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Nonsurgical management of diabetic retinopathy Ghanbari MD 1388:11:30

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Diabetic Retinopathy Diabetic retinopathy is one of the commonest causes of blindness in the UK and America in ages 20-74.

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Pathology: Leakage Leakage Ischaemia Ischaemia Microangiopathy

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1. Leakage

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2.Ischaemia

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Pathogenesis: Chronic hyperglycaemia

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Pathogenesis: chronic hyperglycaemia glycosylation of protein/basement membrane.

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Pathogenesis: chronic hyperglycaemia glycosylation of protein/basement membrane loss of pericytes

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Pathogenesis: chronic hyperglycaemia glycosylation of protein/basement membrane loss of pericytes reduced O 2 transport tissue hypoxia

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Pathogenesis: chronic hyperglycaemia glycosylation of protein/basement membrane loss of pericytes reduced O 2 transport tissue hypoxia Microaneurysms

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Pathogenesis: chronic hyperglycaemia glycosylation of protein/basement membrane loss of pericytes reduced O 2 transport tissue hypoxia vaso-formative factors produced (TGF- & VEGF)

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Pathogenesis: chronic hyperglycaemia glycosylation of protein/basement membrane loss of pericytes reduced O 2 transport tissue hypoxia vaso-formative factors produced (TGF- & VEGF) Neo-vascularisation

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Pathogenesis: chronic hyperglycaemia glycosylation of protein/basement membrane loss of pericytes reduced O 2 transport tissue hypoxia vaso-formative factors produced (TGF- & VEGF) Neo-vascularisation Haemorrhage / Scarring

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1.Haemorrhage

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2.Scaring

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new vessels new vessels grow on posterior vitreous face grow on disc (NVD) grow in the periphery (NVE) grow on iris if ischaemia is severe (NVI)

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(NVE)

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(NVD)

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( rubeosis iridis )

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The natural history of neovascularisation note lack of laser treatment scars

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The natural history of neovascularisation note lack of laser treatment scars

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The natural history of neovascularisation note lack of laser treatment scars

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In summary diabetic patients loose vision from: 1. Retinal edema affecting the fovea 2. Vitreous haemorrhage 3. Scaring/ tractional retinal detachment

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Classification 1: retinopathy No retinopathy mild moderate Severe Very severe proliferative retinopathy non-proliferative retinopathy

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Classification 1: retinopathy No retinopathy mild moderate Severe Very severe proliferative retinopathy non-proliferative retinopathy laser observe / re-screen

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Classification 2: maculopathy No maculopathy observable maculopathy referable maculopathy clinically significant maculopathy

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Classification 2: maculopathy No maculopathy observable maculopathy referable maculopathy clinically significant maculopathy laser observe / re-screen

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Signs of non proliferative retinopathy microaneurysms / dot + blot haemorrhages hard exudate cotton wool patches abnormalities of venous calibre Intra-retinal microvascular abnormailities (IRMA)

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mild non proliferative retinopathy microaneurysms +/or very small blots only

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moderate non proliferative retinopathy microaneurysms dot + blot haemorrhages venous calibre changes in only 1 quadrant (1/4)

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severe non proliferative retinopathy Microaneurysms plus: > 4 per quadrant of dot + blot haemorrhages > 2 quadrants of venous tortuosity/looping > 1 quadrant of IRMA 4,2,1 rule

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Very severe non proliferative retinopathy 2 of 4,2,1 rule

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Proliferative retinopathy New vessels disc (NVD) New vessels elsewhere (NVE) Treated if you see laser scars; untreated if no laser

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What is happening here?

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Classification 2: maculopathy No maculopathy observable maculopathy referable maculopathy clinically significant maculopathy

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1 DD

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Management of DR Medical Surgical laser laser vitrectomy vitrectomy

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Risk factors Duration of diabetes HBP Hyperglycemia Smoking Hyperlipidemia Pregnancy Weight Type 1 diabetes

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Panretinal and macular photocoagulation were established as the gold standard of treatment, supported by the data of the (ETDRS) and the (DRS).

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A number of molecular mechanisms connect hyperglycemia to the vascular damage,: protein kinase C (PKC), vascular endothelial growth factor (VEGF).

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Percent of diabetic patients with retinopathy according to duration of disease in patients under the age of 30 years who were treated with insulin (primarily type 1 diabetes) and patients over the age of 30 years who were not treated with insulin (primarily type 2 diabetes). Retinopathy increased over time in both groups, affecting virtually all patients with type 1 diabetes by 20 years. The increased incidence in type 2 diabetes at three years is a probable reflection of the difficulty in determining the time of onset of that disease. Data from Klein, R, Klein, BE, Moss, SE, et al, Arch Ophthalmol 1984; 102:520,527.

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Risk of sustained progression of retinopathy in patients with type 1 diabetes according to the mean glycosylated hemoglobin values at six-month intervals (green line). Better glycemic control was associated with a lesser rate of progressive retinopathy. The red lines represent the 95 percent confidence intervals. Data from The Diabetes Control and Complications Trial Research Group, N Engl J Med 1993; 329:977.

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Cumulative incidence of progressive retinopathy in patients with type 1 diabetes and very mild to moderate nonproliferative retinopathy who were treated with either conventional (dashed line) or intensive (solid line) insulin therapy for nine years. There was an increasing benefit of intensive therapy over time, although intensive therapy was associated with transient worsening in the first year (p