcoidosis, Goodpasture Syndrome.Goodpasture Syndrome.

MiscMisc: CRF, Oral contraceptives, Hyperlipidemia: CRF, Oral contraceptives, Hyperlipidemia

ClassificationClassification

CVOS classification based on Fluorescein CVOS classification based on Fluorescein angiographic characteristics:angiographic characteristics:

Perfused or Non IschemicPerfused or Non Ischemic –less than 10 –less than 10 disc areas in diameter of retinal capillary disc areas in diameter of retinal capillary non perfusion on angiography.non perfusion on angiography.Non Perfused or IschemicNon Perfused or Ischemic – 10 or more – 10 or more disc areas in diameter if retinal capillary non disc areas in diameter if retinal capillary non perfusion.perfusion.IndeterminateIndeterminate –when there is sufficient –when there is sufficient intraretinal hemorrage to prevent intraretinal hemorrage to prevent angiographic determination of perfusion angiographic determination of perfusion statusstatus

Clinical PresentationClinical Presentation

Sudden visual impairment.Sudden visual impairment.

VA is impaired to moderate to severe degree.VA is impaired to moderate to severe degree.

Pain – usually advanced with NVI, NVG and Pain – usually advanced with NVI, NVG and increased IOP.increased IOP.

Classic clinical picture on dilated examination.Classic clinical picture on dilated examination.

Ischemic Central Retinal Vein Ischemic Central Retinal Vein Occlusion Occlusion

Sudden, painless decrease in visual acuity. Sudden, painless decrease in visual acuity.

Vision ranges from CF to hand movements.Vision ranges from CF to hand movements.

Afferent Pupillary Defect is marked. Afferent Pupillary Defect is marked.

Patients with ischemic occlusion have an average age of 68.5 Patients with ischemic occlusion have an average age of 68.5 years.years.

FundusFundus : Entire venous tree is tortuous, engorged, dilated, and dark : Entire venous tree is tortuous, engorged, dilated, and dark

- Extensive Dot-Blot & Flame Shaped Hemorrhages - Extensive Dot-Blot & Flame Shaped Hemorrhages involving peripheral retina and posterior pole. involving peripheral retina and posterior pole.

- Severe Disc Oedema and Hyperemia.- Severe Disc Oedema and Hyperemia.

- Cotton wool spots may be present- Cotton wool spots may be present

FAFA : marked delay in AV transit time >20 seconds : marked delay in AV transit time >20 seconds

central masking by retinal hemorrhagescentral masking by retinal hemorrhages

extensive areas of capillary non perfusion and vessel wall extensive areas of capillary non perfusion and vessel wall stainingstaining

ERGERG : reduced : reduced

COURSE & PROGNOSISCOURSE & PROGNOSIS

Acute signs resolve within 9-12 months and residual findings like Acute signs resolve within 9-12 months and residual findings like disc collaterals, macular epiretinal gliosis & pigmentary changes disc collaterals, macular epiretinal gliosis & pigmentary changes may remain.may remain.

Poor prognosis because of decreased visual acuity and Poor prognosis because of decreased visual acuity and neovascularization. Visual loss occurs because of macular edema, neovascularization. Visual loss occurs because of macular edema, capillary nonperfusion, overlying hemorrhage (either retinal or capillary nonperfusion, overlying hemorrhage (either retinal or vitreal), or a combination of all of these. Retinal edema usually vitreal), or a combination of all of these. Retinal edema usually gradually subsides except in the macula, where it may persist for gradually subsides except in the macula, where it may persist for many months or years. Macular holes or cysts may form.many months or years. Macular holes or cysts may form.

Rubeosis iridis develop in 50% between 2-4 months which may lead Rubeosis iridis develop in 50% between 2-4 months which may lead to NVG.to NVG.

