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

Diabetic Retinopathy  Diabetic retinopathy is one of the commonest causes of blindness in the UK and America in ages

Pathology: Leakage Leakage Ischaemia Ischaemia Microangiopathy

1. Leakage

2.Ischaemia

Pathogenesis: Chronic hyperglycaemia

Pathogenesis: chronic hyperglycaemia glycosylation of protein/basement membrane.

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

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

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

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

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

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

1.Haemorrhage

2.Scaring

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)

(NVE)

(NVD)

( rubeosis iridis )

The natural history of neovascularisation – note lack of laser treatment scars

The natural history of neovascularisation – note lack of laser treatment scars

The natural history of neovascularisation – note lack of laser treatment scars

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

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

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

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

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

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

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

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

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’

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

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

What is happening here?

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

1 DD

Management of DR  Medical  Surgical laser laser vitrectomy vitrectomy

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

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

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

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.

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.

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 <0.001). Data from The Diabetes Control and Complications Trial Research Group, N Engl J Med 1993; 329:977.

Cumulative rates of developing severe visual loss in untreated eyes with advanced retinopathy and those treated with argon laser or xenon arc photocoagulation. Photocoagulation slowed the rate of progressive disease by more than 50 percent. Data from The Diabetic Retinopathy Study Research Group, Ophthalmology 1981; 88:583. PRP

Cumulative rate of developing severe visual loss in untreated eyes with macular edema and eyes treated with focal laser therapy. Photocoagulation slowed the rate of severe visual loss. Data from Early Treatment Diabetic Retinopathy Study Research Group, Ophthalmology 1991; 98:766. MPC

ضمن عرض پوزش بدلیل حجم بالای LECTUER ادامه اسلایدها امکان پذیر نمیباشد در صورت نیاز به ادامه لطفا به واحد سمعی و بصری مرکز آموزشی درمانی فیض مراجعه و یا با شماره تلفن داخلی 392 تماس حاصل نمائید با تشکر