6.1.10 Recognises, evaluates and manages diabetic eye disease and refers accordingly. Flashcards
See Visit 2. We are only needing to discuss images.
Pathogenesis
Microangiopathy = small vessel disease (capillaries)
i.e., small BVs vulnerable to damage from high glucose levels
Due to (1) microvascular leakage & (2) microvascular occlusion
Microvascular occlusion
- Changes within the capillary bed due to high glucose levels; this can be changes within capillary basement membrane, endothelial wall damage, impaired red blood cell deformability (red blood cells are less bendable), platelets become more sticky
- This means the capillaries are more easily blocked
- Once you start seeing these occlusions, this leads to the production of the growth factor VEGF and IGF-1 to stimulate the retina to grow new vessels & feed the retina
- However, these vessels lack the same structure, and therefore and leakier and more fragile (or on a scaffolding of vitreous which is unstable)
- IRMA develop at the edge of the occluded area
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Microvascular leakage
- Occurs when there is a loss of pericytes
- Pericytes are cells which wrap around capillary walls and are reasonable for the structural integrity
- Leads the outpouching of walls (micro-aneurysms) & microvascular leakage, therefore intra-retinal haemorrhages, and retinal oedema
Signs of DR
- Most exudates, particularly from diabetic eye disease, will appear around IPL and INL (dense shadow with little or no visibility)
- Flame shaped haemorrhages – RNFL near surface
- Dot blot haemorrhages – deeper between plexiform layers
- Exudates – mainly found around IPL and INL
- Oedema – between OPL and INL
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DR Grading scale
R0 – no retinopathy
R1 – mild background retinopathy
At least one of the following features anywhere: dot haemorrhage, cotton wool spot, blot haemorrhage, flame shaped haemorrhage
Rescreen in 12 months for DRS
R2 – moderate background
4 or more haemorrhages in one hemi-field only
Rescreen in 6 months
R3 – severe background / pre-proliferative
4 or more haems
Venous beading / IRMA
R4 – proliferative
Active new vessels
Pre-retinal haemorrhage
Retinal neovasc NVD, NVE
Grading scale of DM
M0 – no maculopathy
M1 – early
Exudates >1 but <2DD from fovea
M2 – advanced
Haemorrhages or exudates within 1DD from fovea
Referral
No referral - Background retinopathy (R1 – R2)
- Microaneurysms, dot/blot haemorrhages
- Exudates >2DD from fovea
Routine - Pre-proliferative – exudates within 2DD of macula (R3 / M1)
- Cotton wool spots, venous beading, IRMA, deep retinal haemorrhages
- Exudates < 2DD of macula
Urgent - Proliferative DR and maculopathy (R4 / M2)
- Retinal neovascularising within disc diameter and/or new vessels elsewhere
- Pre-retinal fibrosis
- Exudates <1DD from fovea
Emergency referral
- Pre-retinal haemorrhage
- Traction retinal detachment
- Rubeosis
Diabetic maculopathy
Maculopathy = features of retinopathy which lie specifically within macular area
Macula specific diabetic pathology that will cause sight loss:
o Macular oedema
o Macular ischaemia – unable to treat (won’t occur without lots of other retinal features of ischaemia)
- Do not need to refer 1 small-isolated dot haem within 1DD of fovea
- SHOULD refer exudate within 1DD of fovea
- SHOULD refer retinal thickening within 1DD
Other complications of DM
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Corneal neuropathy
Reduction in corneal nerve density causing corneal desensitization
Starts with DED symptoms, progresses to breakdown of epithelium, corneal oedema & ulcers
Delayed healing of corneal epithelium
Increased risk of infection & persistent defects
**Cataract **
Age related cataracts (NS/CO/PSC) occur earlier/may progress quicker
Young diabetics may develop ‘diabetic cataract’ = snowflake opacities
Fundamental management of differernt grades of DR
- Good management significantly reduces risk profile
- Smoking cessation
- Managing weight
- Managing diet
- Medications
- Insulin - may cause hypoglycaemia which causes dizzy spells; in rare cases may cause presbyopia when first starting treatment due to shifting fluids which affect the lens; generally stabilises
