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MSc IOVS > Retinal Vascular Disease Lectures > Flashcards

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
Q

What are the main systemic diseases with ocular manifestations?

A

Diabetes
Hypertension
Thyroid disease
Rheumatoid arthritis (Sjorgren’s syndrome)

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26
Q

What condition is characterised by iris Lisch nodules and café-au-lait spots?

A

Neurofibromatosis type I

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27
Q

What inflammatory condition requires urgent referral if it presents with ocular manifestations?

A

Rheumatoid arthritis

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28
Q

How does rheumatoid arthritis present in the eyes?

A

Red eyes
Necrotising keratitis
Sjorgren’s syndrome/dry eyes

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29
Q

Which ophthalmic conditions of systemic origin commonly present in hospital?

A

Peripheral ulcerative keratitis
Uveitis
Retinitis
Ophthalmic neuritis

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30
Q

What are the ophthalmic consequences of diabetes?

A

Cataracts (<40’s)
Risk of retinal vessel occlusion
Cranial nerves III, IV, VI palsies
Diabetic retinopathy

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31
Q

What is the classification of diabetic retinopathy?

A

Background
Pre-proliferative
Proliferative

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32
Q

What are the features of background diabetic retinopathy?

A

Microaneurysms

‘Dot’ and ‘blot’ haemorrhages

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33
Q

What are the features of pre-proliferative diabetic retinopathy?

A

Haemorrhages and microaneurysms
Cotton wool spots
IRMA
Venous abnormalities (beading, loops)

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34
Q

How is moderate and severe pre-proliferative DR classified?

A

Moderate: 1 quadrant venous beading, IRMA
Severe: 4:2:1 quadrants, 4 with haemorrhage or 2 with venous beading or 1 with IRMA

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35
Q

What are the features of proliferative diabetic retinopathy?

A

Neovascularisation (Disk: NVD, elsewhere: NVE)
Pre-retinal/vitreous haemorrhages (worse)
Retinal fibrosis
Tractional retinal detachment (worst)

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36
Q

How is proliferative diabetic retinopathy treated?

A

Anti-VEGF agents

Argon laser therapy

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37
Q

What are the features of diabetic maculopathy?

A

Early vision loss

Macular HMA’s, exudates, oedema

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38
Q

What are the differences on fundoscopy between exudative and ischaemic diabetic retinopathy?

A

Exudative DR causes maculopathy but ischaemic DR usually does not

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39
Q

What is the pathogenesis of diabetic retinopathy prior to microvascular leakage?

A 
Basement membrane thickening
Endothelial/pericyte damage
Capillary venule outpouching
RBC changes, higher platelet viscosity
Hypoxia retina releases VEGF: angiogenesis
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40
Q

What anterior segment sign is seen in proliferative diabetic retinopathy?

A

Rubeosis iridis

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41
Q

What is the earliest clinically detectable change seen in diabetic retinopathy?

A

Microaneurysms

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42
Q

What angiogenic factors are release following retinal hypoxia?

A 
Growth factors (IGF-1, EGF, etc.)
VEGF (protein kinase-C activation)
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43
Q

How can diabetic retinopathy progression be reduced?

A

Less dietary sugar, fat, cholesterol

Statins, laser treatment

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44
Q

How is diabetic maculopathy treated?

A

Diabetes/BP control
Statins, anti-VEGF, laser therapy
Intravitreal steroids (dexamethasone, fluocinolone)

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45
Q

How is ischaemic diabetic retinopathy treated?

A

Diabetes/BP control alone

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46
Q

What is the gold standard treatment for diabetic eye disease?

A

Panretinal photocoagulation

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47
Q

When is VR surgery indicated in diabetic eye disease?

A

Rubeosis iridis, haemorrhages (if sub-hyaloid sleep elevated)
Retinal detachment
Vitreomacular traction (posterior hyaloid, epiretinal membranes)

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48
Q

What types of retinal detachment are there?

A

Tractional
Rhegmatogenous
Combined

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49
Q

How is refractory DMO treated?

