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Retinal Vascular Disease Lectures Flashcards

1
Q

What are the risk factors for diabetic retinopathy?

A 
Diabetes duration
Hyperlipidaemia
Poor glycaemic control
Hypertension
Smoking
Ethnicity (black/Hispanic)
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2
Q

What was the landmark diabetic retinopathy trial?

A

UKPDS (Younis et al, 2002)

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3
Q

What are the common ophthalmic complications of diabetes?

A

Retinopathy
Iridopathy
Unstable refraction

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4
Q

What is the disease process in diabetic retinopathy (DR) that compromises retinal perfusion?

A

Microangiopathy

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5
Q

What components make up retinal capillaries?

A

Endothelial cells (blood-retinal barrier)
Basement membrane
Pericytes

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6
Q

What are the effects of hyperglycaemia on retinal capillaries?

A

Endothelial cell/pericyte apoptosis
More porous basement membrane
Reduced retinal perfusion
VEGF breaks down blood-retinal barrier

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7
Q

What are the two forms of capillary damage in diabetic retinopathy?

A

Exudative (macular oedema)

Ischaemic (neovascularisation)

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8
Q

What signs are seen in exudative diabetic retinopathy?

A

‘Dot’ and ‘blot’ haemorrhages
Intraretinal oedema
Hard exudates

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9
Q

Which investigations may be used to identify fluid in retinal layers?

A

Fundoscopy

OCT

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10
Q

Which investigation may be used to identify retinal vessel leakage?

A

Fluorescein angiography (FA)

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11
Q

What is a retinal micro-aneurysm?

A

Asymmetrical dilatation of weakened capillary wall after pericyte loss

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12
Q

What is the classical appearance of macular oedema on fluorescein angiography?

A

Petal-shaped

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13
Q

What factors lead to capillary occlusions secondary to intravascular coagulation?

A

More platelet stickiness
More leucocyte adhesion
Less endothelial function
Altered haemodynamics

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14
Q

What is the macular consequence of ischaemic diabetic retinopathy

A

Enlargement of the foveal avascular zone (no treatment available)

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15
Q

What fundoscopy signs are seen in severe retinal ischaemia?

A

Extensive haemorrhages
Cotton wool spots
Engorged retinal veins
IRMA

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16
Q

Cotton wool spots are found in which retinal layer? Which imaging form identifies them well?

A 
Nerve fibre layer
Fluorescein angiography (FA)
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17
Q

Proliferative diabetic retinopathy is caused by which angiogenic factor and which cells produce this protein?

A

VEGF

Retinal endothelial cells

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18
Q

What are the stages of angiogenesis?

A 
Invasion
Mitosis
Canalisation
Loop formation
Vascular arcade formation
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19
Q

Which proliferative diabetic retinopathy complications are treatable?

A

Macular oedema

Neovascularisation

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20
Q

What examinations and investigations are carried out for DR patients?

A

Visual acuity/fields
Colour/red-free fundus imaging
Fluorescein angiography
OCT (especially for macular oedema)

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21
Q

What are the diabetic retinopathy classification stages?

A

R0: No retinopathy
R1: Few I/R haemorrhages, hard exudates, cotton wool spots
R2: Many I/R haemorrhages, venous beading/loops, IRMA
R3: Neovascularisation, pre-retinal haemorrhage, fibrosis, tractional retinal detachment

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22
Q

How is diabetic maculopathy classified?

A

M0: No disease
M1a: Exudate <1 disc diameter of foveal centre, >half disc area (<1DD: M1b)
M1c: Microaneurysm, haemorrhage <1DD of foveal centre if best VA <6/12

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23
Q

How do inflammatory retinal disorders commonly present?

A

Vision loss, floaters
Anterior uveitis
Vitreous opacities
White patches/retinal vessels

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24
Q

What neurodegenerative condition is characterised by blunted venules, an elongated foveal tip on OCT and a pale fovea?

