6.1.10: Recognises, evalutes & manages diabetic eye disease & refers accordingly Flashcards

1
Q

What is diabetic retinopathy and what are the risk factors?

A

Dysfunction of the retinal vasculature caused by chronic hyperglycaemia resulting in structural damage to the neural retina.
Poor metabolic control
Risk Factor – Duration of diabetes, Glycaemic control, Hypertension, Pregnancy, Hyperlipidaemia, Smoking,
Age (T1 no DR <13yrs, T2 20% DR at diagnosis), Ethnicity (African, Hispanic, South Asian)

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2
Q

What is the pathogenesis of Diabetic Retinopathy?

A
  1. Damage to the endothelium
  2. Loss of pericytes)
  3. Breakdown of blood-retinal barrier
  4. Thickening of capillary basement membrane
  5. VEGF release
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3
Q

Describe microangiopathy in Diabetic Retinopathy - microvascular occlusion and microvascular leakage?

A

o Microvascular occlusion -> Retinal ischaemia -> Cotton wool spots, capillary closure, AV shunts,
Neovascularisation
o Microvascular leakage -> Breakdown of blood-retinal barrier -> Retinal Haemorrhage, Retinal exudates and oedema

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4
Q

What are key signs of diabetic retinopathy?

A

o Flame Haemorrhages
o Dot-blot
o Exudates
o CWS
o Microaneurysms
o Venous Beading
o NVD
o IRMA (intra – retinal microvascular abnormalities)

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5
Q

Describe background retinoapthy?

A

– Few scattered Microaneurysms, haemorrhages, exudates and cotton wool spots.
o Microaneurysms – early clinical sign of DR, small red dot sometime indistinguishable from haemorrhages (20 - 200microns). Weakening of the capillary walls due to a loss of pericytes resulting in
an outpouching (typically in the INL)
o Exudates – located between inner plexiform and inner nuclear layer, yellow waxy appearance, leakage of
lipoproteins from the capillaries.
o Haemorrhages – Dot and Blot – originate from venous end of capillaries and therefore situated in compact
middle layer. Flame Shaped – originate from the superficial precapillary arterioles and therefore follow RNFL
(more likely hypertensive retinopathy)
o Cotton wool spots (CWS) – retinal microinfarcts as a consequence of retinal ischaemia caused by blockage in axoplasmic transport in retinal nerve fibres. accumulations of neuronal debris within the nerve fibre layer as a result of interruption of normal axoplasmic flow. This debris accumulates in the ganglion cell nerve axons.

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6
Q

Describe pre-proliferative retinopathy?

A

represents increasing retinal ischaemia (sight threatening complication)
o Venous irregularities – Beading, Duplication and Looping – definite indication of ischaemia
o Multiple retinal haemorrhages
o Multiple CWS – Greater than 5
o IRMA (intra – retinal microvascular abnormalities) – AV shunts in the retinal layer. A-V shunt (abnormal connection between an artery and a vein) that bypasses the capillary bed in the retina

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7
Q

Describe proliferative retinopathy?

A

results from retinal hypoperfusion and unregulated growth factor production
o Neovascularisation – New fine brittle vessels grow in front of the plane on the retina (corkscrew in
appearance). NVD – New vessels on disc. NVE – new vessels elsewhere
o Pre-retinal Haemorrhage – Retinal NV grow in front of the plane of the retina and become attached to the
posterior vitreous surface when they bleed blood accumulates in front of retina.
o Vitreous Haemorrhage – occurs when haemorrhage from NV breaks into the vitreous. May cause sudden
onset blob in vision or severe visual loss
o Fibrous Tissue

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8
Q

Describe maculopathy?

A

Results from the leakage of fluid from the retinal capillaries around the fovea (Sight threatening) –
Microaneurysms, haemorrhages and exudates at the macula.
o Focal – Due to focal leakage from microaneurysms and capillaries.
o Diffuse – Diffuse leakage from capillaries throughout the posterior pole
o Ischaemic – Due to hypoperfusion of the macula
M1: DMO, Haems, Exudates - routine referral

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9
Q

What classes as advanced diabetic eye disease?

A

Tractional retinal detachment due to fibrous tissue, Rubeosis Iridis (Neovascular Glaucoma)

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10
Q

What is R0 on SDRGS? no visible retinopathy When is recall?

A

No diabetic retinopathy anywhere
Rescreen 12 months

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11
Q

What is R1 on SDRGS? mild When is recall?

A

Background diabetic retinopathy BDR - mild
The presence of at least one of any of the following features anywhere
dot haemorrhages
microaneurysms
hard exudates
cotton wool spots
blot haemorrhages
superficial/ flame shaped haemorrhages
Rescreen 12 months

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12
Q

What is R2 on SDRGS? Observable background When is recall?