- Novorapid – ingredient insulin aspart, fast-acting and works rapidly to normalise blood sugar levels, begins working after 10-20mins, lasts 3-5 hours
- Levemir – ingredient insulin detemir long acting, subcutaneous injection only, up to 24-hour duration of action
- Metformin (biguanide) (T2) – dry eye and increase risk of angle closure
- Gliclazide – lens changes, refractive error shifts
Background & pre-proliferative - Usually monitoring only
- Pre-proliferative depends how bad bleeds are
Proliferative - PRP, 2-4000 laser burns in peripheral retina
- Reduce VEGF drive, destroy ischaemic retina, lessens amount of retina requiring oxygen by killing off peripheral cells
Advanced proliferative - Multiple sessions of PRP
- Vitrectomy
- Many need to manage retinal detachment / rubeotic glaucoma
Macular oedema - Anti-VEGF agents can arrest or reserve proliferative retinopathy and macular oedema e.g. intravitreal ranibizumab (Lucentis®), less destructive than PRP
- Intravitreal corticosteroids if unresponsive to anti-VEGF: used widely to treat macular oedema, modest improvement of VA, long-acting steroid implants may be used
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Type 1 Vs Type 2
Type 1 diabetes is an autoimmune disease, which means it results from the immune system mistakenly attacking parts of the body. In the case of type 1 diabetes, the immune system incorrectly targets insulin-producing beta cells in the pancreas.
Nobody knows why this occurs, or how to stop it. The immune systems of people with type 1 diabetes continue to attack beta cells until the pancreas is incapable of producing insulin.
Type 2 diabetes is characterised by the body losing its ability to respond to insulin. This is known as insulin resistance.
The body compensates for the ineffectiveness of its insulin by producing more, but it can’t always produce enough. Over time, the strain placed on the beta cells by this level of insulin production can destroy them, diminishing insulin production.
Muscles ?
- 3rd nerve palsy
- Ischaemic will spare the pupil (microvascular damage)
- 3rd, 4th or 6th nerve. 6th is most common!
Cornea
- Epithelial erosions
- Puncate keratitis
- Stromal oedema
- Delayed wound healing
- Reduced corneal sensitivity
- Arcus
Iris
- Rubeosis - vessels seen at iris (neovasc!!) - neovascular glaucoma! Pressure increase
- Pupil size small & irregular - sympathetic denervation
- May be argyll robertson pupil
Lens
- Snowflake cataract - cortical opacities look like snowflakes
- Fluctuation in fluid causing refractive changes. Hyperopia = reduced glucose. Myopia = high glucose due to change in refractive index
- Early onset of NS & age related cataracts
Cotton Wool Spots
Isolated cotton wool spots (one or more) in the absence of any microaneurysm or haemorrhage should be counted as no DR (R0).
Any number of cotton wool spots (CWS) in the presence of other non‐referable features of DR should be graded as background DR (R1).
Venous loops
A venous loop should no longer be referred and should be regarded as a feature of R1.
Photocoagulation scars
Assign a P0 grade if no evidence of previous photocoagulation. Assign a P1 grade if evidence of previous photocoagulation (focal/grid to macula or peripheral scatter).
Dot & Blot Haems
MBH - 8-10+ blot haems across both images generally R2 - referred
These haemorrhages are in the retina’s inner nuclear and outer plexiform layers
Blot haemorrhages are larger than the width of the smallest of the 4 branches of the central retinal vein as it crosses the edge of the disc. This is provided the veins are not very dilated.
Flame haemorrhages are superficial haemorrhages in the nerve fibre layer. Any haemorrhage that is flame shaped or any MA should not be counted as a blot.
Few blot haems with quite widespread dot haems are generally graded R2
IRMA
RMA is considered present if the IRMA can still be seen on the colour image, that has not been enlarged, as well as on the red free.
If an IRMA can only be seen on a red free image and not on the colour image a referral should not be made (returned to annual screening).