A

Macular telangiectasia type 2

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25
What are the main systemic diseases with ocular manifestations?
Diabetes Hypertension Thyroid disease Rheumatoid arthritis (Sjorgren’s syndrome)
26
What condition is characterised by iris Lisch nodules and café-au-lait spots?
Neurofibromatosis type I
27
What inflammatory condition requires urgent referral if it presents with ocular manifestations?
Rheumatoid arthritis
28
How does rheumatoid arthritis present in the eyes?
Red eyes Necrotising keratitis Sjorgren's syndrome/dry eyes
29
Which ophthalmic conditions of systemic origin commonly present in hospital?
Peripheral ulcerative keratitis Uveitis Retinitis Ophthalmic neuritis
30
What are the ophthalmic consequences of diabetes?
Cataracts (<40’s) Risk of retinal vessel occlusion Cranial nerves III, IV, VI palsies Diabetic retinopathy
31
What is the classification of diabetic retinopathy?
Background Pre-proliferative Proliferative
32
What are the features of background diabetic retinopathy?
Microaneurysms | ‘Dot’ and ‘blot’ haemorrhages
33
What are the features of pre-proliferative diabetic retinopathy?
Haemorrhages and microaneurysms Cotton wool spots IRMA Venous abnormalities (beading, loops)
34
How is moderate and severe pre-proliferative DR classified?
Moderate: 1 quadrant venous beading, IRMA Severe: 4:2:1 quadrants, 4 with haemorrhage or 2 with venous beading or 1 with IRMA
35
What are the features of proliferative diabetic retinopathy?
Neovascularisation (Disk: NVD, elsewhere: NVE) Pre-retinal/vitreous haemorrhages (worse) Retinal fibrosis Tractional retinal detachment (worst)
36
How is proliferative diabetic retinopathy treated?
Anti-VEGF agents | Argon laser therapy
37
What are the features of diabetic maculopathy?
Early vision loss | Macular HMA’s, exudates, oedema
38
What are the differences on fundoscopy between exudative and ischaemic diabetic retinopathy?
Exudative DR causes maculopathy but ischaemic DR usually does not
39
What is the pathogenesis of diabetic retinopathy prior to microvascular leakage?
``` Basement membrane thickening Endothelial/pericyte damage Capillary venule outpouching RBC changes, higher platelet viscosity Hypoxia retina releases VEGF: angiogenesis ```
40
What anterior segment sign is seen in proliferative diabetic retinopathy?
Rubeosis iridis
41
What is the earliest clinically detectable change seen in diabetic retinopathy?
Microaneurysms
42
What angiogenic factors are release following retinal hypoxia?
``` Growth factors (IGF-1, EGF, etc.) VEGF (protein kinase-C activation) ```
43
How can diabetic retinopathy progression be reduced?
Less dietary sugar, fat, cholesterol | Statins, laser treatment
44
How is diabetic maculopathy treated?
Diabetes/BP control Statins, anti-VEGF, laser therapy Intravitreal steroids (dexamethasone, fluocinolone)
45
How is ischaemic diabetic retinopathy treated?
Diabetes/BP control alone
46
What is the gold standard treatment for diabetic eye disease?
Panretinal photocoagulation
47
When is VR surgery indicated in diabetic eye disease?
Rubeosis iridis, haemorrhages (if sub-hyaloid sleep elevated) Retinal detachment Vitreomacular traction (posterior hyaloid, epiretinal membranes)
48
What types of retinal detachment are there?
Tractional Rhegmatogenous Combined
49
How is refractory DMO treated?
Iluvien (DEX implant) | PPV +/- ILM peel
50
What are the aims of diabetic vitrectomy?
Relieving antero-posterior/tangential traction, less bleeding Improves laser efficiency
51
What are the consequences of microvascular leakage in proliferative diabetic retinopathy?
Microaneurysms Retinal oedema Hard exudates
52
What features are seen in hypertensive retinopathy?
AV nipping, papilloedema | B/CRVO (biggest cause)
53
What features are seen in thyroid eye disease?
``` Dry, painful eyes Conjunctival injection Lid retraction/oedema Proptosis, diplopia Optic nerve compression ```