FOLLOW UPFOLLOW UP Monthly for 6 months to detect anterior segment neovascularisation, Monthly for 6 months to detect anterior segment neovascularisation,

angle neovascularisation (for risk of NVG)angle neovascularisation (for risk of NVG)

Nonischemic Central Retinal Nonischemic Central Retinal Vein Occlusion Vein Occlusion

Most common typeMost common type

Sudden, unilateral blurred vision.Sudden, unilateral blurred vision.

VA impaired to moderate-severe degree.VA impaired to moderate-severe degree.

APD absent or mild.APD absent or mild.

Fundus : Tortuosity and dilatation Fundus : Tortuosity and dilatation - Dot n Blot & Flame shaped haemorrhages in - Dot n Blot & Flame shaped haemorrhages in

all 4 quadrants, most common in periphery all 4 quadrants, most common in periphery - Cotton Wool spots, Optic Disc and macular edema.- Cotton Wool spots, Optic Disc and macular edema.

FA : Delayed AV transit timeFA : Delayed AV transit time Good retinal capillary perfusion and late leakageGood retinal capillary perfusion and late leakage

COURSE & PROGNOSISCOURSE & PROGNOSIS

Acute signs resolve within 6-12 months and residual Acute signs resolve within 6-12 months and residual findings like disc collaterals, macular epiretinal gliosis & findings like disc collaterals, macular epiretinal gliosis & pigmentary changes may remain.pigmentary changes may remain.

Conversion to ischaemic CRVO occurs in 15% within 4 Conversion to ischaemic CRVO occurs in 15% within 4 months and 34% within 3 years.months and 34% within 3 years.

Cases that do not progresses to ischemic type the Cases that do not progresses to ischemic type the prognosis is good with return of vision to normal or near prognosis is good with return of vision to normal or near normal in 50%.normal in 50%.

Main cause for poor vision is chronic macular edema Main cause for poor vision is chronic macular edema which may lead to secondary RPE changes.which may lead to secondary RPE changes.

Standard InvestigationsStandard Investigations

Blood PressureBlood Pressure

ECGECG

CBC, ESRCBC, ESR

Urine AnalysisUrine Analysis

Protein ElectrophoreseisProtein Electrophoreseis

Random Blood Glucose, LipidRandom Blood Glucose, Lipid

INVESTIGATIONS <50 YRSINVESTIGATIONS <50 YRS

Chest X RayChest X Ray

Thrombophilia screen :Thrombophilia screen :  

Clotting screenClotting screen

Protein C,S defficiencyProtein C,S defficiency

Elevated factor VElevated factor V

Actviated protein C resistanceActviated protein C resistance

Factor V Leiden a major risk factor in females Factor V Leiden a major risk factor in females

Dysfibrogenaemia Dysfibrogenaemia

Prothrombin G20210AProthrombin G20210A

Antiphospholipid antibodiesAntiphospholipid antibodies

Autoantibodies: anti cardiolipin, lupus anticoagulant, ANAAutoantibodies: anti cardiolipin, lupus anticoagulant, ANA

General TherapyGeneral Therapy

Avoid oral contraceptivesAvoid oral contraceptivesAspirinAspirinTreat hypercholesterolemia and hypertensionTreat hypercholesterolemia and hypertensionLower IOPLower IOPAnticoagulants if requiredAnticoagulants if requiredOral steroids and non steroidal Oral steroids and non steroidal immunosuppressive agentsimmunosuppressive agents

If vision drops consider re-occlusion.If vision drops consider re-occlusion.

TREATMENTTREATMENT

IschaemicIschaemic : Laser PRP in eyes with angle neovascularisation : Laser PRP in eyes with angle neovascularisation (1500-3000 burns, spaced one burn apart) avoiding areas of (1500-3000 burns, spaced one burn apart) avoiding areas of haemorrhage.haemorrhage.Laser PRP in patients with NVD/NVE without INV/ANV (Ryan).Laser PRP in patients with NVD/NVE without INV/ANV (Ryan).

