Overview Of Retinal Conditions Clinical and OCT Findings Central Coast Day Hospital Inaugural Optometrist Conference 26th February 2012 Anil Arora.

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Presentation transcript:

Overview Of Retinal Conditions Clinical and OCT Findings Central Coast Day Hospital Inaugural Optometrist Conference 26th February 2012 Anil Arora

What you might rather be doing

What you might feel like right now

100 Things To Do Before You Die (www.bucketquiz.com) Give your mother a dozen red roses and tell her you love her. Shower in a waterfall. Sleep under the stars. Fart in a crowded space Give to a charity. Run a marathon. Reflect on your greatest weakness, and realize how it is your greatest strength. Attend a Sunday morning ophthalmology conference in Terrigal -especially any lectures on retinal conditions and OCT

OPTICAL COHERENCE TOMOGRAPHY IN RETINAL DISEASES Shows accumulation of fluid within the retina and below the retina Changes in the neurosensory retina Cystic changes Alteration of contour or thickness Vitreous – retinal interface abnormalities Irregularity or elevation of the RPE Quantification of the abnormalities and measurement of treatment response OPTICAL COHERENCE TOMOGRAPHY IN RETINAL DISEASES 5

Optical coherence tomography

Normal macula Foveal depression Symmetrical contour Normal thickness of fovea and perifoveal tissues Flat and regular RPE

Important Retinal Conditions Age-related macular degeneration Diabetic retinopathy Retinal detachment and predisposing diseases Central and branch retinal vein occlusion Macular hole Epiretinal membrane Vitreomacular traction syndrome Central serous retinopathy

Age-Related Macular Degeneration Leading cause of blindness in the elderly Prevalence rate rises sharply with each decade In Australia there are about 5 million people 50+ ~ 15% of these will have age-related macular changes 1- 2% or 50-100,000 of these will have significant vision loss from geographic atrophy or from exudative changes

Exudative Macular Degeneration EXAMINATION Visual acuity Variable – depends on size and location of haemorrhage/exudation Amsler grid testing Fundus examination Haemorrhage Elevation by subretinal fluid/blood Drusen Pigment changes/atrophy/scarring

Drusen Accumulation of debris between the RPE and Bruch’s membrane

Exudative changes –SRF and sub-RPE fluid Fovea SRF RPE SRF and RPE detachment RPE thinned and irregular

PED – serous and fibrovascular Serous PED dépression fovéale Fovea RD DSR DEP PED Occult Fibro vascular PED

Role of OCT in ARMD Evaluation of exudative changes Quantification of retinal thickness Response to treatment with anti-VEGF agents

Role Of OCT In ARMD Response to treatment

Diabetic Retinopathy Presence of diabetic microvascular lesions Most frequent ocular complication of DM 1/3rd rule – About 1/3rd of all diabetics have some degree of retinopathy and in about 1/3rd of these have sight-threatening disease After 15 years about 70% of people with diabetes will have some retinopathy

Risk Factors For Retinopathy Development of diabetic retinopathy related to: Duration of diabetes Glycaemic control Hypertension management Serum lipids and cholesterol Other factors eg. pregnancy, nephropathy

Diabetic Retinopathy Two types of retinopathy Nonproliferative retinopathy (NPDR) Early stage diabetic retinopathy Proliferative retinopathy (PDR) Later stage diabetic retinopathy

Nonproliferative Diabetic Retinopathy (NPDR) Also called background diabetic retinopathy. Earliest stage of diabetic retinopathy. Damaged blood vessels in the retina leak fluid and blood into the eye. Cholesterol or other fat deposits from blood, called hard exudates, may leak into retina. Top: Healthy retina Bottom: NPDR with hard exudates

Proliferative Diabetic Retinopathy Characterised by the growth of new blood vessels in response to tissue hypoxia NVD – new vessels at or within 1 DD of the optic disc NVE – new vessels elsewhere in the retina Can lead to: Vitreous haemorrhage Tractional retinal detachment