54
How is thyroid eye disease managed?
Symptomatic treatment Immunosuppression, surgery Emergency: Orbital decompression
55
What are the signs of 3rd cranial nerve palsy?
Ptosis | Inferior, temporal unreactive pupil
56
What are the causes of a 3rd cranial nerve palsy?
Vasculopathy (DM, hypertension) | Aneurysm (refer to surgery!)
57
What is the blood supply of the retina
Internal carotid artery -> Ophthalmic artery -> Central retinal artery Outer third supplied by the choroid Inner two-third's supplied by the central retinal artery
58
What is the blood supply of the choroid?
Short and long posterior ciliary arteries
59
What is are the physical differences between retinal arteries and retinal veins?
Retinal veins are larger and redder than retinal arteries
60
Which retinal layers contain the superficial, intermediate and deep plexus?
Superficial: Inner plexiform layer Intermediate: Inner nuclear layer Deep: Outer plexiform layer
61
What 500μm region of the macula is responsible for the highest visual resolution?
Foveal avascular zone (FAV)
62
What is the blood supply of the retinal photoreceptors?
Choroid
63
What cells make up the inner and outer blood-retinal barriers?
Inner: Endothelial cells Outer: RPE cells
64
How does retinal vein occlusion present?
Sudden painless visual loss | RAPD if ischaemic
65
What investigations do ophthalmologists order if RVO is suspected?
BP OCT Fluorescein angiography
66
What investigations do GP’s order if RVO is suspected?
``` FBC, ESR, thrombophilia screen, CRP, rheumatoid factor U&E’s, serum ACE Blood glucose, cholesterol ECG, X-ray Thyroid function test ```
67
What fundoscopy signs are seen in RVO?
``` Flame and 'blot' haemorrhages Intraretinal oedema Cotton wool spots Engorged retinal veins Collateral retinal vessels ```
68
What are the treatable complications of RVO?
Macular oedema | Neovascularisation (ischaemia)
69
What OCT signs are seen in RVO?
Exudative fluid-filled subretinal/outer nuclear layer spaces | Hyperreflective track lines
70
Who pioneered vitreo-retinal surgery?
Dr Robert Machemer | Professor McLeod
71
What factors affect the need for vitreo-retinal surgery?
``` Haemorrhage time Status of fellow eye Retinal detachment Vitreomacular traction Prior laser Premacular/intragel ```
72
What are the indications for vitreo-retinal surgery?
Rubeosis iridis, haemorrhages Retinal detachment Vitreomacular traction
73
What developments have improved vitreo-retinal surgery?
23-27G needles Bimanual, wide-angle illumination Oculoplasmin
74
What are the indications for surgery in RVO?
Vitreous haemorrhages | Epiretinal membranes
75
How is vitreous haemorrhage graded?
0: None 1: Mild, visible retina 2: Moderate, no visible retina, red reflex present 3: Severe, retina/red reflex not visible
76
Which surgical interventions are used to treat RVO?
Adventitial sheathotomy Chorioretinal anastamoses Radial neurotomy
77
What are the main causes of CRVO?
Central retinal vein thrombosis | Central retinal artery atherosclerosis
78
What are the risk factors for CRVO?
``` Hypertension Diabetes Hyperlipidaemia Obesity Smoking Glaucoma Blood hyperviscosity syndromes ```
79
Why is anti-VEGF given pre-op? When can it be given? Any risks?
Better manipulation, less vitreous bleeding Beneficial in rubeosis iridis 7 days up to 24 hours before surgery Fibrosis risk
80
What is the pathogenesis in central retinal vein occlusion?
Narrowed vein, flow turbulence, partial thrombosis Less venous outflow, high vein pressure Oedema, haemorrhage, ischaemia VEGF, endothelial damage, occlusion, glaucoma
81
What are the 3 classes of retinal vein occlusion?
Ischaemic Non-ischaemic Indeterminate
82
What classification factors suggest ischaemic CRVO?
>10 disc diameters non-perfusion on FFA RAPD (>1.2 logMAR units) (NVI/NVA, <20/200 VA, perimetry, electroretinogram)
83
What classification factors suggest non-ischaemic CRVO?
