Download presentation
Published byAudrey Epps Modified over 10 years ago
1
Overview Of Retinal Conditions Clinical and OCT Findings Central Coast Day Hospital Inaugural Optometrist Conference 26th February 2012 Anil Arora
2
What you might rather be doing
3
What you might feel like right now
4
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
5
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
6
Optical coherence tomography
7
Normal macula Foveal depression Symmetrical contour
Normal thickness of fovea and perifoveal tissues Flat and regular RPE
8
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
9
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 ,000 of these will have significant vision loss from geographic atrophy or from exudative changes
10
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
11
Drusen Accumulation of debris between the RPE and Bruch’s membrane
12
Exudative changes –SRF and sub-RPE fluid
Fovea SRF RPE SRF and RPE detachment RPE thinned and irregular
13
PED – serous and fibrovascular
Serous PED dépression fovéale Fovea RD DSR DEP PED Occult Fibro vascular PED
14
Role of OCT in ARMD Evaluation of exudative changes
Quantification of retinal thickness Response to treatment with anti-VEGF agents
15
Role Of OCT In ARMD Response to treatment
16
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
17
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
18
Diabetic Retinopathy Two types of retinopathy
Nonproliferative retinopathy (NPDR) Early stage diabetic retinopathy Proliferative retinopathy (PDR) Later stage diabetic retinopathy
19
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
20
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
21
Proliferative Diabetic Retinopathy
22
Proliferative Diabetic Retinopathy
With PDR, vision is affected when any of the following occur: Vitreous haemorrhage Traction retinal detachment Neovascular glaucoma Vitreous haemorrhage
23
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
24
OCT scan showing macular oedema
25
Diabetic macular oedema – focal, cystoid and diffuse
26
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
27
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
28
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
29
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.
30
Retinal Detachment
31
Retinal Detachment
32
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
33
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
34
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
35
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
36
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
37
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
38
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
39
Branch Retinal Vein Occlusion
Management Intravitreal Avastin Intravitreal triamcinolone or dexamethasone Retinal laser Manage hypertension and other risk factors
40
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
41
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
42
Macular Hole
43
Macular hole OCT showing a macular hole before and after surgery
44
Stages of a macular hole on OCT
45
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
46
Epiretinal Membrane
47
Epiretinal Membrane With Pseudohole
48
Epiretinal membrane Without pseudohole With pseudohole
49
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
50
Vitreomacular traction syndrome
51
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
52
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
53
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
54
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
55
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
56
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
57
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
58
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
59
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
60
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
61
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
Similar presentations
© 2024 SlidePlayer.com. Inc.
All rights reserved.