Proliferative Diabetic Retinopathy

Proliferative Diabetic Retinopathy With PDR, vision is affected when any of the following occur: Vitreous haemorrhage Traction retinal detachment Neovascular glaucoma Vitreous haemorrhage

Diabetic Macular Oedema Most common cause of decreased vision and blindness in diabetic retinopathy Indicated by findings of microaneurysms, haemorrhages or hard exudates within 2DD of the fovea CSME (Clinically significant macular oedema) Complicated definition, but basically retinal thickening or hard exudates within 500 um of the fovea

OCT scan showing macular oedema

Diabetic macular oedema – focal, cystoid and diffuse

Role of OCT in Diabetic Retinopathy Confirm clinical suspicion of macular oedema Quantification of extent of oedema Diagnosis of macular traction and localised macular tractional retinal detachment in cases of proliferative retinopathy Evaluation of response to treatment – laser and /or intravitreal Avastin/Triamcinolone

Retinal Detachment Often preceded by a vitreous detachment with patient seeing flashes and floaters Usually starts as a blurring or loss of peripheral vision in one area that progresses centrally More likely in those with a history of Myopia Ocular trauma or surgery

Retinal Detachment Most commonly due to a posterior vitreous detachment with a retinal tear developing About 10% of PVD develop a retinal tear Risk of tear much higher if blood or pigmented cells present in vitreous

Retinal Detachment If a retinal tear is found before the retina detaches, it can often be treated with laser photocoagulation or cryotherapy or a combination of these.

Retinal Detachment

Retinal Detachment

Retinal Detachment Surgical Management Scleral buckle/cryotherapy Vitrectomy +/- buckle/cryotherapy +/- endolaser +/- intraocular gas +/- silicone oil +/- perfluorocarbon liquid Pneumatic retinopexy In-rooms procedure Gas injection and positioning

Role of OCT in Retinal Detachment Very limited role as the diagnosis is clinical and treatment in most cases is surgical Useful in assessing reason for poor vision following retinal detachment repair with anatomical reattachment of the retina. May show: Persistent macular oedema/subretinal fluid Damage to photoreceptors Thinned and atrophic retina Epiretinal membrane

Central Retinal Vein Occlusion Common cause of visual loss Usually history of hypertension Two main forms Non-ischaemic Ischaemic 75-80% non-ischaemic at presentation 15% non-ischaemic may convert to ischaemic 50% of ischaemic -->neovascular glaucoma

Central Retinal Vein Occlusion Cause Of Visual Loss In CRVO In non-ischaemic CRVO vision reduction due to macular oedema &/or haemorrhage In ischaemic CRVO vision reduced from macular ischaemia or later by retinal neovascularization with vitreous haemorrhage or from neovascular glaucoma

Central Retinal Vein Occlusion Management Macular oedema Intravitreal Avastin Intravitreal triamcinolone / dexamethasone Macular grid laser in younger patients (<60) Ischaemia and neovascular complications Panretinal photocoagulation Anti-VEGF drugs Management of hypertension and other cardiovascular risk factors

Branch Retinal Vein Occlusion Usually occurs in patients 50 – 70 yo Hypertension is the main risk factor (70%) Occurs at an A-V crossing where vein and artery have a common adventitial sheath Visual loss from macular oedema, haemorrhage or ischaemia

Branch Retinal Vein Occlusion Late Complications Retinal or optic disc neovascularization with vitreous haemorrhage Epiretinal membrane Chronic macular oedema with formation of a foveal cyst or lamellar hole “Atrophic maculopathy” from prolonged macular oedema or ischaemia

Branch Retinal Vein Occlusion Management Intravitreal Avastin Intravitreal triamcinolone or dexamethasone Retinal laser Manage hypertension and other risk factors