<10 disc diameters non-perfusion on FFA
84
Where does ischaemic CRVO occur and what are the consequences?
Lamina cribrosa Gross vision loss RAPD
85
Where does non-ischaemic CRVO occur and what are the vascular consequences?
Retrolaminar region | Fall in perfusion pressure
86
How is macular oedema secondary to CRVO treated?
Panretinal photocoagulation (laser) Intravitreal anti-VEGF 3-monthly Intravitreal steroids
87
What did the CATT study compare?
Lucentis vs Avastin to treat CRVO
88
What risks are associated with CRVO treatment?
Glaucoma Retinal detachment Cataract Endophthalmitis
89
How does the prognosis differ between CRVO and BRVO?
BRVO can usually resolve spontaneously (70% gain >2 lines in 12 months) CRVO prognosis depends on baseline VA
90
In which vascular site can BRVO most commonly be found?
``` Arteriovenous crossings (adventitia fuse) Often supratemporal quadrant ```
91
What are the risk factors for BRVO?
Hypertension Cardiovascular disease High BMI (20 y/o) Glaucoma
92
What is the most common fundoscopy site for arteriovenous crossings in BRVO?
Superior temporal quadrant
93
What classification factors suggest ischaemia BRVO?
Posterior segment neovascularisation | >5 disc diameters non-perfusion on FFA
94
What acute features are seen in BRVO?
Dilated/tortuous retinal veins, swollen optic disc, macular haemorrhage, oedema
95
What chronic features are seen in BRVO?
Macular ischaemia, oedema, pigment change | Epiretinal membranes, SR fibrosis
96
What were the inclusion criteria for the CVOS study?
Macular oedema due to CRVO (FA confirmed) | BCVA <20/50
97
How is BRVO treated?
Laser (first-line): Sectoral for CMO, NVI | Anti-VEGF agents
98
How many participants were involved in the CVOS study?
155
99
What treatment for macular oedema secondary to CRVO did the CVOS study investigate?
Macular grid argon laser
100
How long and often was the follow-up in the CVOS study?
4-monthly for 3 years
101
How was ischaemic CRVO defined in the CVOS study?
>10 disk diameters of non-perfusion on fluorescein angiography
102
What were the results of the CVOS study and when were they published?
1995: No statistically significant difference in visual acuity post-laser treatment
103
What did the BVOS study aim to investigate?
Argon laser to treat: Macular oedema (BRVO) Neovascularisation Vitreous haemorrhages
104
What were the inclusion criteria for the BVOS study?
BRVO >3 months <6/12 visual acuity Non-perfusion on FA
105
How long was the follow-up for the BVOS study?
3 years
106
What treatments for macular oedema secondary to BRVO did the BVOS study investigate?
Argon laser treatment and PRP
107
What were the results of the BVOS study?
>2 lines gained in 65% (treated) vs 37% (sham) | No effect if BRVO >1 year or <6/60 VA
108
Which intravitreal steroids are commonly used in clinical practice?
Triamcinolone (Kenolog) | Dexamethasone (Ozurdex)
109
What are the three main anti-VEGF agents?
Ranibizumab (Lucentis) Bevacizumab (Avastin) Aflibercept (Eylea)
110
What did the GENEVA study investigate?
Dexamethasone (Ozurdex) given over 6 months to treat RVO
111
What were the results of the GENEVA study?
Ozurdex reduced BRVO macular oedema peaking at 2 months but did not last up to 6 months
112
Which study investigated raised IOP through steroid retreatment?
Shasta
113
Which trials involved Ranibizumab (Lucentis) to treat RVO?
BRAVO (BRVO) | CRUISE (CRVO)
114
Which Ranibizumab (Lucentis) trials used laser treatment and PRN dosing as controls respectively?
BRIGHTER | CRYSTAL
115
What treatment duration was involved in the BRAVO and CRUISE trials?
Monthly injections over 6 months
116
What were the results of the BRAVO and CRUISE trials?
>10-letter (BRVO), >14-letter (CRVO) BCVA improvements at 6 months
117
What was the name of the BRAVO and CRUISE extension study? How long did this last?
HORIZON | 1 year
118
What was the name of the HORIZON extension study? How long did this last?
