Classification of Diabetic retinopathy
✍️ Mild non-proliferative diabetic retinopathy (NPDR)
☝️ At least one microaneurysm.
✍️ Moderate non-proliferative diabetic retinopathy (one of the following )
☝️ intraretinal haemorrhages
☝️microaneurysms
☝️ cotton-wool spots
☝️venous beading
☝️intraretinal microvascular abnormalities (IRMA).
✍️ Severe nonproliferative diabetic retinopathy
☝️relies on the 4–2-1 rule
☝️ Intraretinal haemorrhages or microaneurysms in 4 quadrants.
☝️ Venous beading in 2 quadrants.
☝️IRMA in 1 quadrant.
✍️ Very severe non-proliferative diabetic retinopathy
☝️at least two of the criteria for severe NPDR.
✍️ Non-high risk proliferative diabetic retinopathy
☝️new vessels on the disc (NVD) or elsewhere (NVE), but criteria not met for high-risk proliferative diabetic retinopathy (PDR) below.
✍️ High-risk proliferative diabetic retinopathy: at least one of the following:
☝️NVD >1/3 disc area.
☝️NVD plus vitreous or preretinal haemorrhage.
☝️NVE >1/2 disc area plus preretinal or vitreous haemorrhage.
✍️ Advanced proliferative diabetic retinopathy
☝️tractional retinal detachment.
🛑 High risk DR from from severe NPDR to advanced PDR
🛑 Macular exudates or thickening ( maculopathy ) can occur with any severity of retinopathy.
Clinically significant macular edema (CSME)
✍️ Definition one of the following
☝️ Thickening within 500 μm of the macular center
☝️ Hard exudate within 500 μm of the macular center with associated thickening of adjacent retina
☝️ Zone of retinal thickening 1 disc area in size, any part of which is within 1 disc diameter of the macular center
🛑 Asymmetric diabetic retinopathy is usually due to carotid disease (on either side)
🛑 Main cause of vision loss in NPDR
☝️ macular edema
☝️ macular ischemia
🛑 Main causes of vision loss in PDR
☝️ tractional maculopathy
☝️ tractional RD (TRD)
☝️ neovascular glaucoma (NVG)
☝️ vitreous hemorrhage (VH)
🛑 common diabetic sequelae
✍️ Diabetic cataract
☝️ aldose reductase pathway converts glucose into sorbitol and fructose causing osmotic effect
☝️ aldose reductase also converts galactose into galactitol (which causes cataracts in galactosemia)
✍️ Diabetic iridopathy
☝️ iris NV
☝️ lacy vacuolization of iris pigment epithelium in 40%
☝️ glycogen-filled cysts in iris pigment epithelium
✍️ Papillitis
☝️acute disc swelling
☝️ vision usually 20/50
☝️ 50% bilateral
☝️ may have VF defect
☝️ most recover to 20/30
✍️ Isolated cranial nerve palsies
☝️ CN 3 ( including pupil- sparing CN 3 palsy)
☝️ CN 4
☝️ CN 6
✍️ Pupillary abnormalities
☝️ light-near dissociation
✍️ Fluctuation in refractive error
☝️ due to osmotic effect on crystalline lens from unstable blood sugar levels
☝️ Don’t change glasses power if HBA1c > 7
✍️ NVG
Managing diabetic retinopathy
✍️ none/background
☝️ Discharge to community screening service for annual review
☝️ if significant systemic disease,
consider review at 9–12 monthly by hospital eye service
✍️ Pre-proliferative
☝️ Observe 4–6-monthly
☝️ consider early PRP in select cases
* in single eye patient where first eye lost from PDR
* prior to cataract surgery
✍️ Proliferative active
☝️PRP 1 or 2 sessions (≥1,000 × 200 to 500 microns × 0.1s) this should occur on the same day or within 2wk
☝️ In young patients with type 1 diabetes, PRP should be delivered over 3–4 sessions, as increased risk of macular oedema post-PRP if excess burns applied in single session
☝️ anti-VEGF therapies is optional
✍️ Proliferative (regressed)
☝️ Observe 4 to 6 monthly
☝️ signs of decreased neovascularization activity
* regression of vessels ± fibrosis
* resolution of retinal haemorrhages
* decreases in retinal vessel dilatation and tortuosity
✍️ Proliferative with coexisting DMO
☝️ For high-risk cases, consider combined macular laser and PRP (with completion of PRP over three sessions, rather than 1 to 2).
☝️ For low-risk cases, it may be possible to perform macular laser initially, with PRP at subsequent follow-up.
☝️ Anti-VEGF therapies may be of particular use
Managing of diabetic maculopathy
✍️ Focal leakage
☝️ Focal laser photocoagulation (n × 50–100 microns × 0.08–0.1s)
☝️ review at 3 to 4 months
✍️ Diffuse leakage
☝️ grid laser photocoagulation (n × 100–200 microns × 0.1 s)
☝️ review at 3 to 4 months
☝️ Ischaemic
☝️ FFA to confirm diagnosis
☝️ observation may be appropriate
* significant ischaemia
* no response to previous laser
✍️ Persistent maculopathy
☝️Anti-VEGF therapies
* ranibizumab approved for cases with central retinal thickness >400 microns
* intravitreal Kenacort in pseudophakic eyes
☝️ vitrectomy if vitreomacular traction or persistent VH
✍️ Rubeosis
☝️ clear media urgent PRP
☝️ media opacity use anti-VEGF therapies
☝️ monitoring NVG
🛑 indicators for poor prognosis in CSME after laser photocoagulation
☝️ Extensive macular capillary non-perfusion (ischemic maculopathy)
☝️Diffuse disease
☝️Cystoid macular edema (longstanding )
☝️Lamellar macular hole.