A

Background diabetic retinopathy BDR - observable
Four or more blot haemorrhages in one hemi-field only (Inferior and superior hemi-fields delineated by a line passing through the centre of the fovea and optic disc)
Rescreen 6 months (or refer to ophthalmology if this
is not feasible)

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13
Q

What is R3 on SDRGS? Referable background When is recall?

A

Background diabetic retinopathy BDR – referable
Any of the following features:
Four or more blot haemorrhages in both inferior and superior hemi-fields
Venous beading
IRMA
Refer ophthalmology - These patients may be kept under surveillance and will not necessarily receive immediate laser treatment

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14
Q

What is R4 on SDRGS? Proliferative When is recall?

A

Proliferative diabetic retinopathy PDR
Any of the following features:
Active new vessels
Vitreous haemorrhage
Refer ophthalmology - These patients are
likely to receive laser treatment or another
intervention

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15
Q

What is M0 on SDRGS? no maculopathy When is recall?

A

No features 2 disc diameters from the centre of the
fovea sufficient to qualify for M1 or M2 as defined below.
Rescreen 12 months

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16
Q

What is M1 on SDRGS? no maculopathy When is recall?

A

Lesions as specified below within a radius of > 1 but 2 disc diameters the centre of the fovea
Any hard exudates
Rescreen 6 months (or refer to ophthalmology if this
is not feasible)

17
Q

What is M2 on SDRGS? no maculopathy When is recall?

A

Lesions as specified below within a radius of 1 disc
diameter of the centre of the fovea
Any blot haemorrhages
Any hard exudates
Refer ophthalmology - These patients may be kept under surveillance and will not necessarily receive immediate laser treatment.

18
Q

What is the treatment for diabetic retinopathy? What are the complications and issues with these txs?

A
  • Good control of blood sugar, blood pressure and cholesterol levels.
  • Regular diabetic eye screening
    Treatment - Laser Photocoagulation – Outpatient procedure, Local anaesthetic with contact lens, Focal and
    Panretinal photocoagulation.
  • Vitrectomy for vitreous haemorrhage - clears visual axis, reduces VEGF reducing
    neovascularisation especially when combined with anti-VEGF.
    o Panretinal Laser – PRP – scatter therapy for PDR (Proliferative DR). Removes Neovascularisation and
    stops the progression of the growth of these vessels.
    o Focal Laser – Localised laser for DMO (Diabetic Macular Oedema)
    o Issues – Destructive treatment, discomfort with PRP. Multiple session,
    o Complications – Focal – accidental foveal burn, deterioration of ischaemic maculopathy. PRP – limitation of
    driving visual field, scotoma, decreased night vision, choroidal detachment, pre-retinal haemorrhage,
    deteriorating of existing DMO.
19
Q

Describe anti-VEGF treatment and diabetic maculopathy?

A

VEGF levels are increased in the retina and vitreous of eyes with DR. Therapy inhibits
VEGF targets the underlying pathogenesis of DMO. (Central retinal thickness >400microns). Stops intraocular new
blood vessel growth (used in px with vitreous haemorrhages prior to vitrectomy). Causes sudden contract of
fibrous tissue (Tractional RD). Very effective in cases of rubeosis iridis (Avastin currently used). Better than laser
PRP.
o Eylea, Lucentis & Avastin (unlicensed)- Widely used in the treatment of DMO. Lucentis monthly follow up
and injection, Eylea 2 monthly after loading dose

20
Q

Describe intravitreal steroids as a treatment for diabetic maculopathy?

A

Steroids reduce the inflammation of vessels which causes the breakdown of capillaries and pericyte loss
Intravitreal Steroids – generally work longer than anti-VEGF but milder effect on DMO. Released via
slow release implant with in the eye.
o Dexamethasone slow release – 3-6 months
o Fluocinolone – 18- 24 months – only when other treatment fail and IOL Px only
o Complications – Cataract and Glaucoma risk is susceptible individuals.

21
Q

What is the English referral criteria for diabetic retinopathy?

A

o R0 – No Diabetic Retinopathy – Annual Review
o R1 – Background Diabetic Retinopathy – Annual Review (If under screening programme)
o R2 – Pre-Proliferative Retinopathy – Routine Referral
o R3 – Proliferative Retinopathy – Urgent Referral
o M0 – No Maculopathy – Annual Review
o M1 - Maculopathy – Routine Referral
o *If undiagnosed diabetic with DR refer to GP/Into Screening Programme