RETAIN | 4 years
119
How was resolved oedema defined in the RETAIN study?
No subretinal fluid 6 months after the last intravitreal injection
120
Which trials involved Aflibercept (Eylea) to treat RVO?
COPERNICUS GALILEO VIBRANT
121
What were the results of the RETAIN study?
Macular oedema resolved in 50% of RVO patients, 80% >20/40 VA Injections still required
122
What treatment duration was involved in the COPERNICUS and GALILEO trials?
Monthly injections over 6 months
123
What were the results of the COPERNICUS and GALILEO trials?
>21-letter (COPERNICUS), >15-letter (GALILEO) BCVA improvements at 6 months
124
What did the GALILEO study investigate?
18-monthly vs PRN Eylea
125
What did the VIBRANT study investigate?
Monthly Eylea vs laser treatment for BRVO
126
What were the main treatment risks associated with RVO besides injection risks?
Raised IOP Glaucoma Cataracts (30%)
127
When is surgery indicated for RVO? What methods are used?
Vitreous haemorrhages, epiretinal membranes (ask about distortion) Chorioretinal anastamosis, radial neurotomy
128
What RAO screening method is used for those <50 with no vascular risk factors?
Hyper-coagulability screen
129
What investigations and referrals are carried out for RAO’s?
FBC’s: ESR/CRP, glucose, HbA1c Carotid doppler, ECG, echo Stroke referral
130
What are the risk factors for CRAO?
``` Smoking Diabetes Hypertension Hyperlipidaemia Cardiac valve/carotid artery disease, AF Sickle cell disease ```
131
What OCT signs are seen in RAO?
Thickened then thinner retina
132
How is RAO treated?
IV acetazolamide Ocular massage Paracentesis Thrombolytic surgery
133
What are the causes of CRAO?
Atherosclerosis (Lamina cribrosa) Emboli (Carotid arteries/cardiac valves) Thrombi
134
What are the 3 forms of CRAO?
Arteritic (GCA) Non-arteritic (transient/permanent) Non-arteritic with cilioretinal sparing
135
What causes non-arteritic transient CRAO?
Vasospasm from platelet serotonin release in plaques
136
What disease must be excluded when diagnosing CRAO?
Giant cell arteritis (Painful vision loss)
137
What are the symptoms caused by GCA?
``` Headache Jaw claudication Scalp tenderness Proximal weakness/pain Anorexia, weight loss ```
138
How do you find emboli sources in carotid arteries or cardiac valves?
Clinical examination Carotids: Doppler, angiogram Cardiac valves: Echocardiogram
139
When must treatment ideally be administered for CRAO?
Within 6 hours ideally
140
What fundoscopy signs are seen in CRAO?
``` Pale macular oedema Cherry red spot in fovea Emboli (20%) Cattle-trucking RAPD ```
141
What treatment is given for CRAO secondary to GCA?
Methylprednisolone 250g IV 6hrly Prednisolone 80-100mg Temporal artery biopsy
142
How long before vision loss following CRAO is irreversible?
90 minutes
143
How does CRAO present?
Sudden painless severe vision loss | RAPD if ischaemic
144
How is CRAO classified?
Non-arteritic permanent/transient Non-arteritic + cilioretinal sparing Arteritic (due to giant cell arteritis)
145
What investigations are used to diagnose CRAO?
Indirect ophthalmoscopy Fluorescein angiography FBC’s: ESR/CRP (Excluding GCA)
146
What vascular feature (32% of eyes) spares the macula in CRAO?
Cilioretinal artery
147
What is the acute first-line management of CRAO?
``` Isosorbide dinitrate (sublingual) Pentoxifylline (systemic) Inhalation therapy Ocular massage, IV acetazolamide/mannitol Paracentesis ```
148
What are the causes of BRAO?
Emboli | Vessel thrombosis
149
What are the risk factors for BRAO?
``` Migraine (smokers) Trauma Coagulopathy, sickle cell disease COCP Mitral valve prolapse, GCA Toxoplasmosis, syphilis ```
150
How does BRAO present?
Sudden painless vision loss | Visual field defects
151
What are the clinical features of BRAO?
Sudden painless visual loss Visual field defect White swollen retina Cattle-trucking, visible emboli (>60%)
152
What emboli types are seen in BRAO?