A

Iluvien (DEX implant)

PPV +/- ILM peel

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50
Q

What are the aims of diabetic vitrectomy?

A

Relieving antero-posterior/tangential traction, less bleeding
Improves laser efficiency

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51
Q

What are the consequences of microvascular leakage in proliferative diabetic retinopathy?

A

Microaneurysms
Retinal oedema
Hard exudates

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52
Q

What features are seen in hypertensive retinopathy?

A

AV nipping, papilloedema

B/CRVO (biggest cause)

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53
Q

What features are seen in thyroid eye disease?

A 
Dry, painful eyes
Conjunctival injection
Lid retraction/oedema
Proptosis, diplopia
Optic nerve compression
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54
Q

How is thyroid eye disease managed?

A

Symptomatic treatment
Immunosuppression, surgery
Emergency: Orbital decompression

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55
Q

What are the signs of 3rd cranial nerve palsy?

A

Ptosis

Inferior, temporal unreactive pupil

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56
Q

What are the causes of a 3rd cranial nerve palsy?

A

Vasculopathy (DM, hypertension)

Aneurysm (refer to surgery!)

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57
Q

What is the blood supply of the retina

A

Internal carotid artery -> Ophthalmic artery -> Central retinal artery
Outer third supplied by the choroid
Inner two-third’s supplied by the central retinal artery

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58
Q

What is the blood supply of the choroid?

A

Short and long posterior ciliary arteries

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59
Q

What is are the physical differences between retinal arteries and retinal veins?

A

Retinal veins are larger and redder than retinal arteries

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60
Q

Which retinal layers contain the superficial, intermediate and deep plexus?

A

Superficial: Inner plexiform layer
Intermediate: Inner nuclear layer
Deep: Outer plexiform layer

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61
Q

What 500μm region of the macula is responsible for the highest visual resolution?

A

Foveal avascular zone (FAV)

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62
Q

What is the blood supply of the retinal photoreceptors?

A

Choroid

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63
Q

What cells make up the inner and outer blood-retinal barriers?

A

Inner: Endothelial cells
Outer: RPE cells

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64
Q

How does retinal vein occlusion present?

A

Sudden painless visual loss

RAPD if ischaemic

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65
Q

What investigations do ophthalmologists order if RVO is suspected?

A

BP
OCT
Fluorescein angiography

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66
Q

What investigations do GP’s order if RVO is suspected?

A 
FBC, ESR, thrombophilia screen, CRP, rheumatoid factor
U&amp;E’s, serum ACE
Blood glucose, cholesterol
ECG, X-ray
Thyroid function test
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67
Q

What fundoscopy signs are seen in RVO?

A 
Flame and 'blot' haemorrhages
Intraretinal oedema
Cotton wool spots
Engorged retinal veins
Collateral retinal vessels
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68
Q

What are the treatable complications of RVO?

A

Macular oedema

Neovascularisation (ischaemia)

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69
Q

What OCT signs are seen in RVO?

A

Exudative fluid-filled subretinal/outer nuclear layer spaces

Hyperreflective track lines

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70
Q

Who pioneered vitreo-retinal surgery?

A

Dr Robert Machemer

Professor McLeod

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71
Q

What factors affect the need for vitreo-retinal surgery?

A 
Haemorrhage time
Status of fellow eye
Retinal detachment
Vitreomacular traction
Prior laser
Premacular/intragel
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72
Q

What are the indications for vitreo-retinal surgery?

A

Rubeosis iridis, haemorrhages
Retinal detachment
Vitreomacular traction

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73
Q

What developments have improved vitreo-retinal surgery?

A

23-27G needles
Bimanual, wide-angle illumination
Oculoplasmin

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74
Q

What are the indications for surgery in RVO?

A

Vitreous haemorrhages

Epiretinal membranes

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75
Q

How is vitreous haemorrhage graded?

