Diabetic retinopathy, diabetic maculopathy

Question 1

What are the risk factors?

Answer 1

• Most important risk factor is duration of DM (seen in 71-90% of pts w > 10years of DM)
• Poor control of DM
• Cardiovascular disease, e.g. HTN, CVA
• Diabetic nephropathy – correlates to the severity of the diabetic retinopathy (DR)
• Others: HLD, smoking, obesity

Question 2

how does diabetes cause diabetic retinopathy, diabetic maculopathy?

Answer 2

Chronic hyperglycaemia 🡪 Increased retinal blood flow with impairment of autoregulation 🡪 increased shear stress 🡪 increased production of vasoactive substances, vascular leakage, increased fluid accumulation 🡪 macular oedema

Platelet dysfunction and blood viscosity: Focal capillary occlusion, focal retinal ischaemia

Ischaemia 🡪 high VEGF concentration (especially in vitreous) 🡪 neovascularisation

Question 3

what is the definition of mild NPDR?

Answer 3

At least one microaneurysm AND criteria not met for other levels of DR

Question 4

what is the definition of moderate NPDR?

Answer 4

• Haemorrhage /microaneurysm ≥ standard photograph #2A, OR

- Soft exudates (cotton wool spots), venous beading, and intra-retinal microvascular abnormalities (IRMA) definitely

Question 5

what is the definition of severe NPDR?

Answer 5

• Dot or blot haemorrhage in all 4 quadrants more than 20 per quadrant, OR
• Venous beading in ≥ 2 quadrants, OR
• Intraretinal microvascular abnormalities (IRMA) ≥ 1 quadrant

Question 6

what is the definition of PDR?

Answer 6

New vessels AND criteria not met for high-risk PDR

Question 7

what is the definition of high risk PDR?

Answer 7

• Neovascularisation of the disc (NVD) ≥ 1/3 to 1/2 disc area, OR
• Neovascularisation of the disc (NVD) and vitreous or pre-retinal haemorrhage, OR
• Neovascularisation elsewhere (NVE) ≥ 1/2 disc area AND vitreous or pre-retinal haemorrhage

Question 8

what is the definition of clinically significant macular oedema (CSMO)?

Answer 8

• Retinal thickening ≤ 500μm from the centre of the macula, OR
• Hard exudates ≤ 500 μm of the centre of the macula, if associated with retinal thickening; the thickening itself may be outside the 500 μm, OR
• Zone of retinal thickening ≥ 1 disc area (1500 μm), any part of which is located ≤ 1 disc diameter from the centre of the macula

Question 9

what are the symptoms of diabetic retinopathy & maculopathy

Answer 9

• Diffuse macular oedema (can occur at any stage of disease)
• Macular ischaemia (detected by fundus fluorescein angiography FFA – shows expanding foveal avascular zone [FAZ])
• Vitreous haemorrhage (bleed from retinal neovascularisation) – may cause acute LOV but blood is often reabsorbed and vision clears spontaneously
• Tractional retinal detachment (tRD) (after fibrosis from bleed)
• Neovascular glaucoma (NVG), which is a 2’ angle closure glaucoma – NVG initially starts off as open angle, but progresses to close angle after bleed and fibrosis of iris neovascularisation

Question 10

what are the signs of NPDR?

Answer 10

• Cotton wool spots/“soft exudates” (infarct of the nerve fibre layer)
• Hard exudates (leakage of lipid & proteinaceous material due to increased vascular permeability)
• Intra-retinal dot and blot haemorrhages
• Microvascular abnormalities (microaneurysms due to weakened vascular walls from pericyte loss, occluded vessels, dilated or tortuous vessels)

Question 11

what is the treatment for macular oedema (CSMO)?

Answer 11

Grid macular laser: low intensity laser, C shaped around macula to stimulate retinal pigment epithelium RPE (which usually pumps fluid out from retina). NO HIGH INTENSITY LASER -> will destroy macula and cause central scotoma

Intravitreal anti-VEGF, e.g. ranibizumab: effect only lasts 4-6 weeks -> need repeated injections to stabilise condition. Often used in combi w grid laser – relieve oedema rapidly first w anti-VEGF, and then do macula laser (when architecture is clearer).

Question 12

what is the treatment for proliferative diabetic retinopathy (PDR) (neovascularisation)?

Answer 12

Pan-retinal photocoagulation (PRP) continues to be the mainstay of treatment (gold standard), while intravitreal anti-VEGF injections and other modalities remain as adjuncts

Mechanism of action: Photocoagulation destroys peripheral retina to decrease metabolic O2 dd 🡪 reduce ischaemic drive 🡪 reduce VEGF production 🡪 reduce neovascularization, and stimulates anti-angiogenic actors from retinal pigment epithelium (RPE) 🡪 arrests neovascularisation

Treatment is generally restricted to the area outside the temporal vascular arcades

Question 13

what are the complications of diabetic retinopathy?

Answer 13

Visual loss

• Diffuse macular oedema (DMO)
• Macular ischaemia
• 2’ angle closure glaucoma (NVG)
• Tractional retinal detachment (TRD)
• Vitreous haemorrhage

No visual loss
- Diabetic papillopathy