Cholesterol (Hollenhorst plaques) Platelet-fibrin Calcific emboli (Cardiac valves)
153
What are the risk factors for central serous chorioretinopathy?
High BP, pregnancy, renal disease, organ transplant, SLE/PAN/Wegner's, cortisol, steroids, Hispanic/Asian ancestry, ecstasy, stress
154
How does central serous chorioretinopathy present?
Transparent blister, yellow-white dots on retina, fibrin deposits, PED (pigment migration)
155
What is the pathophysiology of central serous chorioretinopathy?
Steroids sensitise choroid to stressors, hyperpermeable centrally, RPE stress, decompensation leads RD, PED, atrophy
156
What types of central serous chorioretinopathy are there?
Acute | Chronic (diffuse retinal pigment epitheliopathy)
157
How does acute central serous chorioretinopathy present?
Recurrent localised detachment, visual loss, 1+ focal leaks (FFA)
158
How does chronic central serous chorioretinopathy present?
Large pigment change, subtle leaks (FFA)
159
How does bullous IRD present?
Asians/steroid use: Shifting fluid, atrophy, bone spicules, telangiectasia
160
How does central serous chorioretinopathy present on FFA?
Mottled hyperfluorescent symmetrical leaks not beyond RD (inkblot), atrophic RPE
161
How does central serous chorioretinopathy present on ICG?
Early hypo then hyperfluorescence (later in CNV), midphase dilation, blurred contours, large vessel silhouettes (rings)
162
How does central serous chorioretinopathy present on OCT?
Thick subfoveal choroid, dilated vessels, RD, RPE defects, ellipsoid loss, thick/granulated photoreceptor outer layer
163
How does central serous chorioretinopathy present on AF?
Confluent hypoAF, mac/peripapillary/granular at macula, descending tracts, choroid folds, drusen, leaks
164
What are the differentials for central serous chorioretinopathy?
POHS, Haradas, posterior scleritis, CNV, melanoma, metastases, haemangioma, optic nerve pit, AMD
165
What is the prognosis of central serous chorioretinopathy following treatment?
90% >6/9 VA but metamorphopsia, brightness, colour issues, 1/3rd recurrent
166
When is central serous chorioretinopathy treated? How is it treated?
Chronic signs, high activity, permanent damage to other eye PDT, laser therapy Diamox, Avastin, anti-mineralocorticoid, steroid antagonist, aspirin 100mg/day
167
What are the risk factors for post-cataract surgery CMO?
Diabetes, uveitis, RVO, epiretinal membranes, age, surgery
168
What is the pathogenesis of post-cataract surgery CMO?
Surgery, inflammatory mediators breakdown blood aqueous barrier and BRB, leaky capillaries, transudate in outer plexiform, inner nuclear layers, microcysts: IR fluid, CMO
169
Which organisation carried out trials for DMO therapy?
Diabetic Retinopathy Clinical Research Network (DRCR.net)
170
What does ETDRS stand for in terms of DR? In which year did this come out?
Early Treatment of Diabetic Retinopathy Study (1985)
171
How is post-cataract surgery CMO treated?
Topical NSAID's/steroids (4-6 weeks), anti-VEGF +/- acetazolamide, triamcinolone, vitrectomy
172
What is the epidemiology of DR, DMO and clinically significant macular oedema?
1/3rd with diabetes have DR, 1/3rd with DR have DMO, 1/3rd with DMO have CSMO (Rule of 1/3rd's)
173
Which questions should diabetic patients be asked?
Last HbA1c test? Aware of blood cholesterol level? Smoking/other risk factors?
174
What are the ideal BP and glucose levels for diabetes patients?
BP: <140/80mmHg Glucose: 48-53mmol/mol
175
According to Keech et al 2007, which drug was linked with reduced DR, PDR, DMO risk?
Fenofibrate
176
Which questions should DMO patients be asked?
Last HbA1c test? Aware of blood cholesterol level? Smoking/other risk factors?
177
What are the ideal BP and glucose levels for DMO patients?
BP: <140/80mmHg Glucose: 48-53mmol/mol
178
According to Keech et al 2007, which drug was linked with reduced DR, PDR, DMO risk?
Fenofibrate
179
What did the FIELD study show?