A

0: None
1: Mild, visible retina
2: Moderate, no visible retina, red reflex present
3: Severe, retina/red reflex not visible

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76
Q

Which surgical interventions are used to treat RVO?

A

Adventitial sheathotomy
Chorioretinal anastamoses
Radial neurotomy

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77
Q

What are the main causes of CRVO?

A

Central retinal vein thrombosis

Central retinal artery atherosclerosis

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78
Q

What are the risk factors for CRVO?

A 
Hypertension
Diabetes
Hyperlipidaemia
Obesity
Smoking
Glaucoma
Blood hyperviscosity syndromes
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79
Q

Why is anti-VEGF given pre-op? When can it be given? Any risks?

A

Better manipulation, less vitreous bleeding
Beneficial in rubeosis iridis
7 days up to 24 hours before surgery
Fibrosis risk

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80
Q

What is the pathogenesis in central retinal vein occlusion?

A

Narrowed vein, flow turbulence, partial thrombosis
Less venous outflow, high vein pressure
Oedema, haemorrhage, ischaemia
VEGF, endothelial damage, occlusion, glaucoma

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81
Q

What are the 3 classes of retinal vein occlusion?

A

Ischaemic
Non-ischaemic
Indeterminate

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82
Q

What classification factors suggest ischaemic CRVO?

A

> 10 disc diameters non-perfusion on FFA
RAPD (>1.2 logMAR units)
(NVI/NVA, <20/200 VA, perimetry, electroretinogram)

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83
Q

What classification factors suggest non-ischaemic CRVO?

A

<10 disc diameters non-perfusion on FFA

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84
Q

Where does ischaemic CRVO occur and what are the consequences?

A

Lamina cribrosa
Gross vision loss
RAPD

85
Q

Where does non-ischaemic CRVO occur and what are the vascular consequences?

A

Retrolaminar region

Fall in perfusion pressure

86
Q

How is macular oedema secondary to CRVO treated?

A

Panretinal photocoagulation (laser)
Intravitreal anti-VEGF 3-monthly
Intravitreal steroids

87
Q

What did the CATT study compare?

A

Lucentis vs Avastin to treat CRVO

88
Q

What risks are associated with CRVO treatment?

A

Glaucoma
Retinal detachment
Cataract
Endophthalmitis

89
Q

How does the prognosis differ between CRVO and BRVO?

A

BRVO can usually resolve spontaneously (70% gain >2 lines in 12 months)
CRVO prognosis depends on baseline VA

90
Q

In which vascular site can BRVO most commonly be found?

A 
Arteriovenous crossings (adventitia fuse)
Often supratemporal quadrant
91
Q

What are the risk factors for BRVO?

A

Hypertension
Cardiovascular disease
High BMI (20 y/o)
Glaucoma

92
Q

What is the most common fundoscopy site for arteriovenous crossings in BRVO?

A

Superior temporal quadrant

93
Q

What classification factors suggest ischaemia BRVO?

A

Posterior segment neovascularisation

>5 disc diameters non-perfusion on FFA

94
Q

What acute features are seen in BRVO?

A

Dilated/tortuous retinal veins, swollen optic disc, macular haemorrhage, oedema

95
Q

What chronic features are seen in BRVO?

A

Macular ischaemia, oedema, pigment change

Epiretinal membranes, SR fibrosis

96
Q

What were the inclusion criteria for the CVOS study?

A

Macular oedema due to CRVO (FA confirmed)

BCVA <20/50

97
Q

How is BRVO treated?

A

Laser (first-line): Sectoral for CMO, NVI

Anti-VEGF agents

98
Q

How many participants were involved in the CVOS study?

A

155

99
Q

What treatment for macular oedema secondary to CRVO did the CVOS study investigate?

A

Macular grid argon laser

100
Q

How long and often was the follow-up in the CVOS study?

A

4-monthly for 3 years

101
Q

How was ischaemic CRVO defined in the CVOS study?

A

> 10 disk diameters of non-perfusion on fluorescein angiography

102
Q

What were the results of the CVOS study and when were they published?