Role of OCT in RVO Assessment of macular oedema Quantification of retinal thickness Response of macular oedema to treatment with intravitreal agents and/or laser Assessment of late complications – epiretinal membrane, lamellar hole

Macular Hole Central visual loss in elderly VA usually 6/36 – 6/60 5 – 10% bilateral Treatment consists of vitrectomy, peeling of the cortical vitreous +/- internal limiting membrane peeling and intravitreal gas injection with one to two weeks of face-down positioning

Macular Hole

Macular hole OCT showing a macular hole before and after surgery

Stages of a macular hole on OCT

Epiretinal Membrane Usually idiopathic, seen in patients over 60 Sometimes after vein occlusion, inflammation Variable effect on vision - blurring, distortion May have associated cystoid macular oedema Pseudohole – may look like macular hole Retinal vessels irregular and tortuous Vitrectomy and peeling if VA 6/18 or worse or even with better vision but troublesome distortion

Epiretinal Membrane

Epiretinal Membrane With Pseudohole

Epiretinal membrane Without pseudohole With pseudohole

Role of OCT in Macular Hole and Epiretinal Membrane Clearly shows hole morphology Differentiates full-thichness hole from lamellar hole or pseudohole Demonstrates associated conditions such as macular oedema, macular cyst and vitreoretinal traction Shows response to treatment eg. closure of macular hole, successful peeling of ERM

Vitreomacular traction syndrome

Vitreomacular traction syndrome Traction on the retina by taut or contracted vitreous gel May be part of a spectrum – VMT may be the result of antero-posterior traction while macular hole may be from tangential traction Shows up well on OCT, sometimes in an asymptomatic patient with a normal retina

OCT in VMT More questions than answers? The more you know the less you understand – LAO TSE The more I learn, the more I learn how little I know - SOCRATES Possible precursor to lamellar hole or macular hole/cyst ? Possible precursor to epiretinal membrane formation? Spectrum of vitreretinal interface disorders – VMT, ERM, macular cyst, lamellar hole, full-thickness macular hole

VMT Treatment Usually vitrectomy with removal of as much cortical vitreous as possible ERM peel if ERM present Intraocular gas fill and face down positioning OCT useful to demonstrate post-op macular structure and release of traction

Central Serous Retinopathy CSR Usually middle-aged male Central visual blur/distortion Micropsia Association with “stress” Can be subtle and easily missed on clinical examination Vast majority recover

OCT in CSR Shows extent of SRF very well – able to show patient Can monitor progress of disease with serial OCT Does not show leakage site in RPE. Need fluorescein angiography

Conclusion Multitude of common and important retinal conditions Clinical diagnosis and an understanding of the potential severity of the condition are vital to good outcomes OCT adds to our ability to diagnose and manage retinal diseases and is increasing our understanding of these conditions

Question 1 OCT is useful in exudative (“wet”) ARMD for all the following reasons EXCEPT: Confirming the presence of subretinal or sub-RPE fluid Assessing and quantifying the amount of fluid present Assessing the size and activity of the choroidal neovascular membrane Assessing response of the exudative changes to treatment

Question 2 OCT is useful in diabetic retinopathy to: Assess the size and number of diabetic microaneurysms Assess hard exudates and cotton-wool spots Assess retinal and/or optic disc new vessels Assess diabetic macular oedema

Question 3 Retinal detachment: Is most commonly due to a posterior vitreous detachment with a retinal tear Is best managed by monitoring with regular OCT examinations Is most common in those with a history of hypertension Usually resolves without treatment over several months

Question 4 The following are true about epiretinal membranes EXCEPT: Can result in blurring and distortion of central vision If visually symptomatic they should be treated with laser photocoagulation May be associated with cystoids macular oedema May spontaneously separate from the retina

Question 5 Central serous retinopathy: Results in loss of central vision if not treated Is managed by using OCT to find the leakage site Is usually due to a leak at the level of the RPE Is typically a disease of elderly females