Non IschaemicNon Ischaemic : Laser PRP : Laser PRP Newer ModalitiesNewer Modalities – Cannulation and infusion of tPA – Cannulation and infusion of tPA

into vein via vitrectomy. into vein via vitrectomy. - Intravitreal Triamcinolone - Intravitreal Triamcinolone

acetonide for CME but its effect acetonide for CME but its effect is short lived. is short lived.

- Optic Nerve Sheathotomy or - Optic Nerve Sheathotomy or Radial optic neurotomy via Radial optic neurotomy via

PPVitrectomy for PPVitrectomy for decompressing the decompressing the central central retinal vein. retinal vein.

Chorioretinal Anastomosis in Non-Ischemic CRVOChorioretinal Anastomosis in Non-Ischemic CRVO

McAllister and Constable reported a surgical technique to create a chorioretinal McAllister and Constable reported a surgical technique to create a chorioretinal anastomosis in patients with non ischemic CRVO. Their current technique is to anastomosis in patients with non ischemic CRVO. Their current technique is to rupture Bruch's membrane first in an area adjacent to the edge of a vein located at rupture Bruch's membrane first in an area adjacent to the edge of a vein located at least three disc diameters from the optic disc with the argon laser; they then use a least three disc diameters from the optic disc with the argon laser; they then use a YAG laser to create a small opening in the sidewall of the adjacent vein.YAG laser to create a small opening in the sidewall of the adjacent vein.In their study there was an average of 2 attempts to create an anastomosis, which In their study there was an average of 2 attempts to create an anastomosis, which was successful in 42% patients in the first series and 67% of patients in the second was successful in 42% patients in the first series and 67% of patients in the second series. In the first series, ischemic central vein occlusion did not develop in any of the series. In the first series, ischemic central vein occlusion did not develop in any of the patients in whom a successful anastomosis was produced, but it did develop in 31% patients in whom a successful anastomosis was produced, but it did develop in 31% of patients in whom such an anastomosis could not be created. All the patients with a of patients in whom such an anastomosis could not be created. All the patients with a successful anastomosis had an improvement in final visual acuity compared with successful anastomosis had an improvement in final visual acuity compared with pretreatment visual acuity. In the group of patients with an unsuccessful pretreatment visual acuity. In the group of patients with an unsuccessful anastomosis, 38% had an improvement in visual acuity, 44% had a worse visual anastomosis, 38% had an improvement in visual acuity, 44% had a worse visual acuity, and 19% had no change. acuity, and 19% had no change. There were some minor complications, such as vitreous and retinal hemorrhages, There were some minor complications, such as vitreous and retinal hemorrhages, that tended to clear well. However, there were some major complications, including a that tended to clear well. However, there were some major complications, including a major fibrovascular proliferation at the sites where surgery was attempted.This major fibrovascular proliferation at the sites where surgery was attempted.This complication can lead to serious, nonclearing vitreous hemorrhages and/or traction complication can lead to serious, nonclearing vitreous hemorrhages and/or traction retinal detachment and may require a vitrectomy for treatment. retinal detachment and may require a vitrectomy for treatment.

NeovascularizationNeovascularization

Most serious complication.Most serious complication.

NVI and NVG occurs in about 25% cases NVI and NVG occurs in about 25% cases of ischemic CRVO`s.of ischemic CRVO`s.

The low incidence of retinal surface The low incidence of retinal surface neovascularization in ischemic central neovascularization in ischemic central retinal vein occlusion is thought to be due retinal vein occlusion is thought to be due to the destruction of endothelial cells, to the destruction of endothelial cells, which provide the source for endothelial which provide the source for endothelial proliferation and neovascularization. proliferation and neovascularization.

BRANCH RETINAL VEIN BRANCH RETINAL VEIN OCCLUSION OCCLUSION

The clinical picture of BRVO is the retinal hemorrages that are segmental in origin

Pathology & MorphologyPathology & MorphologyLeber was probably the first investigator to note the connection between branch retinal vein occlusion and the arteriovenous intersection. Koyanagi found that the majority (77.7%) of his cases of temporal vein occlusion involved the superior retina and later confirmed this anatomic observation, noting that branch retinal vein occlusion always occurs at an arteriovenous intersection. Histologically, where the vein and artery cross, they share a common adventitial sheath, and the venous lumen may be diminished by as much as a third at this crossing.