A

1995: No statistically significant difference in visual acuity post-laser treatment

103
Q

What did the BVOS study aim to investigate?

A

Argon laser to treat: Macular oedema (BRVO)
Neovascularisation
Vitreous haemorrhages

104
Q

What were the inclusion criteria for the BVOS study?

A

BRVO >3 months
<6/12 visual acuity
Non-perfusion on FA

105
Q

How long was the follow-up for the BVOS study?

A

3 years

106
Q

What treatments for macular oedema secondary to BRVO did the BVOS study investigate?

A

Argon laser treatment and PRP

107
Q

What were the results of the BVOS study?

A

> 2 lines gained in 65% (treated) vs 37% (sham)

No effect if BRVO >1 year or <6/60 VA

108
Q

Which intravitreal steroids are commonly used in clinical practice?

A

Triamcinolone (Kenolog)

Dexamethasone (Ozurdex)

109
Q

What are the three main anti-VEGF agents?

A

Ranibizumab (Lucentis)
Bevacizumab (Avastin)
Aflibercept (Eylea)

110
Q

What did the GENEVA study investigate?

A

Dexamethasone (Ozurdex) given over 6 months to treat RVO

111
Q

What were the results of the GENEVA study?

A

Ozurdex reduced BRVO macular oedema peaking at 2 months but did not last up to 6 months

112
Q

Which study investigated raised IOP through steroid retreatment?

A

Shasta

113
Q

Which trials involved Ranibizumab (Lucentis) to treat RVO?

A

BRAVO (BRVO)

CRUISE (CRVO)

114
Q

Which Ranibizumab (Lucentis) trials used laser treatment and PRN dosing as controls respectively?

A

BRIGHTER

CRYSTAL

115
Q

What treatment duration was involved in the BRAVO and CRUISE trials?

A

Monthly injections over 6 months

116
Q

What were the results of the BRAVO and CRUISE trials?

A

> 10-letter (BRVO), >14-letter (CRVO) BCVA improvements at 6 months

117
Q

What was the name of the BRAVO and CRUISE extension study? How long did this last?

A

HORIZON

1 year

118
Q

What was the name of the HORIZON extension study? How long did this last?

A

RETAIN

4 years

119
Q

How was resolved oedema defined in the RETAIN study?

A

No subretinal fluid 6 months after the last intravitreal injection

120
Q

Which trials involved Aflibercept (Eylea) to treat RVO?

A

COPERNICUS
GALILEO
VIBRANT

121
Q

What were the results of the RETAIN study?

A

Macular oedema resolved in 50% of RVO patients, 80% >20/40 VA
Injections still required

122
Q

What treatment duration was involved in the COPERNICUS and GALILEO trials?

A

Monthly injections over 6 months

123
Q

What were the results of the COPERNICUS and GALILEO trials?

A

> 21-letter (COPERNICUS), >15-letter (GALILEO) BCVA improvements at 6 months

124
Q

What did the GALILEO study investigate?

A

18-monthly vs PRN Eylea

125
Q

What did the VIBRANT study investigate?

A

Monthly Eylea vs laser treatment for BRVO

126
Q

What were the main treatment risks associated with RVO besides injection risks?

A

Raised IOP
Glaucoma
Cataracts (30%)

127
Q

When is surgery indicated for RVO? What methods are used?

A

Vitreous haemorrhages, epiretinal membranes (ask about distortion)
Chorioretinal anastamosis, radial neurotomy

128
Q

What RAO screening method is used for those <50 with no vascular risk factors?

A

Hyper-coagulability screen

129
Q

What investigations and referrals are carried out for RAO’s?

A

FBC’s: ESR/CRP, glucose, HbA1c
Carotid doppler, ECG, echo
Stroke referral

130
Q

What are the risk factors for CRAO?

A 
Smoking
Diabetes
Hypertension
Hyperlipidaemia
Cardiac valve/carotid artery disease, AF
Sickle cell disease
131
Q

What OCT signs are seen in RAO?