Fenofibrate prevents DR progression and reduces need for laser
180
What did the ACCORD study show?
40% reduction in DR progression in 4 years with fenofibrate + statin vs statin only
181
Which complications are linked with DR/PDR?
Nephropathy, CV events, peripheral neuropathy, peripheral arterial disease
182
Which complications are linked with DMO?
2x stroke, 2.5x MI risk
183
How has DMO treatment evolved from 1985 to 2015?
ETDRS, Triamcinolone, Avastin, Lucentis, Iluvien, Ozurdex, Eylea
184
What were the results of the ETDRS for laser treatment?
50% less vision loss risk (not in CSMO), Ideal time to consider laser: CSMO onset
185
Which new DMO laser therapies have minimised side effects?
Micropulse laser | PASCAL
186
How is DMO laser therapy hypothesised to work?
Thermal damage to retinal pigments, closes microaneurysms, improves RPE ability to remove fluid
187
What were the results of the ETDRS for laser treatment?
50% less vision loss risk (not in CSMO), onset of CSMO is idea time to consider laser
188
What is the ETDRS DRSS?
``` DR severity grading (very mild, mild, moderate, severe): No DR: 10 NPDR: (20, 35, 43-47, 53A-E) PDR: (61, 65, 71-75, 81-85) ```
189
What were the key DMO Ranibizumab trials?
``` RESOLVE RISE & RIDE RESTORE DRCR.net RETAIN (vs laser) ```
190
What were the 24-month results of the RISE & RIDE study?
Ranibizumab ineffective if given >1-year post-diagnosis, reduces DR progression risk
191
What were the results of the RESTORE study for DMO?
Lucentis alone ideal, high baseline VA maintained, best VA gain seen in those with CRT >400µm
192
What did the RESTORE study evaluate?
Ranibizimab +/- laser for DMO treatment
193
What did the RISE & RIDE study for DMO evaluate?
Monthly Lucentis +/- PRN laser for DMO
194
What were the results of the RESTORE study for DMO?
Lucentis alone ideal, high baseline VA maintained, best VA gain seen in CRT >400µm
195
What did the DRCR.net study evaluate? What were the results?
``` Different Ranibizumab + laser treatments Deferred laser (6 month wait) better with anti-VEGF therapy ```
196
What did the RISE & RIDE study evaluate?
Monthly Lucentis +/- PRN laser
197
What did the RETAIN study for DMO evaluate?
Treat and Extend vs PRN Lucentis for DMO
198
Which study compared Lucentis, Avastin and Eylea for DMO treatment? What were the injection criteria?
``` Protocol T (US) Inject in first 6 months then only if improving, defer if not improved in last 2 visits ```
199
What were the main DMO Eylea studies? What were the results?
VIVID, VISTA (4 or 8 weeks vs laser) | BCVA gain with Eylea
200
When was Eylea approved by NICE for use in the UK for DMO?
June 2015
201
What did the CLARITY study for DMO evaluate? What were the results?
3 doses then PRN Eylea vs laser 8 weeks | DMO improved with Eylea but not if CSMO
202
What were the results of the Protocol T study?
VA change (2 years): Eylea>Lucentis>Avastin Avastin better for CRT reduction
203
Which study evaluted Lucentis vs laser for proliferative DMO? What was the side effect of laser therapy?
DRCR Protocol S | Visual field change
204
What did the CLARITY study for DMO evaluate?
3 Eylea doses then PRN vs laser after 8 weeks
205
What were the main DMO steroid studies? Which agents were used?
DRCR.net (Protocol B): Triamcinolone (Kenalog) MEAD: Dexamethasone FAME: Fluocinolone acetonide (Iluvien)
206
Which steroid is not licensed for use in the eye?
Triamcinolone (Kenalog), intra-articular injection for arthritis
207
What was the result of the DRCR.net (Protocol B) steroid study?
Laser better than Kenalog at 2 years, higher VA gain, lower CRT levels
208
What were the results of the MEAD study?
Dexamethasone indicated if pseudophakic lens, non-steroid responsive DMO
209
What were the results of the FAME study?
33-43% >15 letter BCVA gain but 80-85% needed cataract surgery, 37% needed IOP-lowering drugs

MSc IOVS (4 decks)

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