Some have postulated that turbulent blood flow at the crossing site causes focal swelling of the endothelium and deeper vein wall tissue leading to venous obstruction and sometimes thrombus formation.

Risk FactorsRisk Factors

Systemic hypertensionSystemic hypertensionDiabetesDiabetesHyperlipidemiaHyperlipidemiaGlaucomaGlaucomaSmokingSmokingAge related atherosclerosisAge related atherosclerosisAntiphospholipid antibodiesAntiphospholipid antibodiesElevated plasma homocysteine levelsElevated plasma homocysteine levelsLow serum folateLow serum folateEyes with shorter axial lengthsEyes with shorter axial lengths

CLASSIFICATIONCLASSIFICATION

Major BRVO: At the Optic discMajor BRVO: At the Optic disc

Away from the disc but Away from the disc but involving the branches of macula. involving the branches of macula.

Minor Macular BRVO : involving only macular branchMinor Macular BRVO : involving only macular branch

Peripheral BRVO Peripheral BRVO

Clinical FeaturesClinical Features

VAVA depends on extent of macular involvement. Patients with depends on extent of macular involvement. Patients with macular involvement presents with sudden onset of blurred vision macular involvement presents with sudden onset of blurred vision and metamorphopsia or a relative visual field defect.and metamorphopsia or a relative visual field defect.

FundusFundus: Dilatation and tortuosity of venous segment distal to site of : Dilatation and tortuosity of venous segment distal to site of occlusion and attenuation proximally.occlusion and attenuation proximally.

- Flame shaped, dot n blot haemorrhage, retinal - Flame shaped, dot n blot haemorrhage, retinal edema and occasionally cotton wool spots. edema and occasionally cotton wool spots.

FAFA: Variable delayed venous filling: Variable delayed venous filling

blockage by bloodblockage by blood

Hyperfluorescence due to leakageHyperfluorescence due to leakage

Hypofluorescence due to capillary non perfusionHypofluorescence due to capillary non perfusion

Pruning of vessels in ischaemic areasPruning of vessels in ischaemic areas

COURSE & PROGNOSISCOURSE & PROGNOSIS

Acute phase resolves in 6-12 months and may be replaced by the Acute phase resolves in 6-12 months and may be replaced by the following:following:

- Hard exudates, venous sheathing and variable amount of residual - Hard exudates, venous sheathing and variable amount of residual haemorrhage.haemorrhage.

- Collateral venous channels characterised by slightly tortuous - Collateral venous channels characterised by slightly tortuous vessels between inferior and superior vascular arcades.vessels between inferior and superior vascular arcades.

Prognosis is good due to formation of collaterals within 6 months in Prognosis is good due to formation of collaterals within 6 months in 50% of eyes with return of visual acuity to 6/12.50% of eyes with return of visual acuity to 6/12.

Management of BRVOManagement of BRVO

BRVO is often associated with pre-existing vascular disease. BRVO is often associated with pre-existing vascular disease.

Evaluation for systemic abnormalities, in particular hypertension, Evaluation for systemic abnormalities, in particular hypertension, should be performed. should be performed.

Exclusion of diabetes, hyperlipidaemia, hyperviscosity/coagulation Exclusion of diabetes, hyperlipidaemia, hyperviscosity/coagulation states, antiphospholipid syndrome, or any other predisposing states, antiphospholipid syndrome, or any other predisposing condition should be performed and regular review is required until condition should be performed and regular review is required until the haemorrhages clear.the haemorrhages clear.

Approximately one third to one half of patients with BRVO have Approximately one third to one half of patients with BRVO have recovery of visual acuity to 6/12, or better, without therapy. recovery of visual acuity to 6/12, or better, without therapy.

Thus the treatment of BRVO has focused on management of vision- Thus the treatment of BRVO has focused on management of vision- limiting complications.limiting complications.