A

Thickened then thinner retina

132
Q

How is RAO treated?

A

IV acetazolamide
Ocular massage
Paracentesis
Thrombolytic surgery

133
Q

What are the causes of CRAO?

A

Atherosclerosis (Lamina cribrosa)
Emboli (Carotid arteries/cardiac valves)
Thrombi

134
Q

What are the 3 forms of CRAO?

A

Arteritic (GCA)
Non-arteritic (transient/permanent)
Non-arteritic with cilioretinal sparing

135
Q

What causes non-arteritic transient CRAO?

A

Vasospasm from platelet serotonin release in plaques

136
Q

What disease must be excluded when diagnosing CRAO?

A

Giant cell arteritis (Painful vision loss)

137
Q

What are the symptoms caused by GCA?

A 
Headache
Jaw claudication
Scalp tenderness
Proximal weakness/pain
Anorexia, weight loss
138
Q

How do you find emboli sources in carotid arteries or cardiac valves?

A

Clinical examination
Carotids: Doppler, angiogram
Cardiac valves: Echocardiogram

139
Q

When must treatment ideally be administered for CRAO?

A

Within 6 hours ideally

140
Q

What fundoscopy signs are seen in CRAO?

A 
Pale macular oedema
Cherry red spot in fovea
Emboli (20%)
Cattle-trucking
RAPD
141
Q

What treatment is given for CRAO secondary to GCA?

A

Methylprednisolone 250g IV 6hrly
Prednisolone 80-100mg
Temporal artery biopsy

142
Q

How long before vision loss following CRAO is irreversible?

A

90 minutes

143
Q

How does CRAO present?

A

Sudden painless severe vision loss

RAPD if ischaemic

144
Q

How is CRAO classified?

A

Non-arteritic permanent/transient
Non-arteritic + cilioretinal sparing
Arteritic (due to giant cell arteritis)

145
Q

What investigations are used to diagnose CRAO?

A

Indirect ophthalmoscopy
Fluorescein angiography
FBC’s: ESR/CRP (Excluding GCA)

146
Q

What vascular feature (32% of eyes) spares the macula in CRAO?

A

Cilioretinal artery

147
Q

What is the acute first-line management of CRAO?

A 
Isosorbide dinitrate (sublingual)
Pentoxifylline (systemic)
Inhalation therapy
Ocular massage, IV acetazolamide/mannitol
Paracentesis
148
Q

What are the causes of BRAO?

A

Emboli

Vessel thrombosis

149
Q

What are the risk factors for BRAO?

A 
Migraine (smokers)
Trauma
Coagulopathy, sickle cell disease
COCP
Mitral valve prolapse, GCA
Toxoplasmosis, syphilis
150
Q

How does BRAO present?

A

Sudden painless vision loss

Visual field defects

151
Q

What are the clinical features of BRAO?

A

Sudden painless visual loss
Visual field defect
White swollen retina
Cattle-trucking, visible emboli (>60%)

152
Q

What emboli types are seen in BRAO?

A

Cholesterol (Hollenhorst plaques)
Platelet-fibrin
Calcific emboli (Cardiac valves)

153
Q

What are the risk factors for central serous chorioretinopathy?

A

High BP, pregnancy, renal disease, organ transplant, SLE/PAN/Wegner’s, cortisol, steroids, Hispanic/Asian ancestry, ecstasy, stress

154
Q

How does central serous chorioretinopathy present?

A

Transparent blister, yellow-white dots on retina, fibrin deposits, PED (pigment migration)

155
Q

What is the pathophysiology of central serous chorioretinopathy?

A

Steroids sensitise choroid to stressors, hyperpermeable centrally, RPE stress, decompensation leads RD, PED, atrophy

156
Q

What types of central serous chorioretinopathy are there?

A

Acute

Chronic (diffuse retinal pigment epitheliopathy)

157
Q

How does acute central serous chorioretinopathy present?

A

Recurrent localised detachment, visual loss, 1+ focal leaks (FFA)

158
Q

How does chronic central serous chorioretinopathy present?

A

Large pigment change, subtle leaks (FFA)

159
Q

How does bullous IRD present?

A

Asians/steroid use: Shifting fluid, atrophy, bone spicules, telangiectasia

160
Q

How does central serous chorioretinopathy present on FFA?

A

Mottled hyperfluorescent symmetrical leaks not beyond RD (inkblot), atrophic RPE

161
Q

How does central serous chorioretinopathy present on ICG?

A

Early hypo then hyperfluorescence (later in CNV), midphase dilation, blurred contours, large vessel silhouettes (rings)

162
Q

How does central serous chorioretinopathy present on OCT?

A

Thick subfoveal choroid, dilated vessels, RD, RPE defects, ellipsoid loss, thick/granulated photoreceptor outer layer

163
Q

How does central serous chorioretinopathy present on AF?

A

Confluent hypoAF, mac/peripapillary/granular at macula, descending tracts, choroid folds, drusen, leaks

164
Q

What are the differentials for central serous chorioretinopathy?

A

POHS, Haradas, posterior scleritis, CNV, melanoma, metastases, haemangioma, optic nerve pit, AMD

165
Q

What is the prognosis of central serous chorioretinopathy following treatment?

A

90% >6/9 VA but metamorphopsia, brightness, colour issues, 1/3rd recurrent

166
Q

When is central serous chorioretinopathy treated? How is it treated?

A

Chronic signs, high activity, permanent damage to other eye
PDT, laser therapy
Diamox, Avastin, anti-mineralocorticoid, steroid antagonist, aspirin 100mg/day

167
Q

What are the risk factors for post-cataract surgery CMO?

A

Diabetes, uveitis, RVO, epiretinal membranes, age, surgery

168
Q

What is the pathogenesis of post-cataract surgery CMO?

A

Surgery, inflammatory mediators breakdown blood aqueous barrier and BRB, leaky capillaries, transudate in outer plexiform, inner nuclear layers, microcysts: IR fluid, CMO

169
Q

Which organisation carried out trials for DMO therapy?

A

Diabetic Retinopathy Clinical Research Network (DRCR.net)

170
Q

What does ETDRS stand for in terms of DR? In which year did this come out?

A

Early Treatment of Diabetic Retinopathy Study (1985)

171
Q

How is post-cataract surgery CMO treated?

A

Topical NSAID’s/steroids (4-6 weeks), anti-VEGF +/- acetazolamide, triamcinolone, vitrectomy

172
Q

What is the epidemiology of DR, DMO and clinically significant macular oedema?

A

1/3rd with diabetes have DR, 1/3rd with DR have DMO, 1/3rd with DMO have CSMO (Rule of 1/3rd’s)

173
Q

Which questions should diabetic patients be asked?

A

Last HbA1c test?
Aware of blood cholesterol level?
Smoking/other risk factors?

174
Q

What are the ideal BP and glucose levels for diabetes patients?

A

BP: <140/80mmHg
Glucose: 48-53mmol/mol

175
Q

According to Keech et al 2007, which drug was linked with reduced DR, PDR, DMO risk?

A

Fenofibrate

176
Q

Which questions should DMO patients be asked?

A

Last HbA1c test?
Aware of blood cholesterol level?
Smoking/other risk factors?

177
Q

What are the ideal BP and glucose levels for DMO patients?

A

BP: <140/80mmHg
Glucose: 48-53mmol/mol

178
Q

According to Keech et al 2007, which drug was linked with reduced DR, PDR, DMO risk?

A

Fenofibrate

179
Q

What did the FIELD study show?

A

Fenofibrate prevents DR progression and reduces need for laser

180
Q

What did the ACCORD study show?

A

40% reduction in DR progression in 4 years with fenofibrate + statin vs statin only

181
Q

Which complications are linked with DR/PDR?

A

Nephropathy, CV events, peripheral neuropathy, peripheral arterial disease

182
Q

Which complications are linked with DMO?