COMPLICATIONSCOMPLICATIONS

3 main vision limiting:3 main vision limiting:

- Chronic macular edema- Chronic macular edema

- Macular nonperfusion- Macular nonperfusion

- Vitreous hemorrhage from - Vitreous hemorrhage from Neovascularisation Neovascularisation

Chronic Macular EdemaChronic Macular Edema

Most common cause of persistent poor VA after BRVO.Most common cause of persistent poor VA after BRVO.

Treatment:Treatment:

- Grid laser photocoagulation-Grid laser photocoagulation-(100-200 um, 0.1 sec duration (100-200 um, 0.1 sec duration spaced one burn width apart, away from fovea and intraretinal spaced one burn width apart, away from fovea and intraretinal haemorrhages should be avoided. Follow up should be after 3 haemorrhages should be avoided. Follow up should be after 3 months.months.

- Intravitreal Triamcinolone acetonide(a corticosteriod suspension Intravitreal Triamcinolone acetonide(a corticosteriod suspension which reduces breakdown of blood retinal barrier) but its effect lasts which reduces breakdown of blood retinal barrier) but its effect lasts for only 6 months.for only 6 months.

- Vitrectomy with or without sheathotomy.Vitrectomy with or without sheathotomy.

NeovascularizationNeovascularizationNVD develops in 10% and NVE in about 25% of eyes within 6-12 NVD develops in 10% and NVE in about 25% of eyes within 6-12 months usually but may develop at anytime within first 3 years, only months usually but may develop at anytime within first 3 years, only in eyes that shows large area(>5 disc diameters in diameter) of in eyes that shows large area(>5 disc diameters in diameter) of retinal capillary nonperfusion.retinal capillary nonperfusion.

Neovascularisation is a serious complication which can lead to Neovascularisation is a serious complication which can lead to recurrent vitreous and pan-retinal haemorrhage and tractional retinal recurrent vitreous and pan-retinal haemorrhage and tractional retinal detachment.detachment.

Vitreous haemorrhage due to neovascularization occurs in Vitreous haemorrhage due to neovascularization occurs in approximately half of the eyes with neovascularization. Butner and approximately half of the eyes with neovascularization. Butner and McPherson found that 11.3% of spontaneous vitreous hemorrhages McPherson found that 11.3% of spontaneous vitreous hemorrhages were due to a BRVO, an incidence second only to proliferative were due to a BRVO, an incidence second only to proliferative diabetic retinopathy as a cause of vitreous haemorrhage. diabetic retinopathy as a cause of vitreous haemorrhage.

TreatmentTreatment : Scatter laser photocoagulation covering the entire : Scatter laser photocoagulation covering the entire involved sector with PPV if vitreous Hemorrhage Is present. Follow involved sector with PPV if vitreous Hemorrhage Is present. Follow up should be after 3 weeksup should be after 3 weeks

HEMICENTRAL AND HEMICENTRAL AND

HEMISPHERIC HEMISPHERIC

RETINAL VEIN OCCLUSIONRETINAL VEIN OCCLUSION

The terms hemicentral retinal vein occlusion and The terms hemicentral retinal vein occlusion and hemispheric retinal vein occlusion refer to eyes hemispheric retinal vein occlusion refer to eyes in which approximately half of the venous outflow in which approximately half of the venous outflow from the retina, either the superior or the inferior, from the retina, either the superior or the inferior, has been occluded. In approximately 20% of has been occluded. In approximately 20% of eyes, the branch retinal veins draining the eyes, the branch retinal veins draining the superior and inferior halves of the retina enter superior and inferior halves of the retina enter the lamina cribrosa separately before joining to the lamina cribrosa separately before joining to form a single central retinal vein.form a single central retinal vein.Hemicentral retinal vein occlusion is an occlusion Hemicentral retinal vein occlusion is an occlusion of one of these dual trunks of the central retinal of one of these dual trunks of the central retinal vein within the nerve. Hemispheric retinal vein vein within the nerve. Hemispheric retinal vein occlusion is an occlusion involving the venous occlusion is an occlusion involving the venous drainage from approximately half of the retina, drainage from approximately half of the retina, either the superior or the inferior retinaeither the superior or the inferior retina

ANATOMY OF HCRVOANATOMY OF HCRVO

Hemispheric retinal vein Hemispheric retinal vein occlusionsocclusions

In some eyes, the nasal retina is not drained by a separate vein, but In some eyes, the nasal retina is not drained by a separate vein, but by a branch of either the superior or the inferior temporal vein. It is by a branch of either the superior or the inferior temporal vein. It is the occlusion of one of these veins draining both the nasal retina the occlusion of one of these veins draining both the nasal retina and the superior or inferior retina near the optic disc that accounts and the superior or inferior retina near the optic disc that accounts for the majority of hemispheric retinal vein occlusions. for the majority of hemispheric retinal vein occlusions.

The treatment and classification are similar to that of branch retinal The treatment and classification are similar to that of branch retinal vein occlusion. vein occlusion.

Fluorescein Angiography HCRVOFluorescein Angiography HCRVO

MACULAR BRANCH RETINAL MACULAR BRANCH RETINAL VEIN OCCLUSION VEIN OCCLUSION

Patients complain of blurring or distortion of vision. Patients complain of blurring or distortion of vision.

Superior macular vein occlusions are more common than inferior, Superior macular vein occlusions are more common than inferior, and some degree of macular edema is present in approximately and some degree of macular edema is present in approximately 85% of these eyes.85% of these eyes.

Although small areas of capillary nonperfusion are present in Although small areas of capillary nonperfusion are present in approximately 20% of eyes, neovascularization is not seen. Joffe approximately 20% of eyes, neovascularization is not seen. Joffe and associates pointed out that clues such as small collateral and associates pointed out that clues such as small collateral channels and microaneurysms often suggest the diagnosis. channels and microaneurysms often suggest the diagnosis.

Treatment of macular edema in macular vein occlusion by grid laser Treatment of macular edema in macular vein occlusion by grid laser photocoagulation. photocoagulation.

Macular Oedema- FFAMacular Oedema- FFA

Fluorescence in the Fluorescence in the macula indicates capillary macula indicates capillary leakage and acute phase.leakage and acute phase.

PAPILLOPHLEBITIS PAPILLOPHLEBITIS In 1961, Lyle and Wybar described six young, healthy patients with In 1961, Lyle and Wybar described six young, healthy patients with a unilateral, relatively benign condition characterized by mild a unilateral, relatively benign condition characterized by mild blurring of vision, essentially normal visual acuity, dilated and blurring of vision, essentially normal visual acuity, dilated and tortuous retinal vessels, a varying amount of retinal hemorrhage, tortuous retinal vessels, a varying amount of retinal hemorrhage, optic disc edema and cotton wool spots.optic disc edema and cotton wool spots.

All six patients improved spontaneously, but were left with sheathing All six patients improved spontaneously, but were left with sheathing of retinal vessels and the formation of vessels on the optic disc. Lyle of retinal vessels and the formation of vessels on the optic disc. Lyle and Wybar called this condition "retinal vasculitis" and believed it to and Wybar called this condition "retinal vasculitis" and believed it to be due to a central retinal vein occlusion secondary to an be due to a central retinal vein occlusion secondary to an inflammatory vasculitis of the venous system.inflammatory vasculitis of the venous system.

Lonn and Hoyt agreed with this aetiology, but felt that Lonn and Hoyt agreed with this aetiology, but felt that "papillophlebitis" was a more appropriate descriptive term."papillophlebitis" was a more appropriate descriptive term.

Other C/F – enlarged blind spot on perimetry.Other C/F – enlarged blind spot on perimetry.

FA – mild delay in AV transit time, hyperfluorescence and good FA – mild delay in AV transit time, hyperfluorescence and good capillary perfusioncapillary perfusion