A

2x stroke, 2.5x MI risk

183
Q

How has DMO treatment evolved from 1985 to 2015?

A

ETDRS, Triamcinolone, Avastin, Lucentis, Iluvien, Ozurdex, Eylea

184
Q

What were the results of the ETDRS for laser treatment?

A

50% less vision loss risk (not in CSMO), Ideal time to consider laser: CSMO onset

185
Q

Which new DMO laser therapies have minimised side effects?

A

Micropulse laser

PASCAL

186
Q

How is DMO laser therapy hypothesised to work?

A

Thermal damage to retinal pigments, closes microaneurysms, improves RPE ability to remove fluid

187
Q

What were the results of the ETDRS for laser treatment?

A

50% less vision loss risk (not in CSMO), onset of CSMO is idea time to consider laser

188
Q

What is the ETDRS DRSS?

A 
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
Q

What were the key DMO Ranibizumab trials?

A 
RESOLVE
RISE &amp; RIDE
RESTORE
DRCR.net
RETAIN (vs laser)
190
Q

What were the 24-month results of the RISE & RIDE study?

A

Ranibizumab ineffective if given >1-year post-diagnosis, reduces DR progression risk

191
Q

What were the results of the RESTORE study for DMO?

A

Lucentis alone ideal, high baseline VA maintained, best VA gain seen in those with CRT >400µm

192
Q

What did the RESTORE study evaluate?

A

Ranibizimab +/- laser for DMO treatment

193
Q

What did the RISE & RIDE study for DMO evaluate?

A

Monthly Lucentis +/- PRN laser for DMO

194
Q

What were the results of the RESTORE study for DMO?

A

Lucentis alone ideal, high baseline VA maintained, best VA gain seen in CRT >400µm

195
Q

What did the DRCR.net study evaluate? What were the results?

A 
Different Ranibizumab + laser treatments
Deferred laser (6 month wait) better with anti-VEGF therapy
196
Q

What did the RISE & RIDE study evaluate?

A

Monthly Lucentis +/- PRN laser

197
Q

What did the RETAIN study for DMO evaluate?

A

Treat and Extend vs PRN Lucentis for DMO

198
Q

Which study compared Lucentis, Avastin and Eylea for DMO treatment? What were the injection criteria?

A 
Protocol T (US)
Inject in first 6 months then only if improving, defer if not improved in last 2 visits
199
Q

What were the main DMO Eylea studies? What were the results?

A

VIVID, VISTA (4 or 8 weeks vs laser)

BCVA gain with Eylea

200
Q

When was Eylea approved by NICE for use in the UK for DMO?

A

June 2015

201
Q

What did the CLARITY study for DMO evaluate? What were the results?

A

3 doses then PRN Eylea vs laser 8 weeks

DMO improved with Eylea but not if CSMO

202
Q

What were the results of the Protocol T study?

A

VA change (2 years):
Eylea>Lucentis>Avastin
Avastin better for CRT reduction

203
Q

Which study evaluted Lucentis vs laser for proliferative DMO? What was the side effect of laser therapy?

A

DRCR Protocol S

Visual field change

204
Q

What did the CLARITY study for DMO evaluate?

A

3 Eylea doses then PRN vs laser after 8 weeks

205
Q

What were the main DMO steroid studies? Which agents were used?

A

DRCR.net (Protocol B): Triamcinolone (Kenalog)
MEAD: Dexamethasone
FAME: Fluocinolone acetonide (Iluvien)

206
Q

Which steroid is not licensed for use in the eye?

A

Triamcinolone (Kenalog), intra-articular injection for arthritis

207
Q

What was the result of the DRCR.net (Protocol B) steroid study?

A

Laser better than Kenalog at 2 years, higher VA gain, lower CRT levels

208
Q

What were the results of the MEAD study?

A

Dexamethasone indicated if pseudophakic lens, non-steroid responsive DMO

209
Q

What were the results of the FAME study